A 6-year-old male presented with loose motions and vomiting for 3 days. On examination, he appeared lethargic and had signs of compensated hypovolemic shock including tachycardia, pale skin, and weak pulses. Intravenous fluids were administered which improved the patient's condition. Laboratory tests found dehydration and electrolyte abnormalities. The patient was diagnosed with hypovolemic shock due to gastroenteritis and treated with intravenous antibiotics and fluid resuscitation. After 7 days of treatment, his condition stabilized and he was discharged.
GEMC: Near-Drowning and Drowning: Resident TrainingOpen.Michigan
This is a lecture by Dr. Jim Holliman from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
GEMC: Near-Drowning and Drowning: Resident TrainingOpen.Michigan
This is a lecture by Dr. Jim Holliman from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
An Approach to a Case of Severe Pneumonia with Iron Deficiency Anemia KairviRaval
Hello There,
I Kairvi Raval and my friend Mili Bulsari students of Doctor Of Pharmacy Year 3, Department of Pharmacy Practice of Shree Dhanvantary Pharmacy College- Surat, Gujarat, Affiliated to Gujarat Technological University- Ahmedabad, Gujarat.
Here we have presented a clinical case of Severe Pneumonia with Iron deficiency Anemia, in SOAP format and along with that we tried to bring light towards the disease overview and linked pathophysiology of Severe Pneumonia progressed into Iron deficiency anemia.
Furthermore, Being PharmD candidates Patient Case is our priority so for that we should Acquire accurate knowledge regarding disease epidemiology and recent advances taking place in the drug therapy. so, we've tried to bring light towards the prevalence of pneumonia in India, Emergence of S. Pneumoniae resistance worldwide and recent advances has taken place in antibiotic therapy.
Hope this finds Helpful.
Thanks and regards,
Kairvi Raval
Mili Bulsari
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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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4. There is ACUTE LIFE THREATENING PROBLEM.
So we will activate emergency response system
as appropriate for setting
Rush to resus. room
Call for help - doctors
Attach high flow oxygen.
Attach cardiac monitor and ECG electrodes
5.
6. EVALUATE:
PRIMARY ASSESSMENT:
Airway: Clear
Breathing: Respiratory rate of 48/min , no added sounds ,
spo2 95% off O2, No indrawing , NVB, b/l equal air entry
Circulation: heart rate 140/min, central and peripheral pulses
are WEAK , CRT more than 3 sec, BP 100/60mmhg
Disability: responds to verbal, RBS: 47 mg/dl, pupils = BERL
Exposure: temperature 37.6C , no rashes, dry mucous
membrane, poor skin turgor, sunken eyes
7. After primary assessment we categorize the pt’s state as
compensated shock most likely HYPOVOLEMIC Shock and
intervention was done accordingly:
Maintain IV/IO line
Analyze cardiac rhythm ( sinus tachycardia)
20ml/kg 0.9% Normal saline first bolus was given (push
and pull technique)
4ml/kg 10% Dextrose bolus was given
Pt. was catheterized.
After each bolus, chest was ascultated for crepts, liver for
enlargement and HR for improvement.
3 boluses of N/S was given and pt. improved.
8. SECONDARY ASSESSMENT:
SAMPLE History:
Signs and Symptoms: Loose motion for 3 days, 7
episodes/day, watery in consistency, large in quantity, foul
smelling. Vomiting for 3 day, 3 episodes/ day, large in
quantity, non-projectile, white in color, containing food
particles, asso. With food and water intake. Pt. became
lethargic for which he was taken to ER
Allergies: none
Medication: none
9. Past medical history : INSIGNIFICANT
Last meal: a biscuit and few sips of juices 4
hours ago
Events: His appetite decreased and Pt. became
lethargic for which he was taken to ER.
11. HEAD TO TOE EXAMINATION:
HEENT:
Unremarkable
RESPIRATORY EXAMINATION :
Normal vesicular breathing .
No basal crepts.
CARDIOVASCULAR:
S1+S2+O
Tachycardia.
Apex beat palpable at 4th ICS medial to mid clavicular
line.
12. ABDOMINAL EXAMINATION:
Soft , non distended
No visceromegaly
Gut sounds audible
Severe dehydration present.
PELVIS / EXTREMITIES:
Unremarkable
BACK :
Unremarkable
CENTRAL NERVOUS SYSTEM :
GCS = 15/15
Conscious and Alert now .
14. INTERVENTION:
Deficit – bolus = 1600 - 960 = 640
DEFICIT FLUID: 640ml 0.9% Dextrose saline was given.
320ml over 8 hrs. and rest 320 ml over next 16 hrs.
MAINTENANCE FLUID: 1300 ml 0.9% Dextrose saline
given. 440 ml over 1st 8 hrs and the rest 860 ml in the
next 16 hrs.
Ongoing losses were replaced by 100 ml of 0.9% N/S
Inj. Ceftriaxone 1.2 g IV X OD.
15. LABS INVESTIGATIONS :-
Hb 10.3 10.3
Hct 35 30.8
Tlc 16.3 11
N 85.3 56
L 8 23
Plt 596 565
BUN 29 15
Cre 1.4 0.5
Na 137 135
K 2.9 3.9
Cl 104 100
Ca 9.1 9
Mg 2.5 2.4
Pho 5.2 5.3
16. LABS INVESTIGATIONS
STOOL D/R:
pH = acidic
Consistency = loose
Colour = yellowish
Red cells = nil/ HPF
Pus cells = 10-12/HPF
STOOL C/S: No bacterial growth
17. PROGRESS DURING HOSPITAL
STAY:
Urine output was 2 ml/kg/hr.
Potassium was low. So, KCl was added in maintenance
fluid. 2 mEq KCl in every 100 ml of fluid
By day 2, child was stabilized and orally allowed.
Replacement fluid were given orally in the form of ORS.
UCE were repeated which normalized.
Frequency of stool reduced
Child was discharged after 7 days of IV antibiotic.
20. Shock:
Shock is characterized by body’s inability to deliver
adequate oxygen to meet the metabolic demands of vital
organs and tissues.
Pathophysiology:
After an initial insult triggering shock leading to
inadequate oxygen delivery to organs and tissues,
compensatory mechanisms attempt to maintain BP by
increasing cardiac output, HR and systemic vascular
resistance (SVR) through sympathetic nervous system
activation and neurohormonal response.
21. And to optimize O2 delivery to the tissues, body also
increases O2 extraction and redistributing blood flow
to the brain, heart and kidneys at the expense of skin
and GI tract.
Respiratory compensation includes greater CO2
elimination in response to metabolic acidosis which
resulted due to deficiency in O2 delivery and a shift to
anaerobic metabolism.
These responses lead to an initial
state of COMPENSATED SHOCK but if treatment is not
initiated or inadequate during this period,
DECOMPENSATED SHOCK develops with hypotension
and tissue damage that may lead to MULTIPLE ORGAN
DYSFUNCTION and ultimately to DEATH.
22. TYPES OF SHOCK:
HYPOVOLEMIC SHOCK:
Most common cause of shock, caused by decreased
circulatory volume.
E.g. haemorrhage or fluid loss ( diarrhoea or
CARDIOGENIC SHOCK:
Caused due to impaired heart function.
E.g. Acute coronary syndrome, valve failure,
or acquired myopathies etc.
23. OBSTRUCTIVE SHOCK:
Due to any lesion that creates a mechanical barrier
that impedes cardiac output.
E.g. cardiac tamponade, tension pneumothorax,
pulmonary embolism, etc
DISTRIBUTIVE SHOCK:
Caused by pathologic peripheral vasodilation.
E.g. sepsis, anaphylaxis, neurogenic
28. DEFICIT:
Estimation of deficit: by assessing dehydration.
Mild dehydration = 5-7%
Moderate dehydration = 7-10%
Severe dehydration = 10-15%
Fluid: Isotonic fluids( Ringer lactate or 0.9% DS)
Amount: For every 1% dehydration, 10ml/kg fluid
given.
Technique: Half of the total fluid was given in 1st 8
and the remaining half in the next 16 hrs.