Headache : Most common causes

# Infection

* Common cold
* Flu
* Fever - headaches are common with fever from any type of infection
* Ear infection
* Tooth infection (type of Dental conditions)
* Sinus infection
* Pneumonia
* Measles
* Mumps
* Tonsillitis
* Sinus blockage
* Coughing - too much coughing can cause a form of traction headache.

# Various possible types of headache:

* Migraine
* Cluster headache
* Tension headache
* See also types of headache

# Lifestyle causes

* Hangover
* Excessive alcohol
* Stress
* Fatigue
* Tension
* Tiredness
* Excessive smoking

# Dyspepsia
# Eye conditions

* Glaucoma
* Eyestrain

# Medical procedures

* Spinal tap treatment
* Epidural - this anaesthetic procedure (common for childbirth) can occasionally cause damage to the spinal area and cause headache.

# Systemic or metabolic conditions

* Hypertension
* Thyroid disease
* Anemia
* Kidney failure (type of Kidney disease)
* Uremia
* Lead poisoning - African Folk Remedies - Kohl - headache
* Various toxins - see toxin causes of headache

# Brain or head conditions

* Meningitis
* Encephalitis
* Head injury
* Brain injury
* Mild traumatic brain injury
* Concussion
* Temporal arteritis
* Heatstroke
* Sunstroke
* Blood clots - in the brain, these can cause a stroke.
* Brain aneurysm
* Subdural hematoma
* Stroke
* Transient ischemic attacks
* Subarachnoid hemorrhage
* Brain tumor
* Benign intracranial hypertension
* Trigeminal neuralgia

Giant baby 8.7 kg born in Indonesia

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Management Of a Comatose Child : Emergency

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Malaria : Epidemiology, signs and symptoms

FActs about Malaria

1. Malaria is a life-threatening disease caused by parasites that are transmitted to people through the bites of infected mosquitoes.
2. A child dies of malaria every 30 seconds.
3. There were 247 million cases of malaria in 2006, causing nearly one million deaths, mostly among African children.
4. Malaria is preventable and curable.
5. Approximately half of the world's population is at risk of malaria, particularly those living in lower-income countries.
6. Travellers from malaria-free areas to disease "hot spots" are especially vulnerable to the disease.Malaria takes an economic toll - cutting economic growth rates by as much as 1.3% in countries with high disease rates.

Malaria is caused by parasites of the species Plasmodium. The parasites are spread to people through the bites of infected mosquitoes.

There are four types of human malaria:

Plasmodium falciparum
Plasmodium vivax
Plasmodium malariae
Plasmodium ovale.
Plasmodium falciparum and Plasmodium vivax are the most common. Plasmodium falciparum is the most deadly.




Common symptoms of malaria
In the early stages, malaria symptoms are sometimes similar to those of many other infections caused by bacteria, viruses, or parasites. Symptoms may include:
Fever.
Chills.
Headache.
Sweats.
Fatigue.
Nausea and vomiting.
Other common symptoms of malaria include:
Dry (nonproductive) cough.
Muscle and/or back pain.
Enlarged Spleen

Complications of Malaria( Falciparum):
Cerebral malaria
Algid Malaria
ARDS
Convulsion
Coma
Acute Renal Failure
Hypoglycemia
hyperthermia
hyperparasitemia
severe anemia


Symptomatic diagnosis
Using Giemsa-stained blood smears from children in Malawi, one study showed that when clinical predictors (rectal temperature, nailbed pallor, and splenomegaly) were used as treatment indications, rather than using only a history of subjective fevers, a correct diagnosis increased from 21% to 41% of cases and unnecessary treatment for malaria was significantly decreased.

Microscopic examination of blood films
Field tests
In areas where microscopy is not available, or where laboratory staff are not experienced at malaria diagnosis, there are antigen detection tests that require only a drop of blood. Immunochromatographic tests (also called: Malaria Rapid Diagnostic Tests, Antigen-Capture Assay or "Dipsticks") have been developed, distributed and fieldtested. These tests use finger-stick or venous blood, the completed test takes a total of 15–20 minutes, and a laboratory is not needed. The threshold of detection by these rapid diagnostic tests is in the range of 100 parasites/µl of blood compared to 5 by thick film microscopy. The first rapid diagnostic tests were using P. falciparum glutamate dehydrogenase as antigen.[42] PGluDH was soon replaced by P.falciparum lactate dehydrogenase, a 33 kDa oxidoreductase [EC 1.1.1.27]. It is the last enzyme of the glycolytic pathway, essential for ATP generation and one of the most abundant enzymes expressed by P.falciparum. PLDH does not persist in the blood but clears about the same time as the parasites following successful treatment. The lack of antigen persistence after treatment makes the pLDH test useful in predicting treatment failure. In this respect, pLDH is similar to pGluDH. The OptiMAL-IT assay can distinguish between P. falciparum and P. vivax because of antigenic differences between their pLDH isoenzymes. OptiMAL-IT will reliably detect falciparum down to 0.01% parasitemia and non-falciparum down to 0.1%. Paracheck-Pf will detect parasitemias down to 0.002% but will not distinguish between falciparum and non-falciparum malaria. Parasite nucleic acids are detected using polymerase chain reaction. This technique is more accurate than microscopy. However, it is expensive, and requires a specialized laboratory. Moreover, levels of parasitemia are not necessarily correlative with the progression of disease, particularly when the parasite is able to adhere to blood vessel walls. Therefore more sensitive, low-tech diagnosis tools need to be developed in order to detect low levels of parasitaemia in the field. Areas that cannot afford even simple laboratory diagnostic tests often use only a history of subjective fever as the indication to treat for malaria. Using Giemsa-stained blood smears from children in Malawi, one study showed that unnecessary treatment for malaria was significantly decreased when clinical predictors (rectal temperature, nailbed pallor, and splenomegaly) were used as treatment indications, rather than the current national policy of using only a history of subjective fevers (sensitivity increased from 21% to 41%).


Molecular methods
Molecular methods are available in some clinical laboratories and rapid real-time assays (for example, QT-NASBA based on the polymerase chain reaction) are being developed with the hope of being able to deploy them in endemic areas.

Rapid antigen tests
OptiMAL-IT will reliably detect falciparum down to 0.01% parasitemia and non-falciparum down to 0.1%. Paracheck-Pf will detect parasitemias down to 0.002% but will not distinguish between falciparum and non-falciparum malaria. Parasite nucleic acids are detected using polymerase chain reaction. This technique is more accurate than microscopy. However, it is expensive, and requires a specialized laboratory. Moreover, levels of parasitemia are not necessarily correlative with the progression of disease, particularly when the parasite is able to adhere to blood vessel walls. Therefore more sensitive, low-tech diagnosis tools need to be developed in order to detect low levels of parasitaemia in the field.

Tropical diseases in Asia

Malaria
Cholera
Dysentery
Intestinal Worms
Dengue Fever
Yellow Fever
Schistosomiasis
Leprosy
Filariasis
Trypanosomiasis
Hepatitis
Chlamydia Trachomatis

Pneumonia : xRay Consolidation

Picture a:??? Anyone can explain-post comment

Picture b: Right lower zone Consolidation

Classification: Pneumonia

Early classification schemes

Initial descriptions of pneumonia focused on the anatomic or pathologic appearance of the lung, either by direct inspection at autopsy or by its appearance under a microscope.

A lobar pneumonia is an infection that only involves a single lobe, or section, of a lung. Lobar pneumonia is often due to Streptococcus pneumoniae (though Klebsiella pneumoniae is also possible.)
Multilobar pneumonia involves more than one lobe, and it often causes a more severe illness.
Bronchial pneumonia affects the lungs in patches around the tubes (bronchi or bronchioles).
Interstitial pneumonia involves the areas in between the alveoli, and it may be called "interstitial pneumonitis." It is more likely to be caused by viruses or by atypical bacteria.

The discovery of x-rays made it possible to determine the anatomic type of pneumonia without direct examination of the lungs at autopsy and led to the development of a radiological classification. Early investigators distinguished between typical lobar pneumonia and atypical (e.g. Chlamydophila) or viral pneumonia using the location, distribution, and appearance of the opacities they saw on chest x-rays. Certain x-ray findings can be used to help predict the course of illness, although it is not possible to clearly determine the microbiologic cause of a pneumonia with x-rays alone.

With the advent of modern microbiology, classification based upon the causative microorganism became possible. Determining which microorganism is causing an individual's pneumonia is an important step in deciding treatment type and length. Sputum cultures, blood cultures, tests on respiratory secretions, and specific blood tests are used to determine the microbiologic classification. Because such laboratory testing typically takes several days, microbiologic classification is usually not possible at the time of initial diagnosis.

Combined clinical classification
Traditionally, clinicians have classified pneumonia by clinical characteristics, dividing them into "acute" (less than three weeks duration) and "chronic" pneumonias. This is useful because chronic pneumonias tend to be either non-infectious, or mycobacterial, fungal, or mixed bacterial infections caused by airway obstruction. Acute pneumonias are further divided into the classic bacterial bronchopneumonias (such asStreptococcus pneumoniae), the atypical pneumonias (such as the interstitial pneumonitis of Mycoplasma pneumoniae or Chlamydia pneumoniae), and the aspiration pneumonia syndromes.

Chronic pneumonias, on the other hand, mainly include those of Nocardia, Actinomyces and Blastomyces dermatitidis, as well as the granulomatous pneumonias (Mycobacterium tuberculosis and atypical mycobacteria, Histoplasma capsulatum and Coccidioides immitis).

The combined clinical classification, now the most commonly used classification scheme, attempts to identify a person's risk factors when he or she first comes to medical attention. The advantage of this classification scheme over previous systems is that it can help guide the selection of appropriate initial treatments even before the microbiologic cause of the pneumonia is known. There are two broad categories of pneumonia in this scheme: community-acquired pneumonia and hospital-acquired pneumonia. A recently introduced type of healthcare-associated pneumonia (in patients living outside the hospital who have recently been in close contact with the health care system) lies between these two categories.

Community-acquired pneumonia
Community-acquired pneumonia (CAP) is infectious pneumonia in a person who has not recently been hospitalized. CAP is the most common type of pneumonia. The most common causes of CAP vary depending on a person's age, but they include Streptococcus pneumoniae, viruses, the atypical bacteria, and Haemophilus influenzae. Overall, Streptococcus pneumoniae is the most common cause of community-acquired pneumonia worldwide. Gram-negative bacteria cause CAP in certain at-risk populations. CAP is the fourth most common cause of death in the United Kingdom and the sixth in the United States. The term "walking pneumonia" has been used to describe a type of community-acquired pneumonia of less severity (because of the fact that the sufferer can continue to "walk" rather than require hospitalization). Walking pneumonia is usually caused by the atypical bacteria mycoplasma pneumonia.

Hospital-acquired pneumonia
Hospital-acquired pneumonia, also called nosocomial pneumonia, is pneumonia acquired during or after hospitalization for another illness or procedure with onset at least 72 hrs after admission. The causes, microbiology, treatment and prognosis are different from those of community-acquired pneumonia. Up to 5% of patients admitted to a hospital for other causes subsequently develop pneumonia. Hospitalized patients may have many risk factors for pneumonia, including mechanical ventilation, prolonged malnutrition, underlying heart and lung diseases, decreased amounts of stomach acid, and immune disturbances. Additionally, the microorganisms a person is exposed to in a hospital are often different from those at home . Hospital-acquired microorganisms may include resistant bacteria such as MRSA, Pseudomonas, Enterobacter, andSerratia. Because individuals with hospital-acquired pneumonia usually have underlying illnesses and are exposed to more dangerous bacteria, it tends to be more deadly than community-acquired pneumonia.Ventilator-associated pneumonia (VAP) is a subset of hospital-acquired pneumonia. VAP is pneumonia which occurs after at least 48 hours of intubation and mechanical ventilation.

Other types of pneumonia
Severe acute respiratory syndrome (SARS)
SARS is a highly contagious and deadly type of pneumonia which first occurred in 2002 after initial outbreaks in China. SARS is caused by the SARS coronavirus, a previously unknown pathogen.
Bronchiolitis obliterans organizing pneumonia (BOOP)
BOOP is caused by inflammation of the small airways of the lungs. It is also known as cryptogenic organizing pneumonitis (COP).
Eosinophilic pneumonia
Eosinophilic pneumonia is invasion of the lung by eosinophils, a particular kind of white blood cell. Eosinophilic pneumonia often occurs in response to infection with a parasite or after exposure to certain types of environmental factors.
Chemical pneumonia
Chemical pneumonia (usually called chemical pneumonitis) is caused by chemical toxicants such as pesticides, which may enter the body by inhalation or by skin contact. When the toxic substance is an oil, the pneumonia may be called lipoid pneumonia.
Aspiration pneumonia
Aspiration pneumonia (or aspiration pneumonitis) is caused by aspirating foreign objects which are usually oral or gastric contents, either while eating, or after reflux or vomiting which results inbronchopneumonia. The resulting lung inflammation is not an infection but can contribute to one, since the material aspirated may contain anaerobic bacteria or other unusual causes of pneumonia. Aspiration is a leading cause of death among hospital and nursing home patients, since they often cannot adequately protect their airways and may have otherwise impaired defenses.

Dust pneumonia
Dust pneumonia describes disorders caused by excessive exposure to dust storms, particularly during the Dust Bowl in the United States. With dust pneumonia, dust settles all the way into the alveoli of the lungs, stopping the cilia from moving and preventing the lungs from ever clearing themselves.

Necrotizing pneumonia, although overlapping with many other classifications, includes pneumonias that cause substantial necrosis of lung cells, and sometimes even lung abscess. Implicated bacteria are extremely commonly anaerobic bacteria, with or without additional facultatively anaerobic ones like Staphylococcus aureus, Klebsiella pneumoniae and Streptococcus pyogenes. Type 3 pneumococcus is uncommonly implicated.

Opportunistic pneumonia includes those that frequently strike immunocompromised victims. Main pathogens are cytomegalovirus, Pneumocystis jiroveci, Mycobacterium avium-intracellulare, invasiveaspergillosis, invasive candidiasis, as well as the "usual bacteria" that strike immunocompetent people as well.

USMLE case: surgery or medicine

A 13-year-old boy has a 3-day history of low-grade fever, upper respiratory symptoms, and a sore throat. A few hours before his presentation to the emergency room, he has an abrupt onset of high fever, difficulty swallowing, and poor handling of his secretions. He indicates that he has a marked worsening in the severity of his sore throat. His pharynx has a fluctuant bulge in the posterior wall. Which of the following is the most appropriate initial therapy for this patient?

A.Narcotic analgesics

B.Trial of oral penicillin V

C.Surgical consultation for incision and drainage under general anesthesia

D.Rapid streptococcal screen

E.Monospot test

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Seasonal hyperacute panuveitis (SHAPU) In Nepal

Seasonal hyperacute panuveitis (SHAPU), characterized by an unusual form of unilateral severe hyper acute diffused intraocular inflammation, is one of the mysterious eye diseases of which the definite cause and treatment remains yet to be tound out. In this study, a total of six cases were included. Aqueous and vitreous samples were subjected to direct microscopy and culture (bacterial or fungal). Of the six cases included, two yielded Streptococcus pneumoniae and one Acinetobactor sp. on culture. All three culture positive samples showed pus cells in direct microscopic examination (gram stain). All cases were subjected to vitrectomy and intravitreal antibiotic and steroid injection, along with oral antibiotics and steroid. Five cases were also treated with antiviral agent. After treatment four cases showed reversal of hypotony and three cases recovered some vision.

Moths have been reported to increase the prevalence of this disease. Complications can be as devastating as blindness.

Read NMJ journal Article...Read

Swine Flu 4 vaccines Declared

The US Food and Drug Administration (FDA) announced today that it has approved 4 vaccines against the 2009 influenza A (H1N1) virus, formerly known as "swine flu." The vaccine lots are expected to be available and distributed within the next 4 weeks.

FDA Commissioner of Food and Drugs Margaret A. Hamburg, MD, said she thought Tuesday's approval was good news for the nation's response to the H1N1 influenza virus. "This vaccine will help protect individuals from serious illness and death from influenza," she said.

The approval comes at a time when the Centers for Disease Control and Prevention (CDC) is reporting that visits to physicians around the country for influenza-like illness are increasing and are higher than expected at this time of year. The vaccines that are currently available against 3 seasonal influenza virus strains will not protect against the 2009 H1N1 virus.

The FDA said that the vaccines, based on early data, effectively elicit an immune response in most healthy adults about 8 to10 days after vaccination. Clinical studies are still underway to produce an optimal dose for children, with results expected in the near future.

Meanwhile, the CDC stresses that influenza is primarily spread through person-to-person contact, by the coughing or sneezing of infected people, and recommends that infected people stay home and limit their contact with others to keep from infecting them.

The newly approved vaccines are being made by CSL Limited, MedImmune LLC, Novartis Vaccines and Diagnostics Limited, and Sanofi Pasteur Inc. All 4 firms reportedly use the same processes to manufacture the H1N1 vaccines. As with the seasonal influenza vaccine, some lots of the H1N1 vaccine will contain the preservative thimerosal and others will not. The FDA has been continuing its efforts toward reducing thimerosal used in vaccines.

The FDA warns that persons with known allergies to chicken eggs or any other substance in the vaccine should probably not be vaccinated, although in the ongoing clinical trials, the vaccines have been well tolerated. The most common adverse effect is soreness at the injection site; other adverse effects can include a mild fever, body aches, and fatigue for a couple of days after vaccination. For the nasal spray delivery system, the most common adverse effects were runny nose, nasal congestion in all ages, sore throats in adults, and fever in children aged 2 to 6 years.

The FDA is working with different organizations regarding adverse event monitoring, information sharing, and an overall analysis during and after the 2009 H1N1 vaccination program, according to the news release. "As with any medical product, unexpected or rare serious adverse events may occur," the FDA notes.

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Tetralogy of Fallot

Tetralogy of Fallot

is the most common Cyanotic heart disease in children. The condition causes mixing of deoxygenated blood with the oxygenated blood being pumped out of the heart and into the circulatory system of blood vessels, Causing-

• hypoxemia.
  
  
• cyanosis, a bluish color of the skin, lips, and membranes inside the mouth and nose.

The 4 abnormalities (tetralogy) of the heart described by Fallot include the following:

• Right ventricular hypertrophy: Narrowing or blockage of the pulmonary valve and/or muscle under the pulmonary valve coming out of the right ventricle. This restriction to blood outflow causes an increase in right ventricular work and pressure, leading to right ventricular thickening or hypertrophy.
  
  
• Ventricular septal defect (VSD): This is a hole in the heart wall (septum) that separates the 2 ventricles. The hole is usually large and allows oxygen-poor blood in the right ventricle to pass through, mixing with oxygen-rich blood in the left ventricle. This poorly oxygenated blood is then pumped out of the left ventricle to the rest of the body. The body gets some oxygen, but not all that it needs. This lack of oxygen in the blood causes cyanosis.
  
  
• Abnormal position of the aorta: The aorta, the main artery carrying blood out of the heart and into the circulatory system, exits the heart from a position overriding the right and left ventricles. (In the normal heart, the aorta exits from the left ventricle.) This is not of major importance in infants.
  
  
• Pulmonary valve stenosis (PS): The major issue with tetralogy of Fallot is the degree of pulmonary valve stenosis, since VSD is always present. If the stenosis is mild, minimal cyanosis occurs, since blood still mostly travels to the lungs. However, if the PS is moderate to severe, a smaller amount of blood reaches the lungs, since most is shunted right-to-left through the VSD

Investigations:

CXR - baseline
ECG - yearly to assess rhythm and QRS duration
TTE - regularly (yearly or more frequent if severe PR and RV dysfunction, can be 2 or 3 yearly if very good surgical result and no new symptoms) (NB. It is easy to under estimate the degree of PR by colour follow alone) To assess pulmonary valve function, proximal PA anatomy, RV size and function, LV function, aortic root size and degree of aortic regurgitation.
Catheterisation - for dilatation / stenting of pulmonary arteries
MRI - becoming investigation of choice for proximal pulmonary artery anatomy, RV size and function and assessment of pulmonary regurgitation
Holter - for symptoms and screening for VT or high grade ectopy in those with marked RV dilatation or QRS > 180ms
Exercise test / CPEX - exercise capacity serial assessment, pre-pregnancy counselling

Additional investigations - EP studies for those with symptomatic atrial or ventricular arrhythmias or unexplained syncope or pre-syncope


Indications for intervention

Unrepaired tetralogy of Fallot (at any age)
Significant RVOT or branch PA stenosis (RV pressure > half systemic)
Severe pulmonary regurgitation with dilatation and dysfunction of the RV
Aortic regurgitation
Arrhythmias in presence of repairable haemodynamic sequela

TREATMENT OPTIONS
Surgery (+/- anti-arrhythmia procedures)

Percutaneous pulmonary valve implantation (for those with an RV to PA conduit of suitable size only)

Percutaneous pulmonary artery angioplasty and stenting

Rickets: Clinical features Photo Gallery

Rickets : Valgus deformity ( knock Knee)


Pot Belly in rickets

Bowing of Legs: Genu Varum

Widening of Wrist

Paediatric Case: Your Diagnosis 1

Case : Paediatrics

A 13 year Male child came with complains of swelling of the body starting from the periorbital area for 8 days and then pitting oedema on the legs for 2 days.There is no history of fever but he complains of headache, temporal aggravated by heat and there is Blurring of vision as well.

He complains of occassional productive cough with blood stained sputum.

No H/O sore throat, TB or other disease in tha past.

He is staying at hostel and his senior has tuberculosis.

O/E:

GC: fair

Vitals: BP=140/100, rest stable

JALCyClOD= Pitting Edema, Bilateral legs

Chest/CVS/PA= No Abnormality detected

local: legs=pustular, echtymic rashes.

Xray: fluffy infiltrates bilateral

Urine:frothy,albumin ++,RBC-,pus cell-normal

Photo of rashes:

Diagnosis?

Rickets: Clinical Features

• Head
  • Skull - Craniotabes may occur, in which the bones of the skull soften and flattening of the posterior skull can be seen. These effects may be transient or permanent. Another feature is the prominence of the frontal bones and the major foramen, resulting in frontal bossing or a prominent, sometimes square, forehead (caput quadratum).
  • Teeth - Teeth may erupt later than normal because of undermineralization. Enamel can be of poor quality, resulting in caries.
• Thorax
  • Rachitic rosary - The enlarged ends of the ribs, resembling beads, can be palpable and visible at the costochondral junction. As a result, the sternum can become more prominent, leading to a pigeon breast or pectus carinatum appearance.
  • Harrison groove - The groove is a semicoronal impression over the abdomen at the level of the insertion of the diaphragm, which can be seen in rickets.
• Spine - A mild to more pronounced scoliosis may be seen as a result of rickets.
• Pelvis - A prominent promontory can be found, and the anteroposterior (AP) diameter of the pelvis can shrink as a result of scoliosis. If this persists in girls, it can cause complications later in life during childbirth.
• Extremities
  • Arms
    • Bowing of the long bones, as a reaction to greenstick fractures, results from concurrent osteomalacia.
    • Thickening of the wrist at the level of the epiphysis is not visible radiographically, since the lesion consists of cartilage, although fraying and cupping of the metaphysis is evident.
  • Legs
    • Bowing of the long bones (genu varum)as a result of weight bearing is typical.
    • Anterior bowing of the tibia (saber shin deformity) may occur.
    • Development of knock-knees (genu valgum) may occur because of displacement of the growth plates during active disease.
    • Thickening at the level of the ankle may occur, identical to the process in the wrist.
• Ligaments and muscles - Laxity in the ligaments is increased, and muscle tone is decreased. This combination leads to a delay in motor development.

Rickets : X Rays

Xray: Bowing of legs




Cupping of epiphysis
Splaying of Metaphysis

11 Categories Of Rickets

Because rickets results from a metabolic disturbance, the underlying disease should be diagnosed. The causes of rickets can be classified into 11 main categories:

• Vitamin D deficiency
  • Dietary deficiency
  • Deficient endogenous synthesis
• Gastrointestinal tract disorders
  • Small intestine diseases with malabsorption
  • Partial or total gastrectomy
  • Hepatobiliary disease
  • Chronic pancreatic insufficiency
• Disorders of vitamin D metabolism
  • Hereditary - Pseudovitamin D deficiency or vitamin D dependency (types I and II)
  • Acquired
    • Use of anticonvulsants
    • Chronic renal failure
• Acidosis
  • Distal renal tubular acidosis (classic or type I)
  • Secondary forms of renal acidosis
  • Ureterosigmoidostomy
  • Drug-induced disease
    • Chronic acetazolamine ingestion
    • Chronic ammonium chloride ingestion
• Chronic renal failure
• Phosphate depletion
  • Dietary - Low phosphate intake plus ingestion of nonabsorbable antacids
    • Hereditary - X-linked hypophosphatemic rickets or adult-onset vitamin D–resistant hypophosphatemic osteomalacia
    • Acquired - Sporadic hypophosphatemic osteomalacia (phosphate diabetes), tumor-associated (oncogenous) rickets, osteomalacia, neurofibromatosis, and fibrous dysplasia
• Generalized renal tube disorders
  • Primary renal tube disorders
  • Renal tube disorders associated with systemic metabolic abnormality
    • Cystinosis
    • Glycogenosis
    • Lowe syndrome
  • Systemic disorder with associated renal disease
    • Hereditary - Inborn errors (Wilson disease, tyrosinemia) and neurofibromatosis
    • Acquired - Multiple myeloma, nephrotic syndrome, and kidney transplantation
    • Intoxication-related - Cadmium, lead, outdated tetracycline
• Primary mineralization defects
  • Hereditary
  • Acquired
    • Diphosphonate treatment
    • Fluoride treatment
• States of rapid bone formation with or without a relative defect in bone resorption
  • Postoperative hyperparathyroidism with osteitis fibrosa cystica
  • Osteopetrosis
• Defective matrix synthesis - Fibrogenesis imperfecta ossium
• Miscellaneous
  • Magnesium-dependent conditions
  • Axial osteomalacia
  • Parenteral alimentation
  • Aluminum intoxication
  • Isofosfamide treatment

Moment to Remember : EBOLA and Cholera

Virus : A threat to Human Civilization

Fat Soluble Vitamins: ADEK and deficiency Symptoms

Vitamin A Deficiency
Acne, allergies, loss of appetite, blindness, colds, dry hair, eye sties, fatigue, insomnia, impaired growth, itching and burning eyes, loss of smell, night blindness, dry skin, sinus trouble, steroid synthesis reduction; Decreased immune system function, cancer susceptibility. (Vitamin A is essential for bones and teeth and protects against cold and flu.)

Vitamin D deficiency
DEFICIENCY SYMPTOMS:Brittle and fragile bones, burning in mouth and throat, diarrhea, insomnia, irregular heartbeat, low blood calcium, myopia, nervousness, pale skin, poor metabolism, rickets, sensitivity to pain, soft bones and teeth, Osteoporosis and Osteopenia, and hypocalcemia. Vitamin D also enhances the immune system

Vitamin E Deficiency:
DEFICIENCY SYMPTOMS:Enlarged prostate gland, gastrointestinal disease, dry or falling out hair, impotency, miscarriages, muscular wasting, muscle weakness, sterility. Decreased circulation, slow tissue healing, leg cramps. Vitamin E helps prevent cancer, cardiovascular disease, cataracts and reduces scarring from some wounds. Zinc and Vitamin E work together.

Vitamin K deficiency:
DEFICIENCY SYMPTOMS:Brittle or fragile bones, low platelet count in blood and poor blood clotting, high glucose in blood. Vitamin K plays an essential role in blood clotting and bone formation. Can help to prevent osteoporosis. Vitamin K also converts glucose into glycogen for storage in the liver.