Cricket Tennis Ball
₹6,785.00 – ₹7,654.00
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Description
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Additional information
| Color | Green |
|---|---|
| Balls Range | CANNON |
| Size | JUNIOR, SENIOR |
36 reviews for Cricket Tennis Ball
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Key Take‑Home Points – Antibiotic Prescribing
Topic Core Message
Indication Only prescribe an antibiotic when the patient has
a confirmed or highly suspected bacterial infection. Avoid use
for viral illnesses, allergic reactions, or chronic non‑infectious conditions.
Choice of Agent Pick the narrowest spectrum drug that covers the likely pathogen(s).
Start with first‑line agents (e.g., amoxicillin/clavulanate
for uncomplicated sinusitis) and reserve broad‑spectrum
drugs for confirmed resistant organisms or severe disease.
Dose & Duration Use evidence‑based dosing; most infections are cured in 5–7 days of therapy.
Shorter courses (3–5 days) are often sufficient for many acute
bacterial infections, reducing selection pressure for resistance.
Monitoring Reassess the patient at 48–72 h: symptom improvement and tolerance.
If no improvement or worsening occurs, consider drug failure,
alternative diagnosis, or resistant infection; adjust therapy accordingly.
—
Practical “What‑to‑Do” Checklist
Step Action Rationale
1 Ask the patient: “How many days have you had these symptoms?” Identifies duration of illness.
2 If Doctor: “I’ve looked at your history of cold‑like symptoms that started about a week ago. In many people, the first few days are caused by a virus—nothing you can treat with antibiotics.
>
> You only need antibiotics if a bacterial infection starts to take over. That usually shows up as a new fever or a sudden worsening of pain near your throat or ear. We’ll give you an antibiotic only if we see those signs. Otherwise, I’d like you to keep resting, stay hydrated, and monitor your temperature.”
>
> Patient: “So I don’t need medicine right now?”
>
> You: “Exactly. But let’s agree on a plan: If you develop a fever over 38 °C (100.4 °F) or the pain gets worse in the next 24–48 hours, call us immediately. We’ll then review and may start treatment.”
—
3. Choosing a Threshold for “High” Fever
Source Threshold Evidence / Rationale
American Academy of Pediatrics (AAP) – Red Flags ≥ 38 °C (100.4 °F) Commonly used in pediatric assessment; identifies children who may need urgent
evaluation.
Royal College of Paediatrics & Child Health (UK) – Fever‑related emergencies ≥ 39 °C (102 °F)
for infants 48 h Risk of seizures, meningitis, encephalitis Call a doctor immediately
Severe headache with stiff neck, rash, confusion Possible meningitis/encephalitis Seek emergency
care
Persistent vomiting after fever onset Dehydration; could indicate brain infection Rehydrate and call healthcare provider
Unusual drowsiness or difficulty waking up Sign of brain involvement Call doctor urgently
Seizures or convulsions Can cause brain damage, indicates severe infection Emergency
care required
Behavior changes (irritability, agitation) May signal neurologic complications Contact a health professional
promptly
Breathing difficulties or chest pain Possible lung involvement from influenza Seek medical help
immediately
These symptoms are not exhaustive; if you suspect neurological complications after an influenza infection, consult healthcare professionals for evaluation and treatment.
—
2. Why is Neurologic Involvement Common in Influenza?
The influenza virus can cause widespread
damage through a combination of direct viral invasion, immune-mediated
injury, and vascular insults.
Pathway Mechanism
Direct Viral Entry Hemagglutinin (HA) binds to sialic
acid receptors on neurons and glia. Influenza A viruses
with H1N1, H3N2 subtypes can cross the blood–brain barrier (BBB).
Immune-Mediated Cytokine Storm Elevated IL-6, TNF‑α, IFN‑γ create a systemic inflammatory milieu
that compromises BBB integrity and induces microglial activation.
Vascular Endothelial Damage Endotheliitis leads to thrombosis or hemorrhage.
The endothelial glycocalyx is shed (↑vWF), increasing coagulability.
Metabolic Dysregulation Hypoxia, lactic acidosis, electrolyte shifts impair neuronal
energy metabolism, exacerbating excitotoxicity.
3. Pathophysiology of Acute Respiratory Failure in COVID‑19
Mechanism Description
Diffuse alveolar damage (DAD) Viral cytopathic effect + immune response → hyaline
membrane formation, edema.
Ventilation–perfusion mismatch Loss of hypoxic pulmonary vasoconstriction → shunt physiology.
Microvascular thrombosis Endothelial injury + hypercoagulability → pulmonary emboli and in‑situ microthrombi.
Loss of lung compliance Fibrosis + surfactant dysfunction → stiff
lungs, high plateau pressures.
These mechanisms explain the rapid deterioration despite relatively normal initial imaging
(e.g., CT may show only ground‑glass opacities early on).
2. Pathophysiology behind “Rapidly Progressive”
COVID‑19
The term “rapidly progressive” refers to a sudden shift from mild or moderate symptoms to severe hypoxemia and multi‑organ failure within hours to days.
Feature Underlying Mechanism
Sudden drop in oxygen saturation Diffuse alveolar damage → capillary leak, microthrombi block
ventilation‑perfusion matching.
Severe dyspnea at rest Increased work of breathing
due to stiff lungs (decreased compliance) and increased minute ventilation required.
Hypotension or tachycardia Systemic inflammatory
response leading to vasodilation, capillary leak, myocardial depression.
Rapidly worsening mental status Hypoxia‑induced cerebral dysfunction; metabolic derangements from sepsis.
4.2 Clinical Course and Prognosis
Patients who exhibit the above acute deterioration often progress
rapidly to multi‑organ failure if not promptly
treated. The prognosis depends on:
Timeliness of intervention (intubation, vasopressors).
Severity of organ dysfunction at presentation.
Underlying comorbidities.
Early identification and escalation to critical care settings are crucial for improving outcomes.
5. Summary & Take‑Home Points
Aspect Key Findings
Typical Presentation Fever, cough, dyspnea; possible GI symptoms (diarrhea, nausea).
Risk Factors Age ≥65 yrs, diabetes, hypertension,
chronic kidney disease.
Imaging Bilateral multifocal ground‑glass opacities on chest CT.
Laboratory Elevated CRP, LDH, D-dimer; lymphopenia.
Complications ARDS, septic shock, multi‑organ failure.
Treatment Supportive care, corticosteroids (e.g., dexamethasone),
anticoagulation; consider antivirals/monoclonal antibodies per guidelines.
—
3. Key Points for the Emergency Department
Rapid Identification: Use point‑of‑care CRP or LDH if available; otherwise rely on clinical suspicion and imaging.
Early Steroids: For patients with hypoxia (PaO₂/FiO₂ 200 mg/L AND PaO₂/FiO₂ 48 h Add IL‑6 blockade if not already on it;
review immunosuppression dose.
D-dimer > 5× ULN and platelet count ↓ by >30% Suspect pulmonary embolism; obtain CT‑PA.
Temperature >38.5°C for >24 h despite antipyretics Evaluate for secondary bacterial infection; consider broad spectrum antibiotics if cultures positive or high suspicion.
Patient’s oxygenation improves to SpO₂ > 94% on room air for 3 days Begin weaning from supplemental O₂; assess readiness for discharge.
—
5. Decision‑Tree Logic (Textual Flow)
START
|
+– If patient has a confirmed bacterial infection (culture +ve) OR high clinical
suspicion:
| – Initiate targeted antibiotic therapy.
| – Monitor CRP, procalcitonin weekly.
|
+– Else if inflammatory markers remain elevated but cultures are negative:
| – Continue anti‑inflammatory regimen.
| – Reassess for new infection signs daily.
|
+– If patient develops new fever >38°C or leukocytosis >10×10^9/L:
| – Order CBC, CRP, procalcitonin, repeat cultures.
| – Consider broadening antibiotics if bacterial source suspected.
|
+– If CRP 10 mg/L) or a >50 % increase from baseline signals possible
infection.
– ESR, IL‑6, and white‑cell counts provide additional evidence; the combination of two or more
abnormal markers increases diagnostic confidence.
Escalation steps –
– If thresholds are met, repeat labs within 24–48 h to
confirm persistence or escalation.
– Persistent elevation prompts imaging (CT chest/abdomen) and microbiological sampling (blood cultures, sputum, urine).
– Broad‑spectrum antibiotics are started empirically while awaiting culture results.
Documentation – Each step is recorded in the patient’s chart with timestamps
to ensure traceability and enable review of decision points.
This protocol balances sensitivity for early infection detection with specificity to avoid unnecessary antibiotic exposure.
It also provides anavar 50mg a day results clear
audit trail that can be used in quality improvement or clinical governance reviews,
aligning with NHS standards for safe prescribing practices.
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Anavar, also known by its generic name oxandrolone, has become a staple in many anabolic steroid cycles due to its relatively mild side‑effect profile and efficient conversion into testosterone.
When used correctly, it can help athletes and bodybuilders enhance muscle definition, preserve
lean mass during cutting phases, or support moderate gains during bulking protocols.
The key to success lies in understanding the appropriate dosage ranges, cycle
length, post‑cycle therapy, and how Anavar stacks up against other oral
steroids such as Turinabol.
—
ANAVAR CYCLE GUIDE
Cycle Length
Standard Cycle: 6 to 8 weeks is considered optimal for most users.
Shorter cycles (4–5 weeks) may be suitable
for beginners or those who experience side‑effects early, while longer
cycles risk cumulative estrogenic effects and
liver strain.
Loading Phase: Some protocols begin with a 2‑week loading phase at 20 mg per day
to build tolerance, then increase to the target dose.
Dosage
Moderate Users (Bodybuilding): 20–30 mg per day for men.
This is usually split into two doses (10–15 mg twice
daily) to maintain stable blood levels.
High‑End Users: Up to 40–50 mg per day may be used in advanced cycles,
but the risk of liver toxicity rises. A single daily dose at 25–30 mg is often preferred
for better absorption and fewer fluctuations.
Timing
Morning vs Evening: Taking Anavar in the morning can reduce the likelihood of insomnia or restlessness, while evening doses might help with recovery due to lower cortisol levels
at night.
Split Doses: Splitting the daily amount into two smaller administrations improves consistency and minimizes peak‑to‑trough
swings.
Stacking Partners
Clomid or Nolvadex (SERMs): Essential after a cycle
to restore natural testosterone production. For a 6‑week Anavar cycle, start SERM therapy in week 5 of the cycle to overlap with the taper.
Aromatase Inhibitors (AIs): Not typically needed for Anavar alone
due to low aromatization rates, but may be used if combined with more potent estrogens.
Post‑Cycle Therapy (PCT)
Typical PCT: 4–6 weeks of Clomid or Nolvadex at 50 mg per day.
Begin immediately after the last dose of Anavar.
Monitoring: Check testosterone, LH, and estrogen levels before and after PCT to gauge recovery.
Side‑Effect Management
Liver Stress: Monitor liver enzymes (ALT/AST) if using high doses or extended cycles.
Consider a mild hepatoprotective supplement such as milk thistle.
Water Retention & Blood Pressure: Rare with Anavar, but watch for hypertension in users who
combine it with other estrogens.
ANAVAR CYCLE FOR BULKING
Although Anavar is often associated with cutting due to its lean‑mass preserving properties, it can also be integrated
into a bulking cycle when paired correctly. The goal here
is to promote muscle hypertrophy while limiting fat gain and keeping estrogenic side‑effects low.
Bulking Protocol Outline
Pre‑Cycle Preparation (2–4 weeks)
– Begin with an oral anabolic such as Ostarine or Ligandrol for 4–6 weeks.
– This priming phase stimulates muscle protein synthesis, preparing tissues to
respond to Anavar’s mild anabolic stimulus.
Anavar Phase (Weeks 5–10)
– Dose: 30–40 mg per day split into two administrations.
– Duration: 6 weeks. The extended period allows for gradual accumulation of
lean mass without the rapid water retention seen with
stronger steroids.
Post‑Cycle (Weeks 11–14)
– Transition to a mild aromatase inhibitor or continue the PCT regimen.
– Focus on protein intake and resistance training to consolidate gains.
Training Emphasis
Hypertrophy Sets: 8–12 reps per set, 4–5 sets
per exercise.
Volume: Increase total weekly volume by 10–15 % during the Anavar phase compared to pre‑cycle weeks.
Recovery: Adequate sleep (7–9 hours) and nutrition are critical;
a caloric surplus of 200–300 kcal with high protein intake (1.6–2.2 g/kg body weight) supports muscle growth.
Nutrition
Macronutrient Ratios: Carbohydrates 45–50 % of total calories,
proteins 30–35 %, fats 20–25 %.
Micronutrients: Vitamin D3, magnesium, and omega‑3 fatty acids to aid recovery and mitigate inflammation.
Hydration: Maintain at least 3 liters of water daily to support
metabolic function and prevent mild edema.
TURINOBOL OR ANAVAR: WHICH ORAL STEROID SUITS YOUR GOALS BEST?
When choosing between Turinabol (tetrahydroxyandrostenedione) and Anavar,
consider the following factors:
Feature Turinabol Anavar
Anabolic Potency Higher anabolic strength; can yield noticeable size increases.
Moderate potency; excellent for lean mass preservation.
Estrogenic Activity Minimal aromatization. Extremely low estrogen conversion.
Liver Toxicity Mildly hepatotoxic, especially at higher doses.
Lower liver strain; safe up to 30 mg/day for most users.
Side‑Effect Profile Possible mild gynecomastia in sensitive individuals.
Rare water retention; minimal risk of gynecomastia.
Ideal Use Bulking phases where size is paramount and a slight increase in muscle hardness
is desired. Cutting, maintenance, or early bulking where definition matters
more than bulk.
Cycle Length 6–8 weeks with careful monitoring. 4–6 weeks for beginners; up to 8 weeks for advanced users.
Decision Factors
Goal: Size vs Definition – If your primary aim is rapid, noticeable size gains, Turinabol may edge out Anavar due to its stronger anabolic
drive. For a leaner, more defined look with minimal side‑effects, Anavar remains
the preferred choice.
Tolerance & Health Status – Users with pre‑existing liver concerns
or those prone to estrogenic reactions should favor Anavar because of its lower hepatotoxicity and negligible aromatization.
Training Phase – During a cutting cycle where preserving
lean mass while shedding fat is key, Anavar’s ability to maintain muscle without adding
water makes it ideal. In contrast, during a true bulking phase where caloric surplus and heavier
training are planned, Turinabol can help accelerate muscle growth.
Budget & Availability – Both steroids are widely available, but pricing may
vary by region. Anavar tends to be slightly cheaper due
to higher demand in cutting markets.
FINAL THOUGHTS
Anavar 50 mg (when used responsibly within a 6‑week cycle) offers a balanced
approach between muscle preservation and moderate hypertrophy
while keeping side‑effects manageable. The cycle design should incorporate proper
timing, split dosing, supportive supplements,
and a robust post‑cycle therapy plan to safeguard endocrine health.
When deciding between Anavar and Turinabol, align the choice
with your specific training goals, physiological tolerance, and desired body composition outcome.
By doing so, you can maximize gains, minimize risks, and achieve a physique that reflects both strength and definition.
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