Diabetic Kidney Disease is Silent but Serious. Explained

What is diabetic kidney disease?

Diabetic kidney disease is a type of chronic kidney disease (CKD) caused by diabetes. It develops gradually as high blood glucose damages small blood vessels in the kidneys, impairing their ability to filter waste and excess fluid. Approximately one in three people with diabetes develops diabetic kidney disease. Diabetic kidney disease is often referred to as diabetic nephropathy. It is a serious complication of diabetes where long-term high blood sugar damages the kidneys’ filtering system, leading to chronic kidney disease and, in severe cases, kidney failure.

How does diabetic kidney disease develop?

Step-by-Step Development

1. Early Functional Changes (Hyperfiltration)

In the initial phase, the kidneys become overactive, filtering more blood than normal (glomerular hyperfiltration).
This is due to high glucose levels increasing pressure inside the glomeruli (tiny kidney filters).

2. Structural Damage

Persistent hyperfiltration and high blood sugar cause thickening of the glomerular basement membrane and expansion of mesangial cells (supporting cells in the kidney).
These changes weaken the filter’s integrity.

3. Protein Leakage (Albuminuria)

Damaged filters start leaking albumin (a protein) into urine.
First appears as microalbuminuria (small amounts), then progresses to macroalbuminuria (larger amounts).

4. Inflammation & Fibrosis

Chronic injury triggers inflammation and fibrosis (scarring) in kidney tissue.
This reduces the number of functioning nephrons (filtering units).

5. Declining Kidney Function

As scarring worsens, the glomerular filtration rate (GFR) drops.
Patients develop chronic kidney disease (CKD), with symptoms like swelling, fatigue, and high blood pressure.

6. End-Stage Renal Disease (ESRD)

In advanced stages, kidneys can no longer filter waste effectively.
Dialysis or a kidney transplant becomes necessary.

Key Factors

Hyperglycemia (high blood sugar): Directly damages kidney vessels.
Hypertension (high blood pressure): Adds stress to glomeruli.
Genetic susceptibility: Some individuals are more prone.
Lifestyle factors: Smoking, poor diet, and obesity accelerate progression.

How common is diabetic kidney disease?

Diabetic kidney disease (DKD) is one of the most common complications of diabetes, affecting about 20–40% of people with diabetes worldwide. It is the leading cause of chronic kidney disease and end-stage renal disease globally.

Risk Factors That Increase Prevalence

Poor blood sugar control
Long duration of diabetes
High blood pressure
Obesity and smoking
Genetic predisposition

Diabetic kidney disease is prevalent—affecting up to 40% of people with diabetes—and is a major driver of kidney failure worldwide. Early detection through urine protein tests and strict control of blood sugar and blood pressure are essential to reduce its prevalence.

Diabetic kidney disease symptoms

Early Symptoms (Often Silent)

Initially, there are no noticeable symptoms—damage begins years before patients feel unwell.
Protein in urine (albuminuria): Detected only through lab tests.
A slight increase in blood pressure may appear early.

Progressive Symptoms

"As kidney damage worsens, patients may notice"

Swelling (edema): In feet, ankles, legs, or hands due to fluid retention.
Foamy urine: Caused by excess protein leakage.
Frequent urination: Especially at night.
Fatigue and weakness: From toxin buildup and anemia.
Nausea, vomiting, and loss of appetite: Signs of advanced kidney dysfunction.
Persistent high blood pressure: Both a cause and consequence of kidney damage.

Late-Stage Symptoms

When DKD progresses to chronic kidney disease (CKD) or end-stage renal disease (ESRD):

Severe swelling (legs, around eyes, lungs)
Shortness of breath (fluid overload)
Confusion or difficulty concentrating
Muscle cramps and itchingchronic kidney disease
Dialysis or a transplant may be necessary if the kidneys fail.

How is diabetic kidney disease diagnosed?

Key Diagnostic Steps

1. Urine Tests

Albuminuria (protein in urine):
Microalbuminuria (30–300 mg/day) is an early sign of DKD.
Macroalbuminuria (>300 mg/day) → more advanced disease.
Urine albumin-to-creatinine ratio (UACR): Preferred test, done on a spot urine sample.

2. Blood Tests

Serum creatinine: Measures waste product in blood.
Estimated glomerular filtration rate (eGFR): Calculates kidney function based on creatinine, age, sex, and body size.
Normal: ≥90 mL/min/1.73 m²
CKD: <60 mL/min/1.73 m² (for ≥3 months)

3. Blood Pressure Measurement

High blood pressure is both a cause and consequence of DKD.
Regular monitoring is essential.

4. Additional Tests (if needed)

Kidney ultrasound: To rule out other causes of kidney disease.
Blood tests for electrolytes: To check kidney’s ability to balance minerals.
Biopsy: Usually needed only if the diagnosis is uncertain.

What increases the risk of developing diabetic kidney disease?

Key Risk Factors

1. Duration of Diabetes

The longer someone has diabetes, the greater the risk.
After 20+ years, up to 30–40% of patients may develop DKD.

2. Poor Blood Sugar Control

Chronic hyperglycemia damages the kidney blood vessels.
High HbA1c levels are strongly linked to DKD progression.

3. High Blood Pressure (Hypertension)

High blood pressure (hypertension) increases the stress on kidney filters (glomeruli).
Hypertension is both a cause and a consequence of diabetic kidney disease (DKD).

4. Genetic Susceptibility

Family history of kidney disease increases risk.
Certain ethnic groups (South Asians, African Americans, and Hispanics) are more vulnerable.

5. Lifestyle Factors

Smoking: Accelerates vascular damage.
Obesity: Increases insulin resistance and kidney workload.
High-salt diet: Worsens hypertension.

6. Other Medical Conditions

Cardiovascular disease
High cholesterol
Recurrent urinary tract infections (less common but contributory)

Risks & Trade-offs

Silent onset: DKD often develops without symptoms, so risk factors must be managed proactively.
Compounding effect: Multiple risk factors (e.g., diabetes + hypertension + smoking) dramatically increase the likelihood of kidney failure.
Preventive strategy: Tight glucose and blood pressure control, a healthy lifestyle, and annual screening can reduce risk significantly.

What are the possible complications?

Major Complications

1. Chronic Kidney Disease (CKD)

Chronic Kidney Disease (CKD) causes a progressive decline in renal function.
This condition results in the accumulation of waste products in the bloodstream.

2. End-Stage Renal Disease (ESRD)

Kidneys fail.
Requires dialysis or a kidney transplant for survival.

3. Cardiovascular Disease

DKD greatly increases the risk of heart attack, stroke, and heart failure.
High blood pressure and vascular damage are common in advanced stages.

4. Hypertension (High Blood Pressure)

Hypertension is both a cause and a consequence of diabetic kidney disease (DKD).
Worsens kidney damage and raises cardiovascular risk.

5. Fluid Retention

Fluid retention can cause swelling in the legs, ankles, feet, and around the eyes.
This condition can result in pulmonary edema, a condition where fluid accumulates in the lungs, leading to shortness of breath.

6. Electrolyte Imbalances

Kidneys fail to regulate minerals like potassium, sodium, and calcium.
Can cause dangerous heart rhythm disturbances.

7. Anaemia

Damaged kidneys produce less erythropoietin (a hormone for red blood cell production).
Leads to fatigue, weakness, and reduced quality of life.

8. Bone Disease (Renal Osteodystrophy)

This condition is characterized by an imbalance in the metabolisms of calcium and phosphate.
This condition leads to brittle bones and fractures.

9. Nerve Damage (Neuropathy)

Worsened by kidney dysfunction.
Can cause numbness, tingling, or pain in extremities.

What is the treatment for diabetic kidney disease?

The video about the kidney-saving tips

Core Treatment Strategies

1. Blood Sugar Control

Tight glucose management reduces kidney damage.
Medications: insulin, oral hypoglycemics, and newer agents like SGLT2 inhibitors (empagliflozin, dapagliflozin) and GLP-1 receptor agonists (liraglutide, semaglutide).
These not only lower blood sugar but also protect the kidneys and heart.

2. Blood Pressure Control

Target: usually <130/80 mmHg.
ACE inhibitors (e.g., lisinopril) or ARBs (e.g., losartan) are first-line drugs because they reduce proteinuria and protect kidney function.

3. Lifestyle Modifications

Diet: Low-salt, balanced protein intake, heart-healthy foods.
Exercise: Regular physical activity.
Smoking cessation: Essential to reduce vascular damage.
Weight management: Helps control both diabetes and hypertension.

4. Cholesterol Management

Statins are often prescribed to reduce cardiovascular risk.

5. Monitoring & Early Detection

Conduct annual urine albumin-to-creatinine ratio (UACR) and eGFR tests.
Regular blood pressure checks.

Advanced Stage Treatments

Dialysis: When the kidneys fail to filter waste.
Kidney Transplant: The Best long-term option for end-stage renal disease (ESRD).
Management of complications:
Anaemia (treated with erythropoietin-stimulating agents)
Bone disease (phosphate binders, vitamin D analogues)
Electrolyte imbalances (dietary adjustments, medications)

Conclusion

Diabetic kidney disease is one of the most serious long-term complications of diabetes, affecting nearly a third of patients worldwide. It develops silently, beginning with microscopic changes in kidney filtration and progressing to protein leakage, scarring, and eventually kidney failure if left unchecked. Diabetic kidney disease is not inevitable. With vigilance, healthy choices, and timely medical care, people with diabetes can protect their kidneys and live healthier, longer lives.

Awareness of Tardive Dyskinesia Protects Patients

Define Tardive Dyskinesia

Long-term antipsychotic use causes tardive dyskinesia (TD), a persistent, often permanent movement disease. Grimacing, lip-smacking, tongue-thrusting, and jerky limb and torso movements result.

Jerky movements of arms,

Tardive Dyskinesia Facts

Involuntary, repeated facial, mouth, tongue, trunk, and extremity movements characterize TD, a medication-induced neurological disorder. Long-term use of antipsychotics (both typical and atypical) is the main cause, but other medications that block dopamine, like metoclopramide (which is used for nausea and GI problems), can also cause it. Chronic drug use may lead to the sensitization of brain dopamine receptors.

Symptoms:

Facial grimacing, lip smacking, and chewing motions
Tongue protrusion or writhing
Rapid blinking
Jerky movements of arms, legs, fingers, or toes
Onset: Typically occurs after months or years of pharmaceutical use.
Prevalence: 20-30% of antipsychotic patients experience it, with older agents being more likely to be affected.

Clinical observation of symptoms, after ruling out other disorders such as Huntington's disease, cerebral palsy, or Tourette syndrome, guides the diagnosis.

Risks and Factors

TD can significantly impair quality of life, leading to social stigma and challenges with eating, speaking, and daily duties.
Early detection and prevention are crucial due to their often irreversible nature.
When commencing antipsychotic medicine, patients and caregivers should be taught to watch for minor indicators of aberrant movements.

What mimics tardive dyskinesia?

Mannerisms, compulsions, catatonia, and spontaneous dyskinesias can mimic TD movements. Movement disorder assessment often involves careful examination of many primary and acquired etiologies.

Who is most likely to develop tardive dyskinesia?

TD usually starts in middle-aged or older individuals; however, it can happen at any age after continuous dopamine-blocking drug use. The risk rises with age, especially in individuals over 40–60.

Age of Onset—Key Findings

TD can occur at any age but is less common in younger people.
Symptoms may occur in middle-aged adults after months or years of antipsychotic use.
Elderly persons have a 5–6-fold higher prevalence of TD than younger patients. Low doses of conventional antipsychotics can cause TD earlier in older individuals.
Age-related risk factors include lengthy neuroleptic exposure, early extrapyramidal symptoms (EPS), alcohol addiction history, and frailty and slower drug metabolism in older persons.

Why Age Matters

Aging brains are more susceptible to dopamine receptor alterations, increasing the risk of TD.
Long-term antipsychotic use increases risk due to cumulative exposure.
For older individuals, doctors may utilize lower doses of atypical antipsychotics as a prevention strategy.

Who gets tardive dyskinesia more often?

People at risk for tardive dyskinesia (TD) include those taking long-term antipsychotic or dopamine-blocking drugs, older adults, women, and those with medical or lifestyle risk factors.

Groups at High Risk for TD

Adults over 60
Compared to younger patients, the risk is 5–6 times higher.
Low doses of antipsychotics can cause TD in this group.
Women, especially postmenopausal women, are more susceptible, according to studies.
TD can occur in patients on long-term antipsychotics, both typical (first-generation) and atypical (second-generation).
Typical agents (e.g., haloperidol, chlorpromazine) have a higher risk.
Individuals taking dopamine-blocking GI medications

* Medications such as metoclopramide and prochlorperazine (used for nausea or GI disorders) can also cause TD.

* Early extrapyramidal symptoms (EPS), including tremors, rigidity, or akathisia during treatment, increase the risk of TD later on.

Other risks

Diabetes mellitus (greater prevalence of TD)
Alcohol or substance misuse history
Cognitive impairment or brain injury
Longer neuroleptic exposure

Why It Matters

Tardive dyskinesia (TD) can be irreversible and significantly affect a person's quality of life.
Early monitoring is crucial, with clinicians using the lowest effective dose and monitoring small abnormalities.
Patients and caregivers should learn about risk factors to advocate for safer treatments.

Tardive dyskinesia: permanent?

Sometimes, tardive dyskinesia (TD) is persistent. Some individuals recover after stopping drugs, while others have lifelong difficulties. Early diagnosis and treatment enhance outcomes.

Keys to TD Permanence

There is no single outcome for TD. Some symptoms improve when the medicine is withdrawn, while others persist eternally.
Research indicates TD is chronic, and symptoms may linger after medication discontinuation.
Early intervention improves the likelihood of partial or full improvement in TD when caught early and treated promptly.
FDA-approved treatments: Valbenazine (Ingrezza) and deutetrabenazine (Austedo) may lessen symptoms but may not completely reverse the condition.

Why It Matters

TD can significantly impact quality of life, creating challenges in eating, speaking, and socializing. The best course of action is prevention because it is usually permanent: use the lowest effective dose, check on it frequently, and, if you can, switch to lower-risk medications.
Educate patients and caregivers to recognize early indicators (lip smacking, tongue motions, grimacing) and seek medical attention soon.

Natural tardive dyskinesia treatment

Supportive lifestyle and natural approaches

Review medication with a doctor.
Adjust or cease the offending drug under medical supervision.
Switching to lower-risk antipsychotics like clozapine or quetiapine may reduce symptoms.
Maintaining a healthy diet with antioxidants is crucial.
Diets high in omega-3 fatty acids (fish, flaxseed, walnuts) and antioxidants (berries, leafy greens, vitamin E, and vitamin C) may promote brain health.
Antioxidants may lower oxidative stress linked to TD, according to certain research.
Exercise and physical therapy
Regular aerobic exercise enhances motor control and decreases stress.

Managing involuntary movements and preserving muscle strength are two benefits of physical therapy.

Mind-body exercises

Yoga, tai chi, and meditation help enhance coordination and reduce anxiety, which can increase TD symptoms.
Patients can gain control over their bodies through breathing exercises.
Supplements (medically advised)
Ginkgo biloba may lessen TD symptoms, according to research.
Melatonin potentially regulates dopamine action.
The Vitamin B6 study suggests potential benefits for TD.
Supplements can interfere with drugs, so only take them under medical supervision.
Avoid drinking and smoking.
Both can aggravate neurological symptoms and limit therapeutic efficacy.

Important Notes:

Natural approaches support, not cure. Natural approaches may alleviate tardive dyskinesia (TD) but seldom provide a cure.
Early detection is crucial. A TD is frequently tenacious once established.
Always see a neurologist or psychiatrist before considering supplements or lifestyle modifications, especially if using antipsychotics.
Diet, exercise, antioxidants, and stress reduction can improve brain function and reduce symptoms of TD, which is often permanent. They should enhance medical treatment, not replace it.

Tardive dyskinesia treatment

Main Treatment Methods

Adjusting medication

Reduce or stop the problematic antipsychotic or dopamine-blocking medicine under physician supervision.
Consider switching to lower-risk medicines such as clozapine or quetiapine, which have lower TD risk.
Medical products approved by the FDA
Valbenazine (Ingrezza) and Deutetrabenazine (Austedo) are VMAT2 inhibitors that minimize aberrant movements.
While not a cure for TD, these can greatly alleviate symptoms.

Alternative medications

Clonazepam (a benzodiazepine) may benefit some people.
Clinical investigations demonstrate the benefits of Ginkgo biloba extract.
Amantadine and tetrabenazine (an earlier VMAT2 inhibitor) may be used.

Supportive treatments

Physical and occupational therapy improve motor control and daily functioning.
Speech therapy can aid with speech and swallowing issues in TD.
Botulinum toxin injections: Reduce serious facial movements and focal dystonia.

Risks and Factors

Early identification is crucial, as TD may persist despite treatment.
Acute discontinuation of antipsychotics might increase psychiatric symptoms; thus, it is important to oversee medication adjustments.
VMAT2 inhibitors may produce side effects such as tiredness, depression, and QT prolongation.
Use natural supplements (e.g., ginkgo or melatonin) under physician supervision to prevent drug interactions.

How can we prevent Tardive dyskinesia?

Careful drug use, early monitoring, and lifestyle changes can lower the incidence of tardive dyskinesia (TD). The objective is to reduce high-risk drug exposure and detect symptoms early.

Main Prevention Methods

Use the lowest effective antipsychotic dose. • High-dose use increases TD risk over time. The smallest dose that controls symptoms is the goal for clinicians.
Prefer lower-risk drugs
Atypical (second-generation) antipsychotics like clozapine and quetiapine have reduced TD risk compared to first-generation drugs like haloperidol.
Regular monitoring for early signs
Early detection of TD can be achieved through routine screening methods such as the Abnormal Involuntary Movement Scale (AIMS).
Patients and caregivers should observe minor movements (e.g., mouth smacking, tongue thrusting, and grimacing).
Limit the duration of dopamine-blocking medicines.
Use long-term treatments such as metoclopramide (for nausea/GI difficulties) only when necessary.
Address risk factors.
Older age, female sex, diabetes, and substance misuse raise TD risk. Manage these factors to reduce risk.
Patient and caregiver education
TD symptom awareness enables early reporting and intervention.
Clear risk communication is crucial before therapy begins.

Conclusion

Prolonged use of dopamine-blocking drugs, particularly antipsychotics, can lead to a persistent movement problem known as tardive dyskinesia. TD is often permanent and can greatly impact daily living, but early detection and treatment can help.

Mental health and neurological safety must be balanced, according to TD. Vigilant prescription, early detection, and current medicines can improve symptom control and quality of life, but reversal is not always possible.

Protect Skin from Age Spots

What are age spots? (liver spots)

Small dark spots can occur on the face, shoulders, hands, and other areas. Sunspots, liver spots, and age spots are natural occurrences that develop in sun-exposed areas as we age. While age spots are generally harmless, many people want to prevent or limit their appearance. Sunspots, liver spots, age spots, and lentigines are like freckles but bigger, darker, and clustered. Individuals exposed to the sun typically develop age spots on their face, hands, shoulders, arms, and back. They usually emerge after 50, but sun-exposed individuals can develop them younger.

This article covers age spot prevention and treatment, including practical methods to keep your skin appearing young and healthy.

Identification, symptoms

The spots are flat and elliptical with well-defined edges.
The colour range is light brown to black.
Size ranges from freckles to ½ inch across.
Safe: It does not cause pain or discomfort.

If age spots change in size, colour, or shape, a medical evaluation is recommended, as some skin malignancies, such as melanoma, can mimic them.

Causes of Age Spots

The main causes of age spots

UV Radiation:
The main cause is UV rays, which cause melanocytes to produce more melanin.
Pigment aggregates in the top skin layers cause dark spots over time.
Cumulative Sun Damage:
Decades of sun exposure increase the process.
Younger people who spend a lot of time outdoors or use tanning beds can get age spots earlier.

Additional Contributors

Skin Type: Fair-skinned individuals with easy burning are more susceptible.
Genetics: Family history can increase susceptibility.
Excessive pigmentation may result from hormonal changes during pregnancy, menopause, or hormone therapy.
Some medications, such as antibiotics or diuretics, might enhance photosensitivity and increase the likelihood of age spots.
Lifestyle: Excessive tanning, outdoor work, or recreational sun exposure without protection.

Developing Age Spots Risks

Older age, fair skin, sun exposure, and tanning bed use are the main risk factors for age spots. Photosensitivity medicines, hormones, and genetics can all enhance susceptibility.

Key Risks

Age (50+): Chronic sun damage commonly causes age spots in individuals over 50 years of age. Kids who spend a lot of time in the sun can get sunburn, too.
Skin Type: Fair-skinned individuals are at risk of burning easily. Reduced melanin leads to poorer UV protection.
Long-term, unprotected solar exposure is the main cause. Outdoor workers, athletes, and individuals in sunny climates are particularly susceptible.
Tanning beds: UV radiation replicates sun damage by accelerating melanin synthesis.
Genetics and family history of pigmentation abnormalities or age spots increase the risk.
Hormonal changes in skin pigmentation can occur due to factors such as pregnancy, menopause, or hormone therapy.
Medication: Antibiotics, diuretics, and chemotherapy medicines can increase photosensitivity and danger.

Prevention for Age Spots

UV exposure can cause age spots; thus, sunscreen, protective clothes, and avoiding tanning salons are ideal. Daily skin care and lifestyle changes also matter.

Key Precautions

Use sunscreen daily. • Apply broad-spectrum SPF 30+ sunscreen in the morning, even on cloudy days.
Reapply every 2 hours outside, especially after swimming or sweating.
Wear Protective Clothing: • Wide-brimmed hats, long sleeves, and UV-blocking sunglasses decrease direct sun exposure. • Fabrics designated “UPF” provide further protection.
Avoid peak sun hours.
Limit outside activities between 10 a.m. and 4 p.m., when UV rays are most intense.
Avoid tanning beds
Artificial UV radiation increases skin aging and pigmentation.

Skincare and Lifestyle

The video explains how to prefer Moisturizer

Moisturize regularly.
Hydrated skin resists sun damage better.
Antioxidant-rich diet: Foods rich in vitamins C and E may minimise skin oxidative stress.
Regular skin checks
Check spots for changes in size, colour, or shape to detect skin cancer.
Gentle Exfoliation • Removes dead skin cells and may minimise uneven pigmentation.

Risks and Factors

Incomplete protection: Sunscreen application alone cannot block all UV radiation; layering is necessary.
Differences in skin types: Fair-skinned people need greater protection; darker skin tones have fewer age spots but more hyperpigmentation.
Consistency is key: Daily behaviours are key—sporadic protection won't avoid accumulated damage.

Sun Protection Importance

Consistent use of sun protection, such as sunscreen, can prevent skin cancer, premature ageing, and UV damage. Implement protective measures daily to maintain skin health and appearance.

Sun Protection Matters

Skin Cancer Prevention: UV radiation is the primary cause of skin malignancies, including melanoma.
Regular sun protection considerably reduces risk.
Prevents premature aging:
UV rays degrade collagen and elastin, causing wrinkles, sagging, and age spots.
Use sunscreen to maintain healthy, young skin.
Reduces Pigmentation and Age Spots:
Sun exposure causes dark areas due to excess melanin.
Protects against uneven skin tone and hyperpigmentation.
Ensures Total Skin Health:
Protects against sunburn, dryness, and irritation.
Promotes natural healing and lowers oxidative stress.

Important Safety Measures

Apply broad-spectrum SPF 30+ sunscreen daily, even indoors or on cloudy days.
Protective clothing: Hats, sunglasses, and UPF-rated textiles.
Smart Timing: Avoid direct sunlight from 10 a.m. to 4 p.m.
Lifestyle Choices: Avoid tanning beds, drink, and consume antioxidant-rich meals.

Sun Protection Negligence Risks

Cumulative exposure to UV rays significantly increases the risk of skin cancer.
Accelerated aging can lead to early wrinkles and a leathery texture.
Recurring pigmentation concerns, including age spots and uneven tone.
UV radiation causes eye damage (cataracts, macular degeneration).

Treating Age Spots

Although innocuous, age spots are often treated cosmetically. Topical treatments include retinoids, laser therapy, cryotherapy, chemical peels, and microdermabrasion, and natural therapies are optional. A dermatologist should confirm the diagnosis before starting any treatment, including laser therapy, which can directly target melanin to reduce pigmentation. Rule out skin cancer.

Medical/cosmetic treatments

Topical medications
Hydroquinone creams: Reduce melanin production to lighten spots.
Retinoids (tretinoin): Promote cell turnover, leading to progressive pigmentation reduction.
Combination creams are often prescribed with moderate steroids to achieve better results.

Procedures

Laser therapy can directly target melanin to reduce pigmentation.
Cryotherapy: Freezes aging areas with liquid nitrogen, producing peeling.
Chemical peels: Reveal fresher, less pigmented skin by removing outer layers.
Microdermabrasion: Improves skin tone and texture by gently sanding away the top layer.
Limited evidence for natural/home remedies.

Use of lemon juice, aloe vera, or green tea extracts may have variable results compared to medical therapy.

Vital Considerations

First, a dermatologist may take a skin biopsy to check if the lesion is benign and not melanoma.

Side effects: Treatments may cause, e.g., redness, inflammation, or transient scarring.
Sunscreen is crucial to prevent new age spots following treatment.
Patience needed: Treatments typically take weeks to months to show results.

Post-treatment prevention

Use daily sunscreen (SPF 30+) to prevent recurrence.
Use protective clothes like caps and long sleeves.
Limit peak solar exposure. and avoid tanning beds.

Natural Age Spot Treatments

Some natural remedies for age spots include lemon juice, which contains citric acid and may diminish pigmentation.

Use diluted juice to avoid irritation.
Aloe Vera Gel: Antioxidants and compounds aid skin repair. May fade spots with regular usage.
Apple Cider Vinegar: Acetic acid exfoliates and lightens dark spots. Dilute to avoid skin burns.
Green Tea Extract: Catechins potentially lower oxidative stress and pigmentation.
Vitamin E Oil • Nourishes skin and may reverse UV damage.
Buttermilk or Yogurt: Lactic acid mildly exfoliates for even skin tone.

Vital Considerations

Limited Evidence: Natural remedies have less scientific support than modern treatments.
Consistency needed: Results may take weeks to months.
Patch test for skin sensitivity to citrus, vinegar, or strong botanicals, which may cause irritation.
Natural therapies should supplement dermatologist-approved treatments, not replace them.
Sunscreen is essential to prevent new age spots from forming, regardless of therapies.

Best Practices

Apply treatments before night to prevent sun sensitivity.
Use with daily SPF 30+ sunscreen.
Use consistently but cautiously, stopping if irritation occurs.
Seek medical advice for changes in spot size, shape, or colour.

Conclusion

Age spots, also known as solar lentigines or liver spots, are a form of harmless UV damage. Age spots are harmless, but they indicate solar damage; therefore, continuous sun protection is the best prevention method. Safe and effective cosmetic treatments are available, but a dermatologist should be consulted for personalized advice. It must exclude skin cancer mimics.

Living with Lewy body dementia is challenging.

Lewy body dementia—Overview

Lewy Body Dementia (LBD) is an umbrella term encompassing Dementia with Lewy Bodies (DLB) and Parkinson's Disease Dementia, a progressive brain disorder characterised by abnormal protein clumps (Lewy bodies) that affect thinking, movement, mood, and behaviour, typically starts after the age of 50. Visual hallucinations, alertness fluctuations, Parkinsonian movement difficulties (tremors, stiffness), and REM sleep behavior disorder (acting out dreams) are key symptoms; memory loss may be delayed. There is no cure, but medications and physical, occupational, and speech therapy can help with the symptoms.

LEBD's 7 Stages

A breakdown of the stages:

Stage 1: No Cognitive Decline
Stage 2: Mild Cognitive Decline
Stage 3: Mild Cognitive Decline
Stage 4: Moderate Cognitive Decline
Stage 5: Moderately Severe Cognitive Decline
Stage 6: Severe Cognitive Decline
Stage 7: Severe Cognitive Decline
Unable to communicate or walk; end-stage care.

Differentiation of LBD from Alzheimer's

Changes in alertness and attentiveness might occur within a day.
Early onset of vivid and detailed visual hallucinations, unlike Alzheimer's.
Parkinsonian motor symptoms: tremors, rigidity, and delayed movement.
REM sleep behaviour disorder affects dreaming, sometimes years before dementia symptoms appear.
Medication sensitivity: Antipsychotics can dramatically aggravate symptoms.

Notes:

Patients may regress between stages.
Symptoms can change quickly, unlike with Alzheimer's.
Early detection of hallucinations, sleep disorders, and motor abnormalities can differentiate LBD from other dementias.

Lewy dementia causes

Main Causes and Mechanisms

Lewy bodies (alpha-synuclein protein deposits):
Clump formation in nerve cells, particularly in cognitive, movement, and alertness areas.

Parkinsonian motor symptoms and dementia might result from interference with neurotransmitters such as dopamine and acetylcholine.

Neurochemical disruption:

Dopamine insufficiency causes tremors, stiffness, and sluggish movement.
Acetylcholine disturbance causes memory loss, confusion, and hallucinations.
Brain regions affected: • Cerebral cortex—cognitive impairment, memory issues.
Substantia nigra causes motor symptoms resembling Parkinson's.
The brainstem is responsible for sleep problems, specifically the REM sleep behavior disorder.

Possible Risks

Several factors enhance risk; however, the cause is unknown:

Most instances start after 50, with a median starting age of 76 years.
Genetics: Variants in SNCA (alpha-synuclein) and GBA genes may increase vulnerability.
Parkinson’s disease increases the risk of dementia with Lewy bodies.
Family history: Parkinson's or dementia in relatives may suggest a greater risk.

LBD Causes' Unique Qualities

Lewy bodies drive LBD, unlike Alzheimer's (produced by beta-amyloid plaques and tau tangles).
The overlap with Parkinson's disease dementia demonstrates the impact on movement and cognition.
The formation and spread of protein deposits in the brain are the subject of ongoing studies.

Key Notes

Lewy Body A proteinopathy, dementia is caused by aberrant protein deposition. Lewy bodies harm nerve cells and disrupt brain chemistry, causing cognitive changes, vivid hallucinations, Parkinsonian movement symptoms, and sleep difficulties.

What are the initial signs of Lewy body dementia?

Common Early Signs of LBD:

Changing cognition and alertness
The condition is characterised by intermittent confusion or drowsiness.
Inconsistent focus and attention, sometimes appearing normal.
Visual hallucinations
Typically, early in the disease, patients experience detailed hallucinations of people, animals, or objects that are not physically present.
REM sleep behavior disorder (RBD) • Dream reenactment, talking, or violent movements during sleep.
This can occur years before dementia symptoms.
Parkinsonian motor symptoms
Mild tremors, muscle stiffness, slower movement, or shuffling gait, resembling Parkinson's disease, occur accompanying cognitive impairment.
Executive function issues
Planning, problem-solving, and multitasking become challenging.
Initial memory loss is less noticeable than in Alzheimer's.

Lewy body dementia diagnosis:

Diagnostics for LBD

1. Clinical Criteria

Essential features for diagnosis:
Varying alertness and cognition.
The patient frequently experiences well-formed visual hallucinations.
Parkinsonian movement symptoms (rigidity, tremor, shuffling gait).
REM sleep behavior disorder (acting out dreams).
Supportive features: • Autonomic dysfunction, such as blood pressure fluctuations and incontinence.
Severe antipsychotic medication sensitivity.

2. Medical History & Neurological Exam

The examination includes a detailed evaluation of the symptoms, their onset, and their progression.
A neurological exam evaluates motor function, reflexes, and coordination.

3. Cognitive Tests

Cognitive tests assess memory, attention, problem-solving, and visual-spatial skills.
Attention and executive function problems generally precede memory loss, unlike Alzheimer's.

4. Lab and Imaging Tests

Either MRI or CT scans can rule out brain problems such as strokes or tumours.
DaTscan (dopamine transporter scan): Reports decreased dopamine activity, validating diagnosis.
Blood tests: Rule out metabolic or systemic dementia causes.

5. Differential Diagnosis

LBD is frequently misdiagnosed as Alzheimer's, Parkinson's, or a psychiatric condition.
Evaluating hallucinations, sleep disorders, and fluctuating cognition aids in diagnosing LBD.

Main Obstacles

No one test or biomarker exists; diagnosis relies on clinical judgment.
Symptoms resemble Alzheimer's and Parkinson's, leading to frequent misdiagnosis.

LBD patients are sensitive to antipsychotic medicines, making early identification crucial to prevent symptom worsening.

Lewy body dementia treatment

The video about treatment for Lewy body dementia

Lewy Body Dementia (LBD) has no cure, but drugs, lifestyle changes, and supportive therapies manage symptoms. We want a better quality of life and fewer difficulties.

The medications used for LBD

Cognitive symptoms (memory, attention, confusion): Cholinesterase inhibitors (e.g., rivastigmine, donepezil) may enhance cognition and minimize hallucinations.
Movement symptoms (rigidity, tremor, slower movement): Levodopa may help, but the response is typically weaker than in Parkinson's disease.
Behavioural and psychiatric symptoms: Use antipsychotics cautiously, as many aggravate symptoms. If necessary, quetiapine or clozapine is safer.
Sleep disruptions (REM sleep behaviour disorder): Melatonin or clonazepam may diminish dream enactment.
Patients can manage autonomic symptoms such as blood pressure swings and incontinence by using tailored drugs and making lifestyle changes.

Also, read https://www.medicoverhospitals.in/articles/lewy-body-dementia.

Non-pharmacological approaches

Cognitive stimulation therapy: Structured activities help sustain mental function.
Physical therapy enhances mobility and balance and minimizes fall risk.
Occupational therapy: Adapts everyday routines and environments for safety.
Speech therapy: Aids in swallowing and communication.
Ensure proper sleep hygiene with a regular schedule and relaxing nighttime habits.

Supportive Care

Caregiver education: Understanding shifts in cognition and hallucinations aids family responses.
Environmental changes: Improved lighting, uncluttered spaces, and visual clues lessen confusion.
Proper nutrition and hydration are crucial for overall health and preventing constipation and infections.
It offers mental health counselling to both patients and caregivers, assisting them in managing stress and depression.

Challenges and Risks

Medication sensitivity: LBD patients are sensitive to antipsychotics, which can aggravate motor and cognitive symptoms if misused.
Misdiagnosis can delay therapy because of overlap with Alzheimer's and Parkinson's.
Symptoms intensify over time, necessitating further support while receiving treatment.

Lewy Body Dementia: Fatal?

Lewy Body Dementia (LBD) is life-threatening, but not as quickly as a heart attack or stroke. As a progressive neurological illness, it can cause significant impairment and lower life expectancy.

Why LBD Is Dangerous

Degrade: Cognitive, movement, and independence continuously degrade.
Complications: Swallowing difficulties resulting in aspiration pneumonia, a common cause of death in LBD.
Severe mobility issues: falls, fractures, and infections.
Autonomic dysfunction: blood pressure swings, urinary issues, hunger.
Medication sensitivity: LBD patients may experience adverse reactions to antipsychotics that worsen symptoms or pose risks.

Life Expectancy

Patients typically survive 5-8 years after diagnosis, with some living up to 10-12 years.
Slow or quick decline in progression depends on age, health, and associated disorders.

Life Quality Considerations

Early detection and treatment (cognitive therapy, mobility support, and sleep management) can enhance independence.
Caregiver support is crucial for patients who require more assistance with everyday tasks.
Advanced planning and palliative care are advised as the disease advances.

Conclusion

LBD is a neurodegenerative condition characterized by aberrant deposits of alpha-synuclein proteins in the brain. It is progressive and life-threatening. A unique combination of cognitive decline, Parkinson-like movement symptoms, vivid hallucinations, and sleep difficulties distinguishes it from Alzheimer's and Parkinson's disease.

Due to its fluctuating nature and medication sensitivity, Lewy body dementia is difficult to treat, although early detection, targeted treatment, and strong caregiver support can improve patient comfort and dignity.

Lack of Colour Vision: Getting Used to a Colourful World

Lack of colour vision: getting used to a colourful world

Colour Vision Deficiency: What Is It?

A visual disease known as Colour Vision Deficiency (CVD) causes a person to have difficulty distinguishing certain hues or tones. Although complete colour blindness—seeing exclusively in shades of grey—is extremely uncommon, it is usually referred to as colour blindness.

A diminished capacity to see colour, colour variations, or shade. Usually hereditary, it is caused by defective or absent red, green, or blue light-detecting cone cells in the retina. The most prevalent is red-green deficiency, which affects roughly 0.5% of females and 8% of males with Northern European ancestry.

How Colour Vision Operates

We can sense a wide range of colours because the retina has cones that are sensitive to three wavelengths: long (red), medium (green), and short (blue). These cones convey messages to the brain. If one type of cone pigment is missing or damaged, the brain cannot correctly interpret certain colours.

Colour Vision Deficiency Types

1. The most prevalent colour blindness is red-green.

The most common deuteranomaly, which is moderate and typically has no effect on day-to-day functioning, is characterised by aberrant green cones that make greens appear redder.
Protanomaly: Reds appear milder and greener because of the weak red cones.
Deuteranopia: Red and green are indistinguishable due to the absence of green cones.
Protanopia: The inability to see red and distinguish between red and green due to the lack of red cones.

2. Blue-Yellow color blindness is a rare condition.

Tritanomaly: Reduced sensitivity causes blue cones to confuse pinks and yellows, as well as blues and greens.
Tritanopia: Lack of blue cones makes it difficult to tell blues from yellows.

3. Monochromacy, which is also known as complete colour blindness, is very uncommon.

Rod monochromacy is the inability to see anything other than grayscale.
Blue Cone Monochromacy: Serious eyesight problems; only blue cones function.

4. Other Groupings

Congenital (Hereditary): Usually red-green, present from birth.
Acquired: Usually affects blue-yellow vision and appears later as a result of disease, drugs, or trauma.

Symptoms

The condition often manifests as an inability to distinguish between specific colours, such as red and green traffic lights.
Colours may seem faded, drab, or odd to certain people.
This condition is often observed in children, especially during school-related tasks such as reading colored charts.

Diagnosis

The Ishihara Colour Test is a diagnostic procedure that uses a succession of plates with colored dots that create patterns or numbers.
Additional vision tests: Evaluating colour discrimination under controlled illumination.

Management

Inherited CVD has no known treatment.
Adaptive techniques include: • Using contact lenses or special spectacles that improve colour contrast.
Digital tools and apps are available to aid in colour identification and labeling.
Adaptive techniques also involve modifications to the job or educational environment.

Deficiency in Colour Vision: Who Is at Risk?

Given that the most prevalent forms of Colour Vision Deficiency (CVD) are inherited and associated with the X chromosome, those with a family history of the condition—particularly men—are most at risk. Specific eye conditions, traumas, and drugs can also increase the risk.

Important Risk Groups

Genetic inheritance, which is the most prevalent
CVD is typically inherited from parents via X chromosome genes.
Because men only have one X chromosome, they are far more vulnerable than women, who require abnormalities on both X chromosomes to be impacted.
The most common hereditary kind is red-green deficiency.
Family history: The probability is increased if near relatives have a colour vision impairment.
Diseases of the eyes
Disorders that harm the retina and impair colour perception include diabetic retinopathy, cataracts, macular degeneration, and glaucoma.

Neurological reasons

Acquired CVD may result from conditions that impact the brain or optic nerve, such as multiple sclerosis or stroke.
Toxins and medications
As a side effect, some medications (such as those used to treat heart problems, infections, or mental illnesses) might change colour vision.
Chemical exposure, such as carbon disulfide, may potentially be a factor.
Changes associated with ageing
The most prevalent and permanent type of CVD, particularly in men, is inherited.

Who Needs to Have a Colour Vision Deficiency Test? Who Needs to Be Put to the Test? Why Kids during standard eye exams

Teachers and parents can modify learning materials with the aid of early detection.
This is particularly crucial before classes begin, as colour-coded worksheets and activities are frequently used.
Children of afflicted parents should be tested because most cases are hereditary, especially those with a family history of CVD.
More men than women
Because red-green deficiency is X-linked, men are more likely to have it (prevalence of 8% compared to 0.5% in women).
Those suffering from eye conditions
Diseases such as diabetic retinopathy, cataracts, glaucoma, and macular degeneration can cause acquired colour vision issues.
People who are on specific drugs
Certain medications (such as those used to treat infections, heart disease, or mental illnesses) may alter how colour is perceived.
Employees in occupations where colour recognition is crucial for safety, such as pilots, electricians, train drivers, military personnel, and others, should have their skills checked.
Anyone observing symptoms • Having trouble reading colour-coded material, differentiating traffic lights, or recognising colours that seem dull or different.

Also. read https://ophthalmologybreakingnews.com/what-is-color-blindness

When to Conduct Testing

Childhood: As part of a regular screening for vision.
Adulthood: If symptoms manifest or before starting a career where colour vision is essential.
Later in life: If medication use or eye conditions start to impair vision.

Although there isn't a cure for congenital colour vision deficiency (CVD), people can manage their everyday lives with the aid of supportive therapies and adaptive equipment. If the issue arises due to an acquired eye illness, medication, or injury, treating the underlying cause can improve colour vision.

Options for Management and Treatment

Addressing the root causes

Treating visual problems such as cataracts, glaucoma, macular degeneration, or diabetic retinopathy may enhance colour perception if CVD is associated with them.
If the condition is brought on by drugs or poisons, stopping or switching the medicine may help you see colour normally again.

Contact lenses and special glasses

For red-green insufficiency in particular, glasses with tinted filters (such as EnChroma lenses) might improve colour contrast.
Although outcomes vary, contact lenses with filters may also be beneficial.

Apps and digital gadgets

Apps for smartphones can change screen settings or recognise colours by name.
Users can alter colour schemes on computers and phones with accessibility capabilities to improve visibility.
Environmental modifications and visual aids
Replacing colour coding with labels, patterns, or variations in brightness.
Change the lighting to enhance contrast.
There is a reliance on location cues, such as the consistent green at the bottom and red at the top of traffic lights.
Experimental treatments, including gene therapy, are being investigated to repair damaged cone cells. While this approach has shown encouraging results in animal trials, it is not yet accessible to humans.

Important Things to Think About

Management of inherited CVD emphasizes adaptability rather than treatment; the condition is lifelong.
Treatment for the underlying illness or medication may improve acquired CVD.
Pilots, electricians, and members of the armed forces are examples of occupations that may need accommodations and testing.
Emotional impact: Counselling and raising awareness might assist in normalizing feelings of frustration or isolation that some people experience.

Colorblind glasses: what are they?

Some people with colour blindness can see colours more clearly with colorblind glasses, which use tinted lenses. They are often designed for those with specific types of red-green colour blindness, which is the most prevalent kind.
Unfortunately, colour blindness currently has no known cure. A colorblind person cannot see normally with these special glasses, but they may make certain colours more vivid or visible.
The operation of colorblind glasses
Rods and cones are photoreceptor cells found in the retina, the rear of the eye. Cone cells enable colour vision by responding to colored light from the environment.
Three types of cones are found in an eye with normal colour vision. Red, green, and blue are the colours that one type recognizes.

Colour blindness occurs when:

There are some (or all) of the cones, but they are not particularly effective.
Some or all of the cones are absent.
Colour vision deficit is the medical term for colour blindness. Most people with the syndrome are born with it, but some drugs and illnesses can cause it.
The majority of colorblind individuals are still able to see some colours. Complete colour blindness is quite uncommon.
The most prevalent kind of colour blindness is by far red-green colour deficiency.

Conclusion

A disorder known as Colour Vision Deficiency (CVD) causes the eye's cone cells to fail to detect particular light wavelengths, making it difficult to discern between different hues. It is most frequently inherited, especially in men, because of its X-linked genetic pattern, although it can also be acquired through age, neurological disorders, ocular problems, or drugs.

For most people, colour vision deficiency is a lifelong disability, but with knowledge, testing, and adaptive solutions, people can flourish without significant limits. The cornerstones of management continue to be early detection and supportive tactics.

Hyperemesis Gravidarum: Early Signs and Effective Management

What is Hyperemesis gravidarum?

Hyperemesis gravidarum (HG) is a severe and persistent form of nausea and vomiting during pregnancy that is much worse than regular morning sickness. It can cause electrolyte imbalances, nutritional deficiencies, and dehydration, and people often need to be hospitalized to get treatment like IV fluids and antiemetics. Extreme symptoms include vomiting all the time, feeling worn out, and getting dizzy. It can get in the way of daily life, but with the right care, it can be managed.

Important signs:

Severe, uncontrollable sickness and vomiting, often all day (not just in the mornings). The inability to hold down drinks leads to dehydration. More than 5% of their pre-pregnancy body weight has been lost.
Electrolyte imbalances and ketonuria (ketones in the urine) are two typical signs. This condition can be debilitating, necessitating bed rest and making it challenging to perform daily activities.

Causes and Risk Factors:

The cause is unknown, but it may be linked to pregnancy hormones, especially rising HCG levels.
Some things that put you at risk are having multiples (twins, etc.), a history of motion sickness, headaches, or a family history of these conditions.
For most women, the first signs show up between 4 and 6 weeks into pregnancy.
It usually gets better between 16 and 20 weeks, but in some cases it can last the whole pregnancy.
The treatment focuses on rehydrating (IV fluids), treating sickness (antiemetics), and providing nutritional support.

Importance:

Early diagnosis and treatment are essential to keep both the mother and the baby from having serious problems. With the right care, results are usually satisfactory.

Why do some women have hyperemesis gravidarum

1. Effects of hormones

HCG (human chorionic gonadotropin): High levels of hCG are highly linked to HG, especially in the early stages of pregnancy. When women are pregnant with twins or moles (trophoblastic disease), their hCG levels are often higher, and their symptoms are worse.
Estrogen and progesterone: These hormones slow stomach emptying, which can cause nausea and vomiting.
The placenta makes a hormone called GDF15, which may play a key role, according to a new study published in 2023.

2. Genetic and family history of disease

A history of HG in the family raises the risk.
Differences in genes that affect hormone sensitivity may explain why some women have serious symptoms, and others don't.

3: Risk Factors

"Primigravida" means "first pregnant."
There were multiple pregnancies, such as twins or triplets.
Weight gain.
The patient had a history of HG before pregnancy.
Trophoblastic diseases, such as molar pregnancy, have been identified as contributing factors to weight gain.

4. Other Factors That Contributed

Issues with the pituitary gland can lead to excessive hormone production.
Stress in the mind may make symptoms worse, but it's not thought to be the main reason.
The thyroid may be involved: High levels of thyroid hormones can mimic or exacerbate the symptoms of HG.

Also, read https://www.breathethroughhg.org/hyperemesis-gravidarum

Important Signs of Hyperemesis Gravidarum

Severe sickness and throwing up (often more than three times a day)
Loss of weight (usually more than 5% of pre-pregnancy weight)
Dehydration (because they can't drink enough)
Imbalances in electrolytes (low potassium, sodium, etc.)

Ketosis occurs when the body breaks down fat for energy, which can be detected in urine.

Feeling dizzy, faint, or lightheaded;
Being worn out and weak from not getting enough food or water;
Headaches and confusion (from being dehydrated and having chemical changes)
In severe cases, individuals may experience low blood pressure and a rapid heart rate.

The video explains how hyperemesis can be cured

How to treat heavy periods during the first stage of pregnancy

Different ways to treat hyperemesis gravidarum in the first trimester

1. Care that helps

Hydration: liquid given through an IV to treat dehydration.
Replacing electrolytes: potassium, sodium, and other ions are checked and fixed.
Nutritional support: extra vitamins, especially thiamine to keep Wernicke's encephalopathy from happening.
Getting enough rest and lowering your stress can help ease your symptoms.

2. Measures of diet and lifestyle

Increase the frequency of small meals.
Avoiding triggers such as strong smells and fatty or spicy foods is also recommended.
Wristbands with ginger and massage may help a little.
Some people can handle cold foods better than hot ones.

3. Treatment with drugs (safe in the first trimester)

In the first place, vitamin B6 (pyridoxine) and doxylamine (an antihistamine) are used.
Antihistamines (diphenhydramine, meclizine) are the second line of defence.
Pentazocine and prochlorperazine are phenothiazines.
If the previous treatments are ineffective, the third-line option is Ondansetron; however, caution is advised when using this drug, as some studies indicate a small risk of birth defects, although it is typically prescribed when the benefits outweigh the risks.
Metoclopramide is a dopamine blocker that is usually safe.

4. Cases That Won't Go Away

Patients may need to stay in the hospital and receive water and medicines to help with vomiting.
In cases where other treatments don't work, corticosteroids like methylprednisolone may be considered. However, this should only be done after 10 weeks of pregnancy because of the risk of cleft palate.
Enteral or parenteral nutrients if the person can't eat or drink.

How to treat heavy periods during the second trimester

How to Treat Hyperemesis Gravidarum During the Second Trimester

1. Care that helps

IV water and electrolytes: fix imbalances and dehydration.
Giving extra thiamine stops Wernicke's encephalopathy, especially before giving glucose through an IV.
Nutritional support: oral intake is recommended if it can be managed; if not, enteral feeding (nasogastric or nasojejunal tube) or parenteral nutrition should be used in the worst cases.

2. Treatment with drugs

As a first step, keep giving pyridoxine (Vitamin B6) and doxylamine.
Antihistamines (diphenhydramine, meclizine) and phenothiazines (promethazine, prochlorperazine) are used as a second line of defence.
Third-line: Ondansetron and metoclopramide are still commonly used if the first two don't work.

"Corticosteroids: Methylprednisolone or prednisolone can be given after 10 weeks of pregnancy for HG that doesn't get better. This is because the risk of cleft palate is highest in the first three months of pregnancy."

3. Hospital stays and advanced medical care

Enteral feeding is better than parenteral nutrition because it keeps the gut healthy.
Parenteral nutrition: This is only used in grave, long-term cases where enteral feeding is not possible.
Monitoring involves regularly checking your weight, urine, ketones, electrolytes, and thyroid function.

Problems with hyperemesis gravidarum

Problems for mothers

Electrolyte imbalance and dehydration: Loss of water and electrolytes (sodium, potassium, and chloride) can make you weak, cause irregular heartbeats, and make you confused.
Vitamins and minerals can be lost when you vomit for a long time, especially thiamine, folate, and B12.
Wernicke's encephalopathy (confusion, weakness, and problems with eye movement) can happen if you don't get enough thiamine.
Loss of weight and muscle
It is normal to lose more than 5–10% of your pre-pregnancy weight.
Metabolic acidity can happen when your body breaks down fats for a long time.
Problems with the intestines and liver
Extreme cases may result in elevated liver enzymes and jaundice.
Anxiety, sadness, and being alone because of a long illness are some of the psychological effects.

Fetal Complications:

Low birth weight, a poor diet, and dehydration in the mother can slow the growth of the fetus.
Early Birth
Severe HG raises the chance of giving birth early.
SGA (Small for Gestational Age): Babies may be smaller than expected for their gestational age.
Possible Effects on Neurodevelopment
Some studies show that if a mother is severely malnourished, there may be long-term risks, but the evidence is still growing.
Stopping excessive vomiting during pregnancy

Ways to avoid getting hyperemesis gravidarum

1. Steps to Take Before and During Pregnancy

Prenatal medicines before getting pregnant: starting folic acid and multivitamins early may lower the risk of feeling very sick.
Please identify the factors that may put women at risk. For example, women who have had HG, repeated pregnancies, or molar pregnancies in the past should be closely watched.

2. Changes to your diet

Small meals more often: This keeps your stomach from being empty, which can make you feel worse if you're feeling sick.
Don't use triggers: Foods with strong smells or that are hot, fatty, or greasy tend to make symptoms worse.
High-protein snacks: Protein helps keep blood sugar stable and may also make you feel less sick.
Some people can handle cold or bland things better than hot ones.
Hydration: Drinking lots of water and clear or ginger-based drinks throughout the day.

3. Changes in lifestyle

Rest and less stress: Being worn out and stressed can make you feel sicker.
Wristbands with acupressure may help with motion sickness.
Ginger drinks or supplements have been shown to help with mild nausea caused by pregnancy.

4. Health Care Prevention

Taking antiemetics early: Women who are at a high risk (for example, who have had HG before) may be given vitamin B6 and doxylamine early in their pregnancy.
Taking extra thiamine: stops Wernicke's encephalopathy if puking gets severe.
Close monitoring: HG can't get worse if it's treated early with IV water and medicines.

Conclusion

Hyperemesis gravidarum (HG) is a major problem that can happen during pregnancy. It is difficult to predict and completely avoid because it is caused by many things, including changes in hormones (mainly HCG, estrogen, and GDF15), genetics, and pregnancy-specific risk factors.

HG isn't just "bad morning sickness"; it's a real illness that can put both mom and baby in danger. Early intervention, care from a team of experts, and patient teaching are all essential for lowering risks and improving outcomes.

Acute kidney injury treatment guidelines

Acute Kidney Damage—Overview

When kidney function abruptly decreases within hours to days, waste products build up in the blood and fluid, leading to disruptions in electrolyte and acid-base equilibrium. Serum creatinine rises rapidly, and urine production decreases from 48 hours to 7 days in AKI. The focus is on nephrology and critical care. Pathophysiology: Kidneys fail to filter blood, making waste elimination and fluid management difficult.

Acute kidney injury

Three main AKI categories exist.

Dehydration or cardiovascular illness prevents blood from reaching the kidneys, causing prerenal AKI.
Renal AKI: Kidney injury.
After renal AKI, the kidney drainage channels are blocked.

Treatments and prognoses vary for these three acute renal damage causes. Direct kidney injury is harder to heal and recover from than blood vessel or urinary system obstructions. The optimum therapy and recovery rate depend on early AKI diagnosis.

Symptoms

Low urine flow (oliguria or anuria)
Leg/ankle/eye swelling • Fatigue, disorientation, nausea, or seizures (from toxin buildup)
Symptoms of fluid overload: shortness of breath
Symptoms of electrolyte imbalance include chest pain or tightness.

Treatment

Address underlying causes, such as dehydration, infection, and blockage alleviation.
Provide support by managing electrolytes (potassium, sodium) and blood pressure.
Dialysis: Temporary or permanent if the kidneys cannot recover.
Review medications: Stop nephrotoxic medicines (NSAIDs, aminoglycosides, contrast agents).

Complications:

CKD or irreversible renal damage
Fluid overload causes pulmonary edema.
Electrolyte imbalances could potentially cause arrhythmias.
Increased mortality risk, especially in hospitalised or critically ill patients.

Long-Term Risks

AKI raises the likelihood of renal deterioration such as CKD or ESRD, even after apparent recovery.
Patients with recurrent AKI episodes are more susceptible to repeated insults like dehydration and sepsis.
AKI is a significant risk factor for long-term cardiovascular disease and mortality.

Complications matter

AKI complications can lead to high fatality rates, particularly in ICU patients.
AKI affects the heart, lungs, brain, and immune system, not only the kidneys.
Early recognition and care of problems (fluid balance, electrolytes, and infection control) are crucial for survival. The focus is on prevention.

Prevention/Monitoring

Monitoring creatinine, electrolytes, and urine output daily.
Avoid NSAIDs, aminoglycosides, and contrast dyes as nephrotoxins.
Ensure fluid control to avoid overburden or dehydration.
Dialysis started promptly for severe problems.

Diagnosis

Acute Kidney Injury (AKI) is diagnosed clinically as follows:

Diagnostic Criteria (KDIGO)

AKI is diagnosed if:

• Serum creatinine rise ≥ 0.3 mg/dL within 48 hours • Serum creatinine rise > 1.5× baseline within 7 days • Urine output < 0.5 mL/kg/hour for ≥ 6 hours

Diagnosis Steps

1. Clinic Assessment

History: Recent sickness, dehydration, sepsis, surgery, and medicine use (NSAIDs, antibiotics, contrast dye).
Symptoms include oliguria/anuria, edema, tiredness, disorientation, and nausea.
Risk factors: Diabetes, hypertension, CKD, and ageing.

2. Lab Tests

Elevated serum creatinine and BUN values indicate poor filtration.
Electrolytes: Hyperkalemia, hyponatremia, and metabolic acidosis.
Urinalysis: Proteinuria, hematuria, and muddy brown casts (indicating acute tubular necrosis).
FENa: Identifies prerenal vs intrinsic AKI.

3. Visualizing

Renal ultrasonography detects blockage (hydronephrosis, stones).
CT/MRI: Used for ultrasound inconclusiveness.
Assess renal blood flow with Doppler scans.

4. Additional Diagnostics

Early identification of developing biomarkers: NGAL, KIM-1, and cystatin C.
Renal biopsy: Rare but appropriate for suspected intrinsic diseases such as glomerulonephritis.

Diagnosis Difference

Prerenal AKI is characterized by low perfusion, which can lead to dehydration and shock.
Intrinsic AKI: Kidney injury brought on by toxins and inflammation.
Obstructive postrenal AKI is characterized by the presence of stones and prostate enlargement.

Monitoring:

Monitoring should include daily measurements of creatinine, urine output, and electrolytes, as well as the use of fluid balance charts and ECG monitoring for hyperkalemia-related arrhythmias.

The treatment for AKI depends on the underlying etiology.

This makes discovering the cause crucial. Some frequent AKI treatments are:

Stopping AKI-causing medications
Giving you fluids (orally or intravenously)
If AKI is bacterial, antibiotics
Placing a urinary catheter may help if AKI is caused by a blockage.
Kidney disease and other organ damage may require dialysis.
Most dialysis treatments are temporary until the kidneys recover.
Most individuals with AKI need hospitalization for monitoring and therapy.

Fixing the cause, stabilizing the patient, and preventing complications are the goals of AKI treatment. Management is supportive; no pharmacological cures.

Core AKI Treatment Principles

Determine and address the cause:
In prerenal AKI, restore blood flow by IV fluids, sepsis treatment, and heart failure management.
To treat intrinsic AKI, remove nephrotoxins and cure glomerulonephritis or interstitial nephritis, potentially with steroids.
Post-renal AKI: Address blockage with catheterization, surgery, or stents.
Supportive care:
Ensure fluid balance to prevent dehydration and overburden.
Address electrolyte imbalances, particularly hyperkalemia.
Manage metabolic acidosis; manage acid-base imbalance.
Adjust medications to prevent renal damage.
Dialysis (Renal Replacement Therapy): • Used to treat severe complications such as refractory hyperkalemia, metabolic acidosis, fluid overload, or uremic symptoms (encephalopathy, pericarditis).
The dialysis can be temporary during renal recovery or permanent if the damage is irreparable.

During Treatment Prevention

Track daily weight and urine output.
Regular blood tests (creatinine, electrolytes).
Use contrast dyes sparingly but necessarily.
Adjust medicine dosage for decreased renal clearance.

Challenges, risks

Delays in recognition negatively impact outcomes.
Overhydration can lead to pulmonary edema.
Underhydration might aggravate prerenal AKI.
Dialysis timing is crucial, as late treatment can increase mortality, and early treatment may not be essential.

Keynote

AKI treatment balances renal perfusion, trigger removal, and body support until kidney function recovers. Early diagnosis and monitoring can help prevent chronic renal disease.

To prevent acute kidney injury

Acute renal injury can't always be prevented due to age or hospitalization. There are techniques to protect the kidneys from long-term damage:

Annual checkup. Blood testing at an annual physical can check kidney health. It also helps doctors spot AKI-risk factors early.
Maintain hydration. It's crucial to stay hydrated to avoid AKI. Unless instructed by a doctor, drink 1.5 to 2 liters of water daily. Drink more water on hot days or while sick.
Diarrhea and vomiting need treatment. Dehydration from these symptoms increases AKI risk. Visit a doctor immediately to avoid AKI.

Care for underlying issues.

Treating CKD can avoid acute renal damage. CKD management includes avoiding NSAIDs, smoking, and potassium- and salt-rich meals.
Imaging contrast should be minimized. Discuss the pros and cons of iodine contrast dye with a doctor before specific imaging exams. Doctors may advise against using this dye since it can damage the kidneys.
Know if you have CKD or diabetes, which can cause acute renal injury. Knowing AKI signs can help you get medical care sooner.

Altering Lifestyle for Acute Kidney Injury

You can enhance your health and kidney function after acute renal injury by making these changes:
Regularly check your kidney health with your doctor.
Apples, carrots, green beans, and white rice are low-potassium. With kidney failure, people may have trouble eliminating extra potassium. Heart issues might result from high amounts.
There are foods that are limited in phosphorus. It's in cheese, oats, dark drinks, and nuts. Excess phosphorus in your blood can damage your bones and strain your kidneys.
Trade packaged foods, quick meals, snacks, and processed meats and cheeses for lower salt intake to control blood pressure. Hypertension increases AKI risk.
Hydrate to avoid renal stress and dehydration.
Acute Kidney Injury Prognosis
The source and severity of kidney injury determine AKI prognosis.

Recovery

Recovering from an AKI increases the chance of acquiring other health issues (e.g., kidney disease, stroke, or heart disease) or having another AKI in the future. AKIs raise the risk of renal disease and failure.
Follow up with your doctor to monitor kidney function and healing to protect yourself. To reduce kidney damage and preserve renal function, prevent or treat AKI early.
Many acute kidney damage patients recover completely if the underlying cause is treated promptly. However, repeated AKIs can damage the kidneys.
In the absence of chronic kidney disease, acute kidney damage may raise the risk. AKI can cause progressive CKD in 50% of patients and end-stage renal disease in 3–15%.
Managing your kidney health and treating any symptoms immediately will help you recover and repair any damage.

Conclusion

Kidney function drops suddenly in acute kidney injury, a dangerous, often reversible disorder. It has serious consequences for the kidneys, heart, lungs, brain, and immune system, so early detection and treatment are critical.

Systemic emergencies like AKI include the kidneys. Early detection, tailored therapy, and close monitoring can help many patients recover kidney function and prevent long-term complications. Late detection or poor management can cause permanent harm and death.