During pregnancy, women undergo certain hormonal and physiological changes that can affect their mouths.
EFFECT OF PREGNANCY ON PERIODONTAL TISSUES
PREGNANCY GINGIVITIS
EFFECT OF PERIODONTITIS ON PREGNANCY
PRETERM LOW BIRTH WEIGHT (PLBW) INFANTS
PREECLAMPSIA
Periodontitis is a complex infection initiated by bacteria –tissue destruction.
Host: the organism from which a parasite obtains its nourishment/ an individual who receives a graft
Modulation: the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment
Definition of periodontal pocket, classification, Histopathology of periodontal pocket, microflora involved, pathogenesis, periodontal pocket as a healing lesion, microtopography of root surface, treatment of periodontal pocket
Periodontitis is a complex infection initiated by bacteria –tissue destruction.
Host: the organism from which a parasite obtains its nourishment/ an individual who receives a graft
Modulation: the alteration of function or status of something in response to a stimulus or an altered physical or chemical environment
Definition of periodontal pocket, classification, Histopathology of periodontal pocket, microflora involved, pathogenesis, periodontal pocket as a healing lesion, microtopography of root surface, treatment of periodontal pocket
Oral-systemic link has been termed Periodontal Medicine. Significance: Periodontal disease is preventable and readily treatable, thus providing many new opportunities for preventing and improving several systemic diseases.
FOCAL INFECTION: Localized or Generalized infection caused by dissemination of microorganisms or toxic products from focus of infection.
FOCUS OF INFECTION Confined area that
(1) contains pathogenic microorganisms
(2) can occur anywhere in body
Diseases/Conditions affected by periodontitis
A PREGNANCY, PREECLAMPSIA
B ISCHEMIC HEART DISEASES, STROKE
C DIABETES MELLITUS
D PNEUMONIA, COPD
E OSTEOPOROSIS
F CANCER
G ALZHEIMER’S DISEASE
H. RHEUMATOID ARTHRITIS
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Host modulation therapy is recommended as an adjunct to scaling and root planing in the periodontal therapy. The basic purpose of host modulation therapy is to restore the balance between pro-inflammatory and anti-inflammatory mediators.
Systemic Peridoontology, link between systemic health and periodontology, diabetes and periodontology, Pregnancy and Peridotology,Nutrition and periodontology
Periodontitis is a chronic infectious inflammatory disease caused by microbes; however the presence of microbes is not enough for the cause of its complex nature of disease. Inflammation is the prime cause of periodontal disease. It commences with the aggregation of pathogenic microbes that induce the host to stimulate a cascade of inflammatory response reactions which in-turn leads to the destruction of the host tissues itself. There is a complex interplay of innate and adaptive immune responses which fights against the pathogens by direct interaction or by release of certain molecules including cytokines.
Cytokines are cell signalling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma. Cytokine biology reveals that there are some subsets of cytokines which are pro-inflammatory cytokines which stimulate the inflammatory responses and cause tissue destruction.
A periodontist is expected to have a sound basis of the cytokine profile to understand the pathogenesis of periodontitis and also to discover the new treatment modality of anti-cytokine therapy.
Hormonal changes in female patients and periodontal diseasesPerio Files
Hormonal fluctuations and gingival changes in female patient occurs during Puberty, Menstruation, Pregnancy, Menopause,
Oral Contraceptives, Osteoporosis.
NEED FOR ASSESSMENT: To identify high-risk stages of female patients in prior so that preventive and treatment procedures can be tailored
Oral-systemic link has been termed Periodontal Medicine. Significance: Periodontal disease is preventable and readily treatable, thus providing many new opportunities for preventing and improving several systemic diseases.
FOCAL INFECTION: Localized or Generalized infection caused by dissemination of microorganisms or toxic products from focus of infection.
FOCUS OF INFECTION Confined area that
(1) contains pathogenic microorganisms
(2) can occur anywhere in body
Diseases/Conditions affected by periodontitis
A PREGNANCY, PREECLAMPSIA
B ISCHEMIC HEART DISEASES, STROKE
C DIABETES MELLITUS
D PNEUMONIA, COPD
E OSTEOPOROSIS
F CANCER
G ALZHEIMER’S DISEASE
H. RHEUMATOID ARTHRITIS
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
Host modulation therapy is recommended as an adjunct to scaling and root planing in the periodontal therapy. The basic purpose of host modulation therapy is to restore the balance between pro-inflammatory and anti-inflammatory mediators.
Systemic Peridoontology, link between systemic health and periodontology, diabetes and periodontology, Pregnancy and Peridotology,Nutrition and periodontology
Periodontitis is a chronic infectious inflammatory disease caused by microbes; however the presence of microbes is not enough for the cause of its complex nature of disease. Inflammation is the prime cause of periodontal disease. It commences with the aggregation of pathogenic microbes that induce the host to stimulate a cascade of inflammatory response reactions which in-turn leads to the destruction of the host tissues itself. There is a complex interplay of innate and adaptive immune responses which fights against the pathogens by direct interaction or by release of certain molecules including cytokines.
Cytokines are cell signalling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma. Cytokine biology reveals that there are some subsets of cytokines which are pro-inflammatory cytokines which stimulate the inflammatory responses and cause tissue destruction.
A periodontist is expected to have a sound basis of the cytokine profile to understand the pathogenesis of periodontitis and also to discover the new treatment modality of anti-cytokine therapy.
Hormonal changes in female patients and periodontal diseasesPerio Files
Hormonal fluctuations and gingival changes in female patient occurs during Puberty, Menstruation, Pregnancy, Menopause,
Oral Contraceptives, Osteoporosis.
NEED FOR ASSESSMENT: To identify high-risk stages of female patients in prior so that preventive and treatment procedures can be tailored
Periodontal Disease: A Possible Risk-Factor for Adverse Pregnancy OutcomeDr. Anuj S Parihar
Bacterial invasion in subgingival sites especially of gram-negative organisms are initiators for periodontal diseases. The periodontal pathogens with persistent inflammation lead to destruction of periodontium. In recent years, periodontal diseases have been associated with a number of systemic diseases such as rheumatoid arthritis, cardiovascular-disease, diabetes mellitus, chronic respiratory diseases and adverse pregnancy outcomes including pre-term low-birth weight (PLBW) and pre-eclampsia. The factors like low socio-economic status, mother’s age, race, multiple births, tobacco and drug-abuse may be found to increase risk of adverse
pregnancy outcome. However, the same are less correlated with PLBW cases. Even the invasion of both aerobic and anerobic may lead to inflammation of gastrointestinal tract and vagina hence contributing to PLBW. The biological mechanism involved between PLBW and Maternal periodontitis is the translocation of chemical mediators of inflammation. Pre-eclampsia is one of the commonest cause of both maternal and fetal morbidity as it is characterized by
hypertension and hyperprotenuria. Improving periodontal health before or during pregnancy may prevent or reduce the occurrences of these adverse pregnancy outcomes and, therefore, reduce the maternal and perinatal morbidity and mortality. Hence, this article is an attempt to review the relationship between periodontal condition and altered pregnancy outcome.
32-year-oldprimigravida, CATB2, Covid positive patient with acute onset of facial palsy, fever, sore throat and productive cough referred from a peripheral hospital came for caesarian section. Past history revealed occurrence of juvenile dermatomyositis for which she took steroids for one and a half year which was slowly weaned off. Prevalence of dermatomyositis is 1to 8 in 100,000. She was started on steroids which was to be continued for a week after caesarian section. She was on paracetamol and cefuroxime on admission. Basic investigations were normal. Caesarian section was done in covid theater following covid protocols under subarachnoid anesthesia Baby had an APGAR score of 9 and was covid negative. Mothers’ recovery was slow. Facial deviation got corrected in 4to 5 months. Ptosis persisted even after 9months and is on treatment. Dermatomyositis is an uncommon inflammatory disease that affects mainly proximal muscle limiting day to day activities. But it can affect respiratory, cardiac and gastrointestinal systems, eyes and joints. Diagnosis is by muscle biopsy and an increase in muscle enzymes. Pregnancy during remission period is safe. But pregnancy can provoke the disease. Skin changes usually precedes muscle symptoms, though we could not notify any lesions. Lung involvement is prominent, and covid also carries the same amount of risk with respiratory system. Systemic glucocorticoids are the first line of treatment. Immunosuppressant drugs Azathioprine and methotrexate are added as second line of therapy, though these drugs are unsafe during pregnancy. Intravenous immunoglobulin, give good outcome during pregnancy. Plasmapheresis is also beneficial. Most of the pregnant patients end up in caesariansection. Regionalanesthesia is the choice of anesthesia. Covid patients with respiratory infections, maintaining saturation above90%, choice of anesthesia is usually regional anesthesia.
Key Words: Juvenile Dermatomyositis, COVID, Cesarian Section
Classification of chemical antiplaque agents
1. FIRST GENERATION AGENTS
Poor substantivity and thus used 4-6 times daily.
Reduces plaque score by 20-50%
Examples:
Antibiotics like Penicillin, Erythromycin, Metronidazole
2. SECOND GENERATION AGENTS
Reduce plaque score by 70-90%
Used twice daily
Example: Bisbiguanides, Chlorhexidine, Alexidine
3. THIRD GENERATION AGENTS
Effective against specific periodontal pathogens
Example: Delmopinol
II. Vehicles for delivery of chemical agents
a. Toothpastes
b. Sprays
c. Irrigators
d. Chewing gums
e. Mouthwashes (Listerine, Chlorhexidine, Triclosan, Fluorides, Hydrogen peroxides, Povidone iodine)
Analgesic is a drug that relieves pain by acting on the CNS or on the peripheral pain mechanism without altering consciousness
Opioid analgesics
Non Opioid analgesics (NSAIDs)
NSAIDs are non-steroidal anti-inflammatory drugs. These are not only pain killers but also are anti-inflammatory drugs that are widely used in dentistry. These are weaker analgesics, also called nonnarcotic or aspirin-like or antipyretic analgesics. They do not depress CNS, do not produce physical dependence, and have no abuse liability. They act primarily on peripheral pain mechanisms.
It is a naturally occurring, semi-synthetic, or synthetic type of anti-infective agent that destroys or inhibits the growth of selective microorganisms, generally at low concentrations.
These drugs are used extensively in dentistry for two main reasons: to prevent an infection (chemoprophylaxis) and in the treatment of an infection. Their use in the management of periodontal diseases is often as an adjunct to conventional treatment.
INDICATIONS IN PERIODONTAL DISEASES
1. Patients who do not respond to conventional mechanical periodontal therapy
2. Patients with Aggressive periodontitis and other types of early-onset periodontitis
3. Patients with acute or recurrent periodontal infection
(Periodontal abscess, NUG / NUP, Peri-implantitis, Pericoronitis) associated with/without systemic manifestation)
4. Prophylaxis for medically compromised patients, endocarditis
Soft deposit that form the biofilm on teeth. Plaque is defined as structured, resilient, yellow grayish colored substance that adheres tenaciously to intra oral hard surfaces including restorations. The term plaque is derived from French word, meaning ‘to form a coverage’.Marginal plaque – cause gingivitis.
Supragingival plaque and tooth-associated subgingival plaque – cause calculus formation and root caries. Tissue-associated subgingival plaque- cause tissue destruction in periodontitis.
Cementum is the mineralized dental tissue covering the anatomical root of teeth. It begins at the cervical portion of the tooth at the cementoenamel junction till the apex. It is one of the four tissues that support the tooth in the jaw (the periodontium).
The primary function- Provides attachment to collagen fibres of the periodontal ligament. It therefore is a highly responsive tissue maintaining the integrity of the root, helping to maintain the tooth in its functional position in the mouth, and being involved in tooth repair and regeneration.
Recent advances in periodontal diagnosisPerio Files
First generation:- Conventional probes.
Second generation:- Pressure controlled visual measurement recording probes
Third generation:-Pressure controlled electronic probes with direct computer data capture.
Fourth generation : Aim at recording sequential probing positions along the gingival sulcus.
Fifth generation : Ultrasonic device attached to the 4th generation probe.
*Increase in size of gingiva. Lead to false pockets.
*Difficulties associated with it are:
Difficulty in plaque control; Aesthetic concerns; Affect mastication
Interfere with speech
*TREATMENT:
Gingivectomy is the treatment of choice to remove false pockets.
In case of true pockets (osseous defects), gingivectomy with Flap surgery is done. First Gingivectomy is done. After that flap is raised and osseous surgery is performed (either osteotomy or regenerative depending upon the type of defect). Gingivectomy is done by scalpel or electro cautery/lasers (to minimize bleeding). Gingivectomy can be done only where at least 3mm of keratinized gingiva remains after completion of surgery. So it is contraindicated in patients with lack of sufficient keratinized gingiva
*REASONS OF RECURRENCE:
Responsible factors: Residual local irritation; and systemic or hereditary conditions causing noninflammatory gingival hyperplasia.
Recurrence of chronic inflammatory enlargements immediately after treatment indicates that all irritants have not been removed. Contributory local conditions like food impaction and overhanging margins of restorations are commonly overlooked.
If the enlargement recurs after healing is complete and normal contour is attained, inadequate plaque control by the patient is the most common cause.
All about gingivitis
*definition
*classification
*Signs and Symptoms: Increased GCF, Gingival Bleeding, Color change, Consistency, Surface texture (STIPPLING), Position of Gingiva, Gingival Contour, Size.
Treatment consisits of scaling and root planing. The more inflamed a gingival unit appears clinically, the better the chances of therapeutic measures resulting in a return to normal gingival health
2017 classification of periodontal and periimpalnt diseasesPerio Files
In World Workshop 2017, American Academy of Periodontology (AAP) and European Federation of Periodontology (EFP) with expert participants updated the 1999 classification of Periodontal Diseases.
Since 1999, new evidences have emerged regarding environmental and systemic risk factors, prompting the experts to develop new classification.
All furcation defects need to be classified and their possible prognosis should be defined. The treatment of the furcation defects should be carried out accordingly. Treatment include
Osteoplasty, Odontoplasty, Tunnel preparation, Root resection, Hemisection
A brief description of all topics to recent advances,SDD, host modulation and diabetes, host modulation in smokers, chemically modified tetracyclines, bisphosphonates
It restore alveolar bone to the level existing at the time of surgery or slightly more apical to this level. Aim is to achieve positive bony architecture.
STEPS INCLUDE:
1.VERTICAL GROOVING
2. RADICULAR BLENDING
3. FLATTENING INTERPROXIMAL BONE
4. GRADUALIZING MARGINAL BONE
PREFERRED TREATMENT FOR ONE WALLED PERIODONTAL BONE DEFECTS (HEMISEPTUM)
Evidence based practice is Integration of best research evidence with clinical expertise and patient values.
Advantages: QUALITY OF CLINICAL PRACTICE IMPROVES BY INCORPORATING LATEST EFFECTIVE CLINICAL TECHNIQUES INTO PATIENT CARE.
Dental practitioner should try to adopt quality evidences in dental practice, accept evidence based new practices and letting go existing theories.
Evidence collected should be combined with clinical experience and patient preferences. Positive environment with advancement in science can help facilitate evidence based change in future.
The future of dentistry and periodontics lies in regeneration. The goals of periodontal therapy lies in not only the arrest of periodontal disease progression but also regeneration of the lost periodontal structures. This presentation provides a review of the current understanding of the regeneration of the periodontium and the procedures involved to restore the periodontal tissues around the teeth.
This topic include all the drugs that are locally applied in periodontal pocket so that their levels in GCF should be more than blood.
Advantages:
Can attain higher concentrations at base of pocket
Can use drugs that are not suitable for systemic administration
Patient compliance is not required
Alternative for patients predisposed to adverse drug reactions from systemic administration.
Reduced risk for drug resistant microbe development
Lower total drug dose
INDICATIONS:
As an adjunct to mechanical therapy in pockets of 5 mm or greater depth
In patients who are systemically compromised & cannot undergo periodontal flap surgery
Localized recurrent pockets with supportive periodontal therapy
In refractory periodontitis (that is resistant to treatment)
Inflammation and Immunity in periodontitis pptPerio Files
Local destruction of periodontium occurs mostly by activation of immune and inflammatory response, initiated by plaque. First innate immune response is activated followed by specific immune response.
Useful for BDS and MDS students
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
HI,
HERE YOU WILL FIND ALL TYPES OF PPTS OF PERIODONTICS FOR BDS AND MDS
PLS SUBSCRIBE TO MY YOUTUBE CHANNEL FOR MORE UPDATES
https://youtu.be/5zN5MZ-YGP8
Thanks for watching bye!!!
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Antimicrobial stewardship to prevent antimicrobial resistanceGovindRankawat1
India is among the nations with the highest burden of bacterial infections.
India is one of the largest consumers of antibiotics worldwide.
India carries one of the largest burdens of drug‑resistant pathogens worldwide.
Highest burden of multidrug‑resistant tuberculosis,
Alarmingly high resistance among Gram‑negative and Gram‑positive bacteria even to newer antimicrobials such as carbapenems.
NDM‑1 ( New Delhi Metallo Beta lactamase 1, an enzyme which inactivates majority of Beta lactam antibiotics including carbapenems) was reported in 2008
5. PREGNANCY GINGIVITIS (INDEX)
Pathogenesis
Effect on Microbiota
Effect of Estrogen and Progesterone
Effect on Immune system
Clinical Features
Treatment
6. During pregnancy there is increased
levels of sex steroid hormones
Main estrogen in plasma in
is estradiol; and main progesterone is
progestin
7. By the end of 3rd trimester, plasma
peak levels of these hormones are 100
ng/ml and 6ng/ml which is 10-30
times more than menstrual levels
8. PREGNANCY GINGIVITIS
Gingival inflammation, initiated by plaque, and
exacerbated by these hormonal changes in 2nd
and 3rd trimester of pregnancy, is referred as
Pregnancy Gingivitis. (seen in 30-100% cases)
First described in 1877
9. Gingival inflammatory changes
usually begin in 2nd month of
pregnancy, and in severity to 8th
month, after which there is abrupt
decrease related to reduction of sex
steroid hormone secretion.
12. . There is 55 fold increase in P.
Intermedia in subgingival
plaque
Gestational hormones act as
growth factors for P. Intermedia
by satisfying the
napthoquinone requirement
bacteria
13. .
Campylobacter level is directly
related to estradiol level
Bacteroides melaninogenicus also
increases in pregnancy (55 fold) and
in those taking contraceptives (16
fold)
15. Effect of Estrogen
Estrogen stimulates proliferation of gingival fibroblasts, synthesis
and maturation of the gingival CT.
Cause increase in leakage of leukocytes and plasma proteins from
post capillary venules by affecting the endothelial lining,
contributing to enhanced gingival inflammation↓ Keratinization along with increase in epithelial glycogen results in
decreased effectiveness of the epithelial barrier
16. Effect of Progesterone
Increased Circulatory levels of Progesterone enhances capillary
permeability and dilatation by forming gaps in endothelial
lining of vessels, resulting in increased gingival exudate
This increased gingival exudate effect caused by
progesterone is of long duration as compared
same effect produced by histamine that is of
short duration.
17. Effect of Progesterone
It inhibits collagenase activity thus resulting in
accumulation of excess collagen in connective
tissue, causing enlargement.
Increased Progesterone levels ↓ the degree of
keratinization of gingival epithelium
18. These hormones also rate of folate metabolism in oral
mucosa.
Since folate is required for tissue maintenance (DNA
formation), increased metabolism could deplete folate
stores and inhibit tissue repair.
Thus folic acid tablet is always recommended in
pregnancy
20. .
↓ Neutrophil chemotaxis and phagocytosis, along with ↓ T-cell responses causes
the suppression of immune system to plaque
Progesterone in particular stimulates the production of inflammatory mediator
PGE2
Peripheral blood lymphocytes showed a decreased response to bacterial
antigens
21. .
↓ IL-6 production by human gingival fibroblasts (upto 50%)
↓ CD4 T and B lymphocytes during pregnancy, thus CD4/CD8 ratio also
decreases, leading to an immunodeficient state.
↓ levels of Plasminogen activator inhibitor type 2 (PAI-2), an important inhibitor
of tissue proteolysis
23. Pregnancy Gingivitis
Gingival enlargement occur in 2 forms:
1. marginal and generalized
2. single or multiple tumor like masses
24. 1. Marginal enlargement
Generalized enlargement, more prominent interproximally than on
facial/lingual surface.
Enlarged gingiva is bright red or magenta, soft, friable and has a smooth
shiny surface
Spontaneous bleeding or on slightest provocation
25. 2. Tumor like enlargement
discrete, mushroom shaped, flattened spherical mass that protrudes
from gingival margin / interproximal space
Tends to expand laterally, and pressure from tongue and cheek
perpetuate its flattened appearance
Dusky red or magenta, with smooth, glistening surface that often
exhibits numerous deep red, pinpoint markings.
26. Superficial lesion, that do not invade underlying bone.
Usually painless, unless complicated by plaque accumulation.
Site – anterior papilla of maxillary teeth (most common)
Gingiva is involved in 70% of cases, followed by tongue, lips and
buccal mucosa.
27. Histopathology
Angiogranuloma
Both marginal and tumor like enlargements consisting of central
mass of CT with numerous diffusely arranged, newly formed
engorged capillaries
Chronic inflammatory infiltrate
Thickened stratified squamous epithelium, with prominent rete
pegs, intercellular bridges, and leukocytic infiltration.
28. TREATMENT
Pregnant women need to be educated on the consequences of pregnancy on
gingival tissues and thoroughly motivated in plaque control measures, with
professional treatment as required.
They are likely to be more comfortable to receive dental treatment during
the second trimester than in the first or third trimester of pregnancy,
although emergency treatment is permissible at any stage during pregnancy
29. Scaling and root planing
Treatment of tumor like gingival enlargements consist of surgical excision
The enlargement recurs unless all irritants are removed.
30. Penicillin and cephalosporin are relatively safer but
patient obstetrician consultation is warranted.
Paracetamol is the safest anti inflammatory drug
31. When to Treat
Gingival lesions in pregnancy should be treated as soon as they are
detected, although not necessarily by surgical means. 2nd trimester is the
safest period of surgical excision.
SRP and adequate oral hygiene measures may reduce the size of the
enlargement. Gingival enlargements do shrink after pregnancy, but they
usually do not disappear.
32. Lesions should be removed surgically during pregnancy only if they interfere
with mastication or produce an esthetic disfigurement that the patient
wishes to remove.
After pregnancy, the entire mouth should be reevaluated, radiographs
should be taken, and the necessary treatment undertaken.
Emphasis should be on 1) preventing gingival disease before it occurs (by
doing scaling in each trimester) and 2) treating existing gingival disease
before it worsens.
36. Preterm low birth weight (PLBW)
infants
Periodontitis is a remote gram negative infection that may play role in PLBW
infants (PLBW < 2500gm)
Premature and low-birth-weight (PLBW) infants are 40 times more likely to
die during the neonatal period. Such infants who survive the neonatal
period, face a higher risk of several neurodevelopment disturbances, health
problems (such as asthma, upper and lower respiratory infections and ear
infections) and congenital anomalies.
37. Offenbacher and co-authors in 1996 from a case controlled study
suggested that women who delivered preterm low birth weight (PLBW)
infants had poorer periodontal health than mothers with normal birth
weight infants. They found the presence of higher levels
of Porphyromonas gingivalis, Bacteroides forsythus, Actinobacillus
actinomycetemcomitans and Treponema denticola organisms normally
associated with periodontal disease in mothers of PLBW babies as
compared to normal controls.
38. In periodontal disease, transient bacteremia can occur leading to selective
colonization of undesired sites. Study by Han et al (2004) have shown that
hematogenous injection of orally related F. nucleatum in mice resulted in
preferential localization to placental blood vessels from which it crossed
the endothelium to the amniotic fluid and induced premature delivery and
stillbirths in a pattern similar to that seen in humans. This supports the
hypothesis that after transient bacteremia, oral bacteria like
F.nucleatum translocates to pregnant uterus and possibly to the fetus
hematogenously.
39. Bacterial migration from periodontal tissues into blood circulation, also
stimulate the production of inflammatory mediators and increased
prostaglandin PGE2 production responsible for uterine contraction and the
onset of preterm delivery.
F. nucleatum and P. gingivalis had been isolated from amniotic fluid and
cord blood in cases of preterm birth and neonatal sepsis by Gauthier S et
al (2011) and Katz J et al (2009) respectively.
40. Proposed mechanisms are-
Translocation of the periodontal bacteria to fetoplacental unit
Systemic dissemination of endotoxins on fetoplacental unit
Systemic dissemination of inflammatory mediators (IL-1, IL-6, TNF-α,
PGE2) on fetoplacental unit.
41. MECHANISM:
41Periodontal Infection
Bacteria & their products in
amnion
Inflammatory response with
cytokine production in
amnion
Increased amniotic
prostaglandin production
Preterm labour with
LBW infants
42. PREVENTION
Hence periodontal disease appears to be an independent risk
factor for PLBW (preterm low birth weight infants) and there is
need to expand preventive measures by introducing oral health
programs as an integral component of prenatal care for
pregnant mothers.
44. Preeclampsia
Preeclampsia is a pregnancy-specific disorder characterized by
increase in systolic arterial pressure (≥140 mmHg) and/or
diastolic pressure (≥90 mmHg) and proteinuria (≥300 mg/24 h),
after 20 weeks of gestation. It is dangerous for both mother and
fetus. Periodontitis is considered as a risk factor for it.
Etiology: An increased systemic inflammatory response to pregnancy
45. Preeclampsia
It is characterized by an abnormal vascular response to
placentation, manifesting as generalized vasospasm, activation
coagulation system and reduced organ perfusion affecting the
kidney, liver and brain.
Periodontal disease burden pregnant women systemically with
endotoxins, inflammatory cytokines and oxidative stressors at
the maternal-fetal interface, thus acting as vascular stressor
that plays a role in development of Preeclampsia in pregnancy.
46. Normal pregnancy is considered as mild pro-inflammatory state whereas
preeclampsia indicate more severe level of inflammation. The subgingival bacteria,
their products and pro-inflammatory cytokines may enter the bloodstream, reach
maternal–fetal interface, trigger/worsen maternal inflammatory response, increases
prostaglandin and cytokines levels in the plasma, causing complications in
pregnancy.
47. Prevention
Maternal periodontal disease is a preventable disease in
contrast to preeclampsia, which can be treated but is difficult to
prevent. Hence, maternal periodontal disease must be taken as
an independent risk factor for adverse pregnancy outcomes
during evaluation of the pregnant women.
48. The study by Jaiman G et al (2018) showed that birth weight of
newborn was significantly less in the preeclamptic group
suggesting that maternal preeclampsia could increase risk for
low birth weight infants.