Brief Presentation on clinical examination of Respiratory System with Report of Normal case
references:
macleod's clinical examination 13th edition
hutchinson clinical methods
R Alagappan - Manual of Practical Medicine, 4th Edition
Brief Presentation on clinical examination of Respiratory System with Report of Normal case
references:
macleod's clinical examination 13th edition
hutchinson clinical methods
R Alagappan - Manual of Practical Medicine, 4th Edition
HYPERTHYROIDISM PART-1 BY DR BASHIR ASSOCIATE PROFESSOR MEDICINE SOPORE KASHMIRProf Dr Bashir Ahmed Dar
This slide presentation on hyperthyroidism is divided into two parts.Part-1 deals with causes of hyperthyroidism.I have tried to explain and give clear understanding about the causes of hyperthyroidism which to my knowledge is made very simple and easily understandable.
Part-2 deals with signs symptoms and treatment.Treatment part has been explained in detail.I hope you will enjoy reading it.
TUBERCULOSIS HAS BEEN EXCLUDED BECAUSE IN INDIA TUBERCULOSIS IS THE MOST COMMON CAUSE OF CHRONIC COUGH AND REST OTHER CAUSES OF CHRONIC COUGHS ARE IGNORED
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
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
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
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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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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.
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.
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
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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
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.
3. Definition
Cough is physiological protective
mechanism which is characterized by
explosive expectoration following a deep
inspiration. Its function is to clear the
tracheobronchial tree of excessive
secretions and foreign body.
4. Cough is often a clue to presence of Respiratory
disease.
Cough provide an essential protective function for human
airways and lungs.
Withought an effective cough reflex we are at risk for -
•retained airway secretion
•Aspirated material
•Predisposing infection
•Respiratory compromise
At the other extreme, excessive coughing
•can be exhausting
•Can be complicated with – emesis, syncope,
muscular pain, rib fracture
•And can aggravate hernia and urinary incontinence.
COUGH
5. Weak or ineffective cough compromises the ability to
clear lower respiratory tract infection, predisposing to more serious
infections and their sequelae.
Causes of impaired cough
•Decrease respiratory muscle strength.
•Chest wall deformity
•Impaired glottic closure or tracheostomy
•Abnormal airway secretions
•Central respiratory depression (anesthesia, sedation or
coma)
Impaired cough
6. Cough mechanism
Spontaneous cough is triggered by stimulation of sensory nerve
endings that are thought to be Primarily Rapidly adopting
receptor and C-fibers.
both chemical (Capsaician) and mechanical stimuli may initiate
the cough.
Afferent nerve ending richly innervate the Pharynx, Larynx, Air
way to the level of terminal bronchioles and also found in
External auditory meatus & Esophagus.
Sensory signal travel via the Vagus and Superior laryngeal
nerve.
7. transient upper airway occlusion
generating positive intra thoracic
pressure as high as 300mmhg.
rapid expiratory flow are generated.
maximizes the velocity of exhalation
Cough reflex involve a highly orchestrated series of involuntary muscular actions.
Bronchial smooth muscle contraction
together with dynamic compression of
airway narrows airway lumen
Vocal cord adduct
Expiratory muscle contract
With sudden release of laryngeal
contraction
8. Acute
Less than 3 wk
R.T.I. ,
Aspiration,
Inhalation of
noxious chemical
or smoke .
Sub-acute
3-8 wk
Tracheobronchitis-
pertussis
post viral tussive
syndrome
Chronic
More than 8 wk
Cardiopulmonary
d’s-
inflammatory,
infectious,
neoplastic and
cardiovascular
etiology.
Cough History
9. Cough of less than 8 wk duration may be
the early manifestation of a disease causing
chronic cough.
Acute cough occurring in context of more
serious disease such as pneumonia, aspiration,
CHF, pulmonary embolism is usually easy to
diagnose due to the presence of other clinical
features.
10. Assessment of chronic cough
•Regardless of cause cough often worsen when one first lies down at night
or with talking or in association with hyperpnea of exercise; it frequently
improve with sleep.
Exception- pertusis, asthma
•Physical examination seeks clue to the presence of cardiopulmonary
disease, including finding such as wheezing or crackles on chest
examination.
•Examination of auditory canal and tympanic membranes, nasal passage
ways and nails.
•Cough may be manifestation of systemic disease such as Sarcoidosis or
Vasculitis.
•In virtually all instances, evaluation of chronic cough merits a chest
radiograph.
11. Chronic cough with a normal chest
radiograph
When initial assessment with chest examination
and radiograph is normal.
Cough variant asthma
Gastro-esophageal reflux
Post-nasal drainage
Medication (ACE inhibitor)
12. The characteristic of cough originating at
various level of RT
ORIGIN COMMON CAUSE CLINICAL FEATURE
Pharynx Post-nasal-drip History of chronic rhinitis
Larynx Laryngitis, tumor Voice or swallowing altered, harsh or painful
voice
Whooping cough, croup Paroxysm of cough, often associated with strider
Trachea Tracheitis Raw restrosternal pain with cough
Bronchi Bronchitis(acute), COPD Dry or productive, worse in morning
Asthma Usually dry, worse at night
Bronchial carcinoma Persistent (often with haemoptysis)
Lung
Parenchyma
Tuberculosis Productive, often with haemoptysis
Pneumonia Dry initially, productive later
Boncheiectasis Productive, change in posture induce sputum
production
Pulmonary edema Often at night (may be productive of pink, frothy
sputum)
Interstitial fibrosis Dry, irritant and distressing
13. DRY COUGH
•URTI
•Initial phase of TB
•TPE
•Cigrette smooking
•Brochogenic
carcinoma
•Compression of
trachea
•Funtional
WET COUGH
(Foul smell)
•Lung abscess
•Bronceactasis
•Infected cavity
•Gangrene of lung
•Fungal infection
(Mucoid)
•Acute bronchitis
•Bronchopneumonia
•Post nasal drip and
sinusitis
14. Color Condition
Reddish Hemoptysis
Blackish Industrial infections, Cole miner cough
Rusty/khaki Pneumonia
Yellow Actinomycosia
Creamy yellow Staphylococcal infection
Frothy pink Pulmonary edema
Mucoid brown to red Klebseila infection
Current jelly Bronchogenic carcinoma, influenza
Green Pseudomonas infection
Blood oyster TB
Sputum color associated with various conditions
22. Sitopaladi Churna
Sitopala– 16 parts
Vamshalochana– 8 parts
Pippali – 4 parts
Ela – 2 parts
Twak – 1 part.
How dose work-
Dilating respiratory tract
Expectorant (moderate)
Strengthening action
Enhancing immunity
Stimulate apatite and digestion
Reduce inflammation
Vata and kapha Shamak
dose – 1 – 3 grams two or three times a day
along with half a teaspoon of ghee and a teaspoon of honey
23. Lavangadi Vati
Lavanga –10 g
Maricha– 10 g
Aksha –10 g
Sara of Khadira–30 g
Water decoction of Babbula – Acacia Arabica
(Vaidyajivana, Shwasa Kasa Chikitsa, 7)
productive and non productive cough, cold and
allergic rhinitis.
balances Vata and Kapha.
dosage: 1 – 2 tablets 2 – 3 times a day
24. Eladi Vati
Ingredients:
Ela–6g
Patra –– 6 g
Twak–6 g
Pippali–24 g
Sita –- 48 g
Madhuka–48 g
Kharjura–48 g
Draksha–48 g
Madhu –48 g
balances Pitta.
cough, cold, fever, hiccups, hoarse voice,
vomiting, dizziness, haematemesis, excessive
thirst etc.
Usual dose is – 1 – 2 tablets 2 – 3 times a day
25. Talisadi Churna
Ingredients:
Talisa – 1 part
Maricha – 2 part
Shunti – 3 part
Pippali – 4 part
Vamshalochana – 5 part
Ela – ½ part
Twak – ½ part
Sharkara – 32 part
Bronchodialator
Mucolytic
Antitussive
Antiinflammatory
Antimicrobial
26. Vyaghri haritaki
Ingredients-
Kantakari- 1 tula(54 ser)
Haritaki-100
Guna-100 pal
Trikatu-6 pal
Chaturjat-1 pal
Shahad-6 pal
All kasa, pinas, shwas,
swarkshay, rajyakshma
Anupan- shritshit jal or dugdh