1. Chronic heavy metal poisoning can result from excessive long term exposure to certain metals through occupational, environmental, or nutritional sources. Common heavy metals that can cause toxicity include arsenic, lead, copper, iron, and mercury.
2. Heavy metals are absorbed through ingestion, inhalation, or skin contact and accumulate in tissues like the liver, kidneys, and bones, causing a variety of symptoms depending on the metal.
3. Diagnosis involves tests of blood, urine, hair or other tissues to detect heavy metal levels. Treatment focuses on chelation therapy using agents like BAL, penicillamine, or DMSA to remove metals from the body. Supportive care is also provided for affected organ systems
Precipitation formation
Precipitation condition and precipitation purity
Methods in Precipitation titration
Mohr method
Volhard method
Fajans method
Titrations with precipitating agents are useful for determining certain analytes e.g. Cl- can be determined when titrated with AgNO3.
Detection of end point:
Chemical
-Precipitation Type - Mohr’s method
-Adsorption – Fajan’s method
-For silver analyses –Volhard method
Sensors –Potentiometric or amperometric
The chemical types are also classified into:
1.Indicators reacting with titrant forming specific color.
2.Adsorption indicators.
Anatacid || B pharmacy First Year || Presentation || kkwagh ||
This presentation is helpful for your study
This Presentation Contain
• Introduction
• characteristics of ideal antacid
• classification of antacid
• Some common use antacid
Precipitation formation
Precipitation condition and precipitation purity
Methods in Precipitation titration
Mohr method
Volhard method
Fajans method
Titrations with precipitating agents are useful for determining certain analytes e.g. Cl- can be determined when titrated with AgNO3.
Detection of end point:
Chemical
-Precipitation Type - Mohr’s method
-Adsorption – Fajan’s method
-For silver analyses –Volhard method
Sensors –Potentiometric or amperometric
The chemical types are also classified into:
1.Indicators reacting with titrant forming specific color.
2.Adsorption indicators.
Anatacid || B pharmacy First Year || Presentation || kkwagh ||
This presentation is helpful for your study
This Presentation Contain
• Introduction
• characteristics of ideal antacid
• classification of antacid
• Some common use antacid
This slide contains the details from topic, "Dental Product", B.Pharm 1st Semester, Pharmaceutical Inorganic Chemistry.
Dental Product
Desensitizing Agent
Dental Caries
Dentifrices
Role of Fluoride
Limit tests, Introduction, Definition,
Limit Test For Chlorides
Limit Test For Sulphates
Limit Test For Iron
Limit Test For Lead
Limit Test For Arsenic
Official compound of iodine and iodine contain preparation. Iodine uses, preparation, assay, storage, their physical, chemical properties and deficiency .
DEFINATION
TYPES OF COUGH
CLASSIFICATION OF EXPECTORANT AND MECHANISM OF ACTION
DEFINATION OF EMETICS
MECHANISM OF ACTION OF EMETICS
COMPOUND RELATED TO EXPECTORANT.
Iron poisoning (physical appearance, sources- dietary and environmental, uses- industrial and biological, usual fatal dose, toxicokinetics, mode of action, clinical features, diagnosis, treatment, autopsy features
This slide contains the details from topic, "Dental Product", B.Pharm 1st Semester, Pharmaceutical Inorganic Chemistry.
Dental Product
Desensitizing Agent
Dental Caries
Dentifrices
Role of Fluoride
Limit tests, Introduction, Definition,
Limit Test For Chlorides
Limit Test For Sulphates
Limit Test For Iron
Limit Test For Lead
Limit Test For Arsenic
Official compound of iodine and iodine contain preparation. Iodine uses, preparation, assay, storage, their physical, chemical properties and deficiency .
DEFINATION
TYPES OF COUGH
CLASSIFICATION OF EXPECTORANT AND MECHANISM OF ACTION
DEFINATION OF EMETICS
MECHANISM OF ACTION OF EMETICS
COMPOUND RELATED TO EXPECTORANT.
Iron poisoning (physical appearance, sources- dietary and environmental, uses- industrial and biological, usual fatal dose, toxicokinetics, mode of action, clinical features, diagnosis, treatment, autopsy features
Clinical symptoms and management of Arsenic poisoningSoujanya Pharm.D
This presentation includes Introduction & physical appearance of arsenic, usual fatal dose, toxicokinetics and mode of action of arsenic, Clinical (toxic) symptoms, diagnosis and management of Arsenic poisoning
This presentation gives the description that which heavy metals are toxic for human health and how they interact with the metabolic processes and cause different diseases in human beings. There are also the threshold values given to help prevent the toxicity....
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
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
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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.
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
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
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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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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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.
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.
2. Heavy metals
Metallic elements in trace quantities are essential for various biological
processes.
- activate enzymes
- facilitate exchange and utilization of oxygen and carbon dioxide.
Common source
Through food, excessive exposure (nutritional, occupational, or
environmental)
progressive accumulation and toxicity
serious consequences.
3. Arsenic
- Twentieth most common element in the earth’s crust, having a concentration
of 1.8 ppm.
- Commonest source of acute heavy metal poisoning, and is second only to
lead in the incidence of chronic toxicity.
PHYSICAL APPEARANCE
Arsenic is a metalloid.
Silver-grey or tin-white, shiny, brittle,
crystal- line and metallic-looking element.
USUAL FATAL DOSE
- 200 to 300 mg for arsenic trioxide.
- Arsenate (pentavalent form) <TOXIC arsenite (trivalent form)
Reason- less water soluble.
- The most toxic form is arsine gas (25 to 30 ppm can be lethal in 30 minutes).
4. TOXICOKINETICS AND MODE OF ACTION
Absorption - oral, inhalational, and cutaneous routes
redistributed to the liver, lungs, intestinal wall, and spleen
binds to the sulfydryl groups of tissue proteins replaces phosphorus in the
bone, deposited also in hair
*doesn’t cross BBB, but crosses placenta readily.
intrauterine death of the foetus
less severe intoxications it can cause respiratory distress of the newborn
6. DIAGNOSIS
1. Urine level
If the 24 hour excretion of arsenic exceeds 100 mcg, it is indicative of toxicity.
• However, ingestion of seafood can interfere with interpretation since
considerable concentrations of organic arsenicals such as arsenobetaine and
arsenocholine may be present in shellfish, cod, haddock, etc., although it is
not associated with toxic effects. In such cases, the analysis must be
repeated after 2 days of “no fish” diet.
2. Blood level
Less reliable than urine level
Blood level of arsenic < 7 mcg/100 mL (70 mcg/L) is generally considered in
the normal range.
3. Hair level
Cannot discriminate between external deposition and toxic accumulation,
pubic hair instead of scalp hair should be sent for quantitation.
7. 4. Radiography
Since arsenic is radiopaque, abdominal x-ray
may reveal its presence in the gastrointestinal tract in acute poisoning.
5. Additional investigations
a. Monitor CBC, serum electrolytes, urinalysis (for proteinuria, haematuria
or pyuria), liver and renal function tests.
b. Obtain an ECG and institute continuous cardiac monitoring in
symptomatic patients.
c. Obtain a chest radiograph in patients with severe poisoning or pulmonary
effects.
d. Initial and periodic biological monitoring and medical surveillance are
required for employees exposed to arsenic.
8. TREATMENT
1. Supportive measures: gastric lavage, intravenous fluids, cardiac
monitoring, etc.
2. Chelation therapy: This can be done with BAL (British Anti Lewisite
or dimercaprol), penicillamine, DMSA (Dimercapto succinic acid),
or DMPS (Dimercapto propane sulfonic acid).
The usual agent employed is BAL at a dose of 3 to 5 mg/kg
intramuscularly every 4 hours until the urinary arsenic excretion dips
below 50 mcg/24 hours. Usual duration of therapy is 7 to 10 days.
In patients who are not allergic to penicillin, penicillamine can be given
orally at a dose of 100 mg/kg/day, 6th hourly for 5 days.
3. Haemodialysis or exchange transfusion.
CASE STUDY: A devastating health crisis (endemic hydroarsenicism)
began to unfold in West Bengal in the early 1980s due to exposure to
arsenic laced well water.
9. Lead
Commonest metal involved in chronic poisoning.
One of the first metals known to man, widely used for domestic, industrial, and
therapeutic purposes.
PHYSICAL APPEARANCE
Elemental lead - highly lustrous, heavy, silvery-grey metal, bluish tint as it
tarnishes in air.
Quite soft and malleable.
Its salts occur as variously coloured powders or liquids and are used widely in
industry and at home, producing cumulative toxicity on chronic exposure.
Uses:
sugar of lead sindoor
white lead surma
litharge
10. USUAL FATAL DOSE
The average lethal dose is said to be 10 gm/70 kg
100 mg/kg for tetraethyl lead.
TOXICOKINETICS
Absorption – oral, inhalation, skin
Stored in bones as phosphate and carbonate.
Accumulated in radius, tibia, and femur
“lead lines” observed on x-ray
skeletal lead are released from bone into the blood stream toxicity
symptoms
Excreted primarily in the urine (about 65%) and bile (about 35%).
11. MODE OF ACTION
- Lead combines with sulfhydryl enzymes decreases haeme synthesis by
inactivating the enzymes involved results in anaemia.
- Increases haemolysis - immature red cells are released into circulation
- CNS oedema decreased nerve conduction
- CVS, Kidney, reproductive organs, gout.
CLINICAL FEATURES
a. Mild toxicity (BL 40-60 mcg/100ml)
– Myalgia
– Paraesthesia
– Fatigue
– Irritability
– Abdominal discomfort.
12. b. Moderate Toxicity (BL 60 to 100 mcg/100 ml) :
– Arthralgia (especially nocturnal)
– Muscular exhaustibility
– Tremor
– Headache
– Diffuse abdominal pain
– Anorexia, metallic taste, vomiting – Constipation
– Weight loss
– Hypertension.
c. Severe Toxicity (BL more than 100 mcg/100 ml) :
– Lead palsy: Wrist drop or foot drop
– A bluish black lead line on gums (Burton’s line)
– Lead colic: Intermittent severe abdominal cramps.
– Lead encephalopathy
13. DIAGNOSIS
1. Blood
2. Urine
3. Bone
TREATMENT
1. Severe acute poisoning with encephalopathy:
a. BAL 4 mg/kg immediately (in children).
b. Cranial CT scan, if cerebral oedema
- Diuretics
» Mannitol 20%: Adult: 1 to 1.5 gm/kg by infusion over 10 to 20 minutes. Child:
0.5 to 1 gm/kg by IV infusion over 10 to 20 minutes.
» Glycerol: 0.3 to 1 gm/kg orally.
» Loop Diuretics: Furosemide and/or ethacrynic acid (as an adjunct)
» Corticosteroids: Dexamethasone
low dose - 16 mg/day in divided doses.
high dose— 1 to 2 mg/kg/day in divided doses.
14. c. KUB: to rule out lead chips in GI tract.
d. For seizures: intravenous diazepam
e. Foley catheterisation
f. CaNa2 EDTA 75 mg/kg/day IV infusion.
15. Copper
PHYSICAL APPEARANCE
lustrous, ductile, malleable, odourless solid with a distinct golden-red or reddish-
brown colour.
Third most abundant trace element in the body
Important catalyst for heme synthesis and iron absorption.
USUAL FATAL DOSE
About 10 to 20 grams of copper sulfate.
DIAGNOSIS
1. Serum caeruloplasmin level
2. Blood copper level
3. Urine level
4. Radiography
16. CLINICAL FEATURES
a. Chronic inhalation of copper sulfate cause vineyard sprayer’s lung disease
histiocytic granulomatous lung.
Liver damage is also common.
b. Chronic contact with swimming pool water containing algicidal copper
chemicals green hair discolouration.
c. Cooking in copper or brass vessels;
leaching of copper containers in which carbonated water, citrus fruit juices, and
other acidic beverages have been stored.
copper poisoning due to verdigris.
d. Chronic copper toxicity -- hallmark of Wilson’s disease,
an autosomal recessive genetic disorder in which there is deficiency of
caeruloplasmin. Discolouration of the peripheral part of the cornea by deposition
of copper in parenchymal tissue.
e. Metal fume fever, wheezing and rales.
f. Skin exposure can produce severe irritation, itching, erythema, dermatitis and
eczema.
17. TREATMENT
1. Haemodialysis
2. Administration of egg white or milk orally
3. Stomach wash
4. Use of chelators
D-penicillamine
Dimercaprol
Unithiol
Calcium disodium edetate
5. Symptomatic measures
6. Eye exposure
7. Dermal exposure
8. Disorder of hair colour
18. Iron
PHYSICAL APPEARANCE
silvery white in colour
it is an essential element and deficiency results in anaemia.
USUAL FATAL DOSE
The usual fatal dose corresponds to about 200 to 250 mg of elemental iron per
kg of body weight.
TOXICOKINETICS
Iron poisoning occurs when serum iron level exceeds the total iron-binding
capacity (TIBC), resulting in free circulating iron in the bloodstream.
19. MODE OF ACTION
Free Iron causes:
Massive postarteriolar dilatation which results in venous pooling.
Increased capillary permeability resulting in decreased plasma volume.
Oxidation of ferrous to ferric iron releasing hydrogen ions.
Subsequent hydration of ferric iron results in metabolic acidosis.
Inhibits mitochondrial function leading to hepatic damage, hypoglycaemia,
and hypoprothrombinaemia.
Inhibits thrombin-induced conversion of fibrinogen into fibrin.
Has a direct corrosive action on the GI mucosa.
20. CLINICAL FEATURES
Stage I (0.5 to 2 hours)
Stage II (recovery- false security)
Stage III (2 to 12 hours after Stage I)
Stage IV (2 to 4 days)
Stage V (days to weeks)
DIAGNOSIS
1. x-ray
2. Serum iron level
3. Total leucocyte count (TLC)
4. Chelation challenge test
5. Qualitative desferrioxamine colour test (QDCT)
21. TREATMENT
1. Stomach wash
2. Magnesium hydroxide solution (1%)
3. Correction of hypovolaemia, and metabolic acidosis.
4. Chelation therapy:
Chelation can be done either with desferrioxamine (parenteral) or deferiprone
(oral).
22. Mercury
PHYSICAL APPEARANCE
heavy, silvery liquid
USUAL FATAL DOSE
The amount of ingested mercury that would be fatal to a man is estimated at 100
grams.
Mercuric chloride: 0.5 to 1 gm/70 kg
Mercurous chloride : 1.5 to 2 gm/70 kg
TOXICOKINETICS
Inhalation elemental Hg absorbed through alveolar membrane enters blood
stream converted to mercuric ions(Hg2+) renal tubular damage during
excretion.
24. DIAGNOSIS
1. x-ray.
2. Blood mercury level
3. Urine mercury level
4. Hair analysis
TREATMENT
1. Chelation therapy—
– BAL (British Anti Lewisite)
- 100 mg by deep IM, every 4 hours for 48 hours, followed by 100 mg every 8
hours for 8 to 10 days.
OR
– DMPS ( 2,3 DiMercapto Propane-1-Sulfonate)
- 5 mg/kg IV, or 6 infusions of 250 mg/day, followed by 100 mg orally twice a day
for 24 days.
OR
– DMSA (Meso 2,3 DiMercapto Succinic Acid, or Succimer)
- 30 mg/kg/day orally for 5 days, followed by 20 mg/day for 14 days.