childhood hypertension is unique presentation by Dr. Hemraj Soni,
very compressive, complied,upgraded, presentation......will definative helpfull for paediatrician n resident doctor............
diagnosing hypertension in children
work up for increased blood pressure
guide line for controling hypertension in pediatrics
treatment of hypertension
hypertensive crisis/emergency
childhood hypertension is unique presentation by Dr. Hemraj Soni,
very compressive, complied,upgraded, presentation......will definative helpfull for paediatrician n resident doctor............
diagnosing hypertension in children
work up for increased blood pressure
guide line for controling hypertension in pediatrics
treatment of hypertension
hypertensive crisis/emergency
Hypertension in pediatric has been increased around the world. there is a lot of factors plays a role in this increased. Here, we described the AAP 2017 protocol for pediatric
this slide was prepared for NCD programme June, 2012, the informations shown here were taken from both JN7 and NICE guideline.useful for family practitioners, community clinic doctors.Thanks
Mr. AMF 62 years presented with central chest pain on exertion for last 4 monthsHypertension(BP-220/120 mmHg) for last 4 years, taking 4 anti hypertensives.Diabetes for last 5 years (HbA1c-9.3%).Smoking for 8 years.Dyslipedemic for 3 years. H/o 5 times hospital admissions due to heart failure in last 3 years.ECG-Anterior wall ischemiaEF-58%During careful clinical exam- renal bruit on left side.Coronary angiogram done and revealed DVD. Renal angiogram showed significant left renal artery stenosis. Coronary angioplasty and left renal artery angioplasty done.
Mr AMF now have no chest pain on exertion after 3 months of coronary angioplasty.
Now BP is controlled (130/85 mm Hg), taking B blockers and ARB due to intolerance of ACE inhibitors.
No hospital admission during this period.
Diabetes and serum lipids are controlled.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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.
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
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
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
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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
2. •Objectives
•How to measure the blood pressure?
•When to measure B/P?
•What is the definition of hypertension ?
•what is the approach to a child with
hypertension?
3. How to measure the blood pressure?
We should consider 4main items when measuring
the child blood pressure
1– the circumstances
2– the child
3– the sphygmomanometer
4– the procedure it self
4. 1- the circumstances
•The child should take a 5 minutes rest before
measuring the blood pressure ,trying to calm
down the child, for two reasons
•1– to avoid stress hypertension
•2– to build a lovely , kindly circumstances to
avoid crying and anger which may interfere with
the measuring process..
5. 2– the child
the child should be in sitting position better
supported back with feet reaching the floor and
the cubital fossa supported at the heart level
6. 3– the sphygmomanometer
**Choose the appropriate size of the cuff
It should cover at least 70% of the distance between the
acromion and the olecranon..
**the bladder length should be > 80 of the arm circumference ,
and width should be > 40 % of the arm circumference..
7. Recommended Dimensions
for Blood Pressure Cuff Bladders
Maximum Arm
Age RangeWidth (cm)Length (cm)Circumference (cm)*
Newborn4810
Infant61215
Child91822
Small adult102426
Adult133034
Large adult163844
Thigh204252
*Calculated so that the largest arm would still allow the bladder to encircle
the arm by at least 80 percent.
8. 4– the procedure
** try to inflate and deflate slowly..
** try to feel the systolic blood pressure by
pulse ..
9. POINTS TO BE REMEMBERED
**BP should be recorded in all 4 limbs.
**Cuff should not be applied two tight (low Bp
recording) or too loose (high BP recording).
•**BP monitoring subsequently should be
taken in the same limb and position.
•**Normally the BP is 10-20mm Hg higher in
lower limbs compared to the upper limbs.
10. Objectives
•How to measure the blood pressure?accomplished
•When to measure
B/P?
•What is the definition of hypertension ?
•what is the approach to a child with
hypertension?
11. When to measure the B/P
** children above 3 years
_____________________
Children older than 3 years who are seen in
medical care settings should have their BP
measured at least once during every health
care episode..
12. Children under 3 years
**History of prematurity, very low birth weight, or other
neonatal complication requiring intensive care
**Congenital heart disease (repaired or nonrepaired)
**Recurrent urinary tract infections, hematuria, or
proteinuria
**Known renal disease or urologic malformations
Family history of congenital renal disease Solid organ
transplant
**Malignancy or bone marrow transplant
**Treatment with drugs known to raise BP
**Other systemic illnesses associated with hypertension
(eg, neurofibromatosis, tuberous sclerosis)
**Evidence of elevated intracranial pressure
13. Objectives
•How to measure the blood pressure?accomplished
•When to measure B/P? accomplished
•What is the definition and causes of
hypertension ?
•what is the approach to a child with hypertension?
14. definition
•Hypertension is defined as average SBP and/or
diastolic BP that is 95th percentile for
gender , age and height on 3 or more
occasions
15. CLASSIFICATION OF HYPERTENSION
Normal = less than 90 th percentile for age sex and height
Pre-hypertension = >90th percentile but
<95th percentile.
Or As with adults, adolescents with BP levels‡120/80
mmhg.
Stage 1 hypertension = 95th to 99th percentile + 5 mmhg.
Stage 2 hypertension = > 99th percentile + 5 mmhg.
16. White-coat hypertension
A patient with BP levels above the 95thpercentile
in a physician’s office or clinic who is
normotensive outside a clinical setting.
(Ambulatory BP monitoring is usually required
to make this diagnosis.)
22. Renal Causes Renal Parenchymal diseases (78%)
Renal vascular diseases (12%)
Cardiovascular CoA(2%)
Condition with large stroke volume (PDA, AV fistula)
Endocrine Hyperthyroidism
Excessive Catecholamine levels (Pheochromocytoma)
Adrenal dysfunction (CAH 11b, 17 a hydroxylase
deficiency)
Hyperaldosteronism (Conn's Syndrome, Renin
Producing Tumors)
Hyperparathyroidism
Neurogenic Raised ICT, Poliomyelitis, LGB.
Drugs and Chemical Sympathomimetic drugs , Amphetamines, Steroids,
OCP, Heavy matal poising (Hg, Lead), Cocaine,
Cyclosporine
Miscellaneous Hypercalcemia, After Coarctation repair, Pre eclampsia
etc.
CAUSES OF HYPERTENSION IN PEDIATRIC POPULATION
23. CLINICAL MANIFESTATION OF
HYPERTENSION
Many children with mild hypertension are
asymptomatic and hypertension is diagnosed
as a result of routine BP measurement.
Severe hypertension may be symptomatic like
headache, dizziness, nausea, vomiting,
irritability, personality changes..
Occasionally with complications like
neurological, CHF, Renal dysfunction, Stroke.
24. Clinical approach to a child with
hypertension
When we make a diagnosis of hypertension
careful and professional approach should be
followed so as to reach a final diagnosis which
me be if treated clear the hypertension state
In such approach we should begin with history ,
then clinical examination followed by
laboratory investigations and imaging studies
25. HISTORY
Present and Past History
Neonatal
- prematurity, BPD, umbilical artery catheterization .
Cardiovascular
-History of CoA or surgery for it, history of palpitation , Headache, excessive
sweating (excessive catecholamine levels).
-Renal-
History of obstructive uropathy, UTI, radiation, trauma or surgery to kidney area.
Endocrine-
weakness, fiushing, weight loss, muscle cramps (hyperaldosteronism). Constipation
Medication/Drugs
- Corticosteroids, amphetamines, cold medications, antiasthamatic drugs, OCP,
cyclosporine/tacrolimus, cocaine.NSAIDs Stimulant medications (eg, dexedrine,
methylphenidate) Beta-adrenergic agonists (eg, theophylline) ,Erythropoietin,
Tricyclic antidepressants, Recent abrupt discontinuation of antihypertensives
26. PHYSICAL EXAMINATION
Accurate measurement of BP in all limbs.
Complete physical examination.
Delayed growth/short stature (renal disease)
Bounding peripheral pulses (PDA, AR)
Weak or absent femoral pulses or BP differential between arms and legs
(CoA)
Abdominal bruits (Renal Vascular Disease)
Abdominal mass(Wilms tumor, neuroblastoma, pheochromocytoma)
Palpable kidneys (Polycystic kidney disease, hydronephrosis, multicystic
dysplastic kidney, mass)
31. Classification of Hypertension in Children
and Adolescents:
Therapy Recommendations
NoneNormal
Do not initiate therapy unless there are
compelling indications such as chronic
kidney disease (CKD), diabetes mellitus,
heart failure, left ventricular hypertrophy
(LVH).
Prehypertension
Initiate therapy based on indications for
antihypertensive drug therapy or if there
are compelling indications as above.
Stage 1 hypertension
Initiate therapy.Stage 2 hypertension
32. MANAGEMENT
Prehypertension or
asymptomatic, Stage 1 Primary HTN
( who do not have evidence of end-organ damage or
diabetes
)
Lifestyle modifications
(Non-pharmacologic interventions)
re-evaluated in six months
Not controlled
Antihypertensive
33. Non pharmacologic interventions-
Weight reduction.
Low salt intake*.
Regular aerobic exercise.
Dietary Approaches- fresh vegetables, fruits, and low-fat
dairy
Avoidance of smoking.
*Can start with recommending “no added salt” with ultimate goal of achieving the current recommendation
of 1.2 grams/day total for 4- to 8-year-olds and 1.5 grams/day for children 9 years and older
34. CLASSIFICATION OF DRUGS
ACE inhibitors Captropil, Enalapril
Angiotensin AT 1, antagonists Losartan
Calcium channel blockers Nifedipine, Verapamil.
Diuretics Hydrochlorthizide, Furosemide,
Spironolactone
b adrenergic blockers Propranolol
a+b adrenergic blockers Labetalol
a adrenergic blockers Prazosin
Central sympatholytics Clonidine
Vasodilators Arterial (Hydralazine, Minoxidil),
Mixed (Sodium nitropruside)
35. Indications for antihypertensive drug
therapy
Symptomatic hypertension
Secondary hypertension
Hypertensive target organ damage
Diabetes( types 1 & 2)
Persistent hypertension despite non
pharmacologic measures
36. Goals of antihypertensive therapy
•Reduction of BP to < 95th percentile without
any concurrent conditions .
•Reduction of BP to <90th percentile with
concurrent conditions (eg.Hyperlipidemia ,End
organ damage, Obesity, CKD Complications
etc)
37. How should I treat?
Step-1 - Starting with a single antihypertensive in small
dose and proceeding to full dose .
Step-2 - If it produce no clinical improvement, a second
antihyprtensive drug should be added or substituted.
initial antihypertensive therapy
a Calcium channel blocker (CCB) or an Angiotensin
converting enzyme (ACE) inhibitor, unless there is a
compelling reason to use an agent from another class
38.
39. Monitoring and follow-up
There are no specific, published guidelines regarding
frequency of monitoring and follow-up after
initiation of therapy, but in the beginning it would be
reasonable to measure a child’s blood pressure at
least weekly and arrange for follow-up every three
months.
Once the child has achieved target BP’s on a medication
regimen, clinic follow-up can be spaced to every six
months.
40. COMBINATION THERAPY
SYNERGISTIC COMBINATIONS.
Drugs increasing renin
activity+ Drugs decreasing
renin activity
ACE inhibitors , Diuretics
+
b blockers
Sympathic inhibitors and
vasodilators cause fluid
retention. Add diuretics
b blockers + Thiazide,
Lasix
ACE inhibitors + Diuretics Envas + Thiazide, Lasix
a Blocker + b blocker Prazosin + Propranolol
41. SECONDARY HYPERTENSION
Treatment should be aimed at removing the cause of
hypertension whenever possible.
Curable forms of Hypertension
Renal Unilateral kidney disease (Nephritis,
Pyelonephritis, hydronephrosis)
Cardiovascular CoA, Renal artery stenosis, thrombosis.
Adrenal Pheochromocytoma, Neuroblastoma,
hyperaldosteronism
Miscellaneous Drugs/ OCP etc.
43. CONCLUSIONS
Hypertension is a silent killer. All children >3 years of
age attending OPDs should have their BP recorded
(Special circumstances in children < 3 years).
Thorough history and physical examination followed by
relevant investigations can clinch the cause of
hypertension.
Hypertension is a curable disease.