Wednesday, January 17, 2018
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Prevention of Typhoid Fever


Enteric group of fever (typhoid fever) includes typhoid and para typhoid (A, B and C ) fever, which are bacterial infections characterized in their typical form by continuous fever, serve headache, enlargement of spleen, diarrhea and sometimes rose spots appearing on the trunk.

Source of Infection and Mode of Transmission

Bacteria are passed in the feces and urine of infected persons, who may be patients or carriers showing no sign of disease. When these bacteria are ingested infection occurs. Transmission may occur by direct or indirect contact with such feces or urine in any of the following ways:

a. Directly by the hands of patient, a convalescent, or a carrier

b. Flies transmitting germs from uncovered excreta or latrines and urinals to kitchens

c. Careless passage of feces or urine directly into streams or rivers or in the neighborhoods of streams, river and walls

d. Sitting latrines, cesspits, septic tanks and streams or rivers

e. Dust

Preventive Measures

These comprise strict adherence to general sanitary measure keeping in view the mode of transmission. Strict water and food discipline should be observed.

a. Protection of water supplies from pollution and sterilization by chlorination or by boiling

b. Proper sanitary disposal of human excreta

c. Latrines and refuse bins should be cleaned regularly

d. Strict fly control by instituting anti fly measures be adopted

e. Protection of food from files and dust

f. Sterilize milk by boiling or pasteurization

g. Properly supervise processing, preparation and serving of all foods especially those that are earth raw, vegetables as well as fruits be thoroughly washed in drinking water before consumption

h. Prohibit eating and drinking from unauthorized sources and places which do not conform to proper sanitary standards

i. Maintain high standard of kitchen hygiene and personal cleanliness of personal employed in cooking or handling food

j. Evacuation of suspected cases to the nearest hospital

k. Carryout TAB inoculation of all individuals and their families once every year

l. Anyone who has suffered from infectious hepatitis, enteric fever or dysentery should not be employed as cooks or cook in the kitchen for at least six months after their discharge from hospital


Prevention and Control of Dengue Fever


Dengue fever is a disease that occurs following the bite of an infected mosquito Aedes Aegypti. This type of mosquito has peculiar white spotted body and legs. It breeds in clean water and has a flight range of only 100-200 meters.

Measures for Prevention and Control of Dengue Fever

Water is must for breeding of mosquitoes. No standing water means no mosquitoes. Hence eliminating the source of breeding or denying access of mosquitoes to water is the first measure to control the emergence of dengue fever.

Prevention of dengue fever is the responsibility of every one and not just authorities. Fly proofing is a must and anyone having any sign of illness must report to a doctor immediately.

Anti Larval Measures 

a. Prevent water collection in the form of small puddles

b. All used bottles, tins and other containers should be properly disposed off

c. Temephos should be sprayed/sprinkled once a week or used engine oil may be used once a week on the ponds or water collections, which can not be drained.

Anti –Adult Mosquito Measures

  • Adult mosquitoes are killed by insecticides which should be sprayed in living accommodation
  • Insecticides to be sprayed are as under:

Knock Down Insecticides

Sprayed in rooms and other buildings with permethrine oil spary, as and when required.

Residual Insecticides

Sprayed on walls /ceilings of all buildings with deltamethrin wettable powder on monthly basis.

Personal Protective Measures

  1. Mosquito nets may be used while in bed during night and by those who may rest during the day . Mosquitoes nets if sprayed upon with based deltamethrin afford better protection. Such nets should be kept hanging on the beds at all times
  2. Mosquito repellent oils should be applied on exposed parts of the body during night at intervals of three hours, except when actually sleeping under mosquitoes nets .
  3. Full sleeve cloths and long dresses should be worn to cover as much of the body as possible.

Prevention of AIDS


AIDS is a viral infection. A person having HIV/ AIDS  can transmit the infection to a healthy individual. The HIV virus may be present in the blood, semen, rectal fluids of infected men and blood, vaginal fluids and breast milk of infected women.

The different modes of transmission are:

a. A healthy man can get HIV /AIDS if he does or receives sexual intercourse from an infected man through rectal or oral route.

b. A healthy woman can acquire HIV/AIDS if she does sexual intercourse with an infected man through vaginal, rectal or oral route.

c. HIV can be transmitted from mother to child during pregnancy, labor or by breast feeding.

d. Sharing syringes with HIV infected drug addicts.

e. In hospitals HIV can be transmitted through contaminated needles, dental and surgical instruments.

f. Transfusion of blood and blood products without proper screening for HIV.

g. HIV is not transmitted by casual contact, such as kissing, hugging, shaking hands, sharing personal objects or eating and drinking in same utensil

Once a person is infected with HIV, he usually does not develop any major illness in the beginning . The virus keeps on multiplying in his blood and after a period of 7 to 10 years destroys his immune systems, leaving him defenseless against a number of infections and cancer. If he does not receive appropriate treatment at this stage, he suffers from serious infections and some types of cancer and eventually dies. The treatment of HIV is difficult and expensive. The treatment continues throughout the rest of life of patient

Even if a person does not die of the disease, he is socially cut of from society, friends and relatives. He is deprived of employment and also suffers financially.

Prevention Measures for AIDS

  1. The best way to prevent having HIV/AIDS is to have sex with spouse only.
  2. As the highest risk of transmission HIV/AIDS is a man having sex with man so such a relation should be avoided .
  3. The risk of getting HIV/AIDS is more if there are multiple sex partners so it is better to have one sex partner.
  4. It is better to know the HIV status of partner before having sex.
  5. Latex condoms should be worn whenever sex is done with someone other than spouse.
  6. Proper technique of using condoms must be ensured.

Post Exposure Prophylaxis

Post exposure prophylaxis means giving anti –HIV drugs to someone who is seriously exposed to the risk of acquiring HIV, such as health worker accidentally pricked by a syringe used for injections in HIV infected patient, or someone having sex with a person who turns out to be patient of HIV.

Post exposure prophyalxis should be started immediately and there is little or no benefit of giving it after 3 days of exposure. It should be continued for one month.

Clinical Case: Bad Obstetric History

pregnancy week 10

Clinical Case

A 28 years old presented with 12 weeks gestation. She has previous history of one intrauterine death at 35 weeks. How will you proceed?


We will proceed by taking detailed history and carrying out investigations.

Detailed history:

Detailed history will include specific emphasis to following points:

  • Metabolic disease
    • Diabetes mellitus
  • Preecclampsia
  • Drug history
  • Antiphopholipid syndrome
  • Fetal heart present
    • Never
    • Disappeared before loss
    • Present still
  • Family history of thromboemolic phenonmenon
  • Consanguinous marriage


Both general and specific investigations will be carried out.

  • General:
    • Blood complete count
    • Blood group and cross match
    • TSH, Blood sugars
    • FSH, LH and prolactin
    • LFTs
    • RFTs
  • Specific:
    • Ultrasonography
    • Hormonal profile


8 Things to Memorize in Pediatrics


It always pays to memorize the following in pediatrics.

Heart Rate

New born 120-140 / min
Infant (less than 1 year) 80-120 / min
Up to 5 years 75-120 / min
5-15 years 70-110 / min

Most common causes of tachycardia in pediatrics are

(1) Fever

(2) Anemia

Respiratory Rate

New born 30-60 / min
Infant (less than 1 year) 20-40 / min
1-3 years 20-30 / min
4-10 years 15-25 / min
Over 10 years 15-20 / min

Blood Pressure

(Systolic = at 6 years it is 100mmHg, add 2.5 mmHg/year after 6)                    

(Diastolic = age in years+60)

New born 70/40 mmHg

(35-60mmHg by flush method)

Infant (less than 1 year) 80/55 mmHg
Up to 5 years 90/60 mmHg
5-15 years 100-110/70 mmHg


(Active=Increase temperature by 10c)

(Place thermometer in armpit for 2 min)

Normal temperature 97.50 F – 99.50 F

Fronto-Occipital Circumference (FOC)

At birth = 35cm

First 3 months = 6cm rise

Next 3 months = 3cm rise

Next 3 months = 2cm rise

At 1 year = 47cm

2,3,5 years = 1,1,1 cm rise

Rule of 0.5 (after 5th year) = 6 years to 12 years = 51 + 0.5cm/year 

(i.e. at 6years=51.5 

at 12 years = 54/55cm)

New born 35cm
3 months 41cm
6 months 44cm
9 months 46cm
1 year 47cm
2 years 49cm
3 years 50cm
5 years 51cm
6 years 51.5cm
7 years 52cm
8 years 52.5cm
9 years 53cm
10 years 53.5cm
11 years 54cm
12 years 54-55cm


At birth = 50cm

Within 1st year = 25cm rise

1st to 2nd year = 10cm rise

2nd to 3rd year = 10cm rise

 Formula = (From 2-12 years [age in yearsx6]+77 cm)

My Rule of 6 (after 3rd year) = 4 years to 12 years = 95 + 6cm / year

(i.e. at 4 years = 101cm , at 12 years = 149cm)

New born 50 cm
1 year 75 cm
2 years 85 cm
3 years 95 cm
4 years 101 cm
5 years 107 cm
6 years 113 cm
7 years 119 cm
8 years 125 cm
9 years 131 cm
10 years 137 cm
11 years 143 cm
12 years 149 cm


At birth = 2.5-3.5 kg

3-12 months = age in months + 9


1-6 years = [age in years x 2]+8


7-12 years = [age in years x 7]-5


Rule of 7

New born 7 lbs 2.5-3.5 kg
6 months 14 lbs 7.5 kg
1 year 21 lbs 10 kg
2 years 28 lbs 12 kg
3.5 years 35 lbs 15 kg
7 years 49 lbs 22 kg
10 years 70 lbs 32.5 kg
11 years 82 lbs 36 kg
12 years 89 lbs 39.5 kg


Dentition is variable

  • First deciduous tooth eruption = 6 months
  • Deciduous teeth eruption (20 teeth) completed by = 2.5 years
  • Shedding of deciduous teeth = 6 years to 12 years
  • Permanent teeth appearance = 6 years to 22 years

X Ray Skull: Thalassemia

x ray skull thalassemia

The x ray below depicts lateral view of skull in thalassemia patient.

x ray skull thalassemia



Co-trimoxazole is the mixture of trimethoprim with sulfamethoxazole, with sulfamethoxazole 400 mg and trimethoprim 80 mg in ratio of 5:1.

Trimethoprim has a large volume of distribution, so its dose is decreased. It is quickly absorbed. Plasma protein binding of trimethoprim is also less than sulfamethoxazole.

Advantages of Using Co-Trimoxazole

  1. Bactericidal (Individual drugs are bacteriostatic)
  2. Wide antibacterial spectrum
  3. Increased efficacy
  4. Less dose of each drug
  5. Less incidence of toxicity
  6. Have same half life (TMP 11 hrs. SMZ 10 hrs.)
  7. Both inhibit the same metabolic pathway, so synergize each others effect.
  8. Decreased chances of resistance (because if bacterium is resistant to one drug, it will be sensitive to other)


Can be given orally or I/V. After oral administration absorption is good, peak plasma levels appear within 2 hours. Given I/V for infectious conditions.

Trimethoprim is a weak base with pH of 7 .2. It is found in bile, sputum, high concentration in CSF, also concentrates in acidic media of prostate and vagina.

Plasma protein binding of trimethoprim is 40-45% while that of sulfamethoxazole is 60%.

Volume of distribution of trimethoprim is 9 times more than sulfamethoxazole.

Most products are excreted in urine; traces of drug appear within 24 hours. Dose is adjusted as required (esp. in renal insufficiency).

Mechanism of Action

Anti bacterial spectrum

Combination has wider antibacterial spectrum.

  1. Gram positive
  2. Gram negative bacteria
  3. Some enterobacteria
  4. Shigella
  5. Salmonella Typhi and Para typhi
  6. Klebsiella Nocardia
  7. Pneumocystis Jiroveci
  8. Escherichia coli
  9. Serratia
  10. MRSA
  11. Staphylococcus aureus
  12. Staphylococcus epidemidis
  13. Proteus
  14. Brucella

Clinical Uses

  1. Respiratory infections:

Highly effective in:

  1. Chronic bronchitis
  2. Community acquired Pneumonia
  3. Otitis media in children
  4. Acute maxillary sinusitis
  5. Pneumocystis Jiroveci Pneumonia
  6. Non tuberculous mycobacterial infections –esp. AIDS
  7. Hemophilis influenzae
  8. Streptococcus Pneumoniae
  9. Moraxella Catarrhalis
  10. Klebsiella Pneumoniae


Has no activity in Pharyngitis

2. GIT Infections:

  1. Although amoxicillin is good, trimethoprim is highly effective in Shigellosis
  2. Typhoid Fever (SMX 800mg: TMP 160mg BD) (cephalosporin or ceftriaxone are 1st line for typhoid fever. Use as alternative
  3. Systemic Salmonella infection (Typhoid Fever) for Salmonella Typhae and Paratyphae, effective when used for prophylaxis given for 3 months

3. UTI:

  1. Said to be effective against uncomplicated and chronic & recurrent UTI. Given either 800 mg x 160 mg or small dose is administered for management of chronic recurrent UTI in 200 mg SMZ 40 mg TMP BD dose.
  2. As highly concentrated in acidic media effective in Prostatitis
  3. Acute Gonococcal Urethritis

Other drugs used in UTI include ampicillin, fluroquinolones, and in uncomplicated refractory cases even sulfonamides can be used.

  1. Brucellosis

Drug of choice is doxycycline, streptomycin and gentamicin.

Co-trimoxazole is used as alternative.


Also used in sensitive MRSA.

Intravenous Uses:

  1. I/V preparation is ideally used for Pneumocystis Pneumonia
  2. Gram negative bacterial sepsis
  3. Shigellosis
  4. Typhoid Fever
  5. UTI

I/V preparations are used when drugs cannot be given orally or patient is uncooperative.

Adverse Effects

As the main component is sulfonamide, all effects are also seen and include:

  1. Hematological

Trimethoprim –megaloblastic anemia, leukopenia, thrombocytopenia, granulocytopenia

Prevented by simultaneous administrations of folic acid 6 – 8 mg/D which does not enter bacteria for 3-6 weeks

2. Hypersensitivity reactions -rashes, fever, vasculitis

3. CNS effects –headache, depression, hallucinations

4. GIT disturbance – nausea, vomiting, glossitis & stomatitis.

5. HIV patients with Pneumocystis pneumonia or immune compromised show fever, rashes, leukopenia, diarrhea, elevation of hepatic aminotransferases, hyperkalemia, hyponatremia.

Nephrotic Syndrome

nephrotic syndrome

Nephrotic syndrome is a kidney disorder characterized by proteinuria greater than 40mg/m2/hour or 50mg/kg/day, first morning urine protein to creatinine ratio of greater than or equal to 3mg/mg, hypoalbuminemia less than 3g/dl in the presence of edema and hyperlipidemia greater than 200mg/dl.

Four cardinal features which are hallmark of nephrotic syndrome are:

  • Proteinuria
  • Hypoalbuminemia
  • Edema
  • Hyperlipidemia


There are approximately 2-7new cases per 100,000 kids in western hemisphere, with peak incidence at around 1.5-6 years of ag. This disease is relatively more common in boys with high prevalence in South East Asia.


Nephrotic syndrome can be classified as primary, secondary and genetic. Primary nephrotic syndrome is further classified as idiopathic and post glomerulonephritis nephrotic syndrome.

Primary Nephrotic Syndrome

Primary nephrotic syndrome is associated with glomerular diseases intrinsic to the kidney and not related to systemic causes. Among all the kids diagnosed with nephrotic syndrome, more than 85 percent are found to have minimal change disease.

Different varieties include:

  • Minimal Change Nephrotic Syndrome
  • Focal Segmental Glomerulosclerosis
  • Membranous Nephropathy
  • Membranoproliferative Glomerulonephritis
  • IgA Nephropathy
  • Idiopathic Crescentic Glomerulonephritis

Congenital Nephrotic Syndrome

There is a really long list of congenital nephrotic syndromes but few imp ones are listed here:

  • Finnish Type Congenital Nephrotic Syndrome
  • Focal Segmental Glomerulosclerosis
  • Diffuse Mesangial Sclerosis
  • Denys Drash Syndrome
  • Frasier Syndrome

These are clinically rare entities that result from podocin, nephrin  and cation channel 6 gene mutations and usually present in first 3 months of life.

Secondary Nephrotic Syndrome

By definition secondary causes are the causes that start extrinsic to kidney and later on progress to involve them. They include infections, like hepatitis B and C, HIV, syphilis and malaria, drugs like penicillamine, gold salts and NSAIDs, autoimmune diseases like SLE, various forms of vascultis like Henoch Schonlein Purpura, allergic reaction to bee sting and food allergens and metabolic diseases like diabetes.

Steroid Sensitive Nephrotic Syndrome

Therapeutically speaking nephrotic syndrome is classified on the basis of response to steroid therapy. Features suggesting steroid sensitive disease are age between 1 and 10 years, absence of macroscopic hematuria, normal BP, normal complement levels and normal renal function.

Steroid Resistant Nephrotic Syndrome

Conventionally steroid resistant disease is said to have occurred when urinary remission cannot be achieved within 8 weeks of prednisone therapy of 60mg/m2/day. 

But currently it is defined as when there is failure to achieve urinary remission after 4 weeks of prednisolone therapy and 3 doses of IV methyl prednisolone pulse therapy on alternate days.


Relapse of nephrotic syndrome is defined as recurrence of nephrotic range proteinuria in association with recurrence of edema once the patient has become completely asymptomatic.

Frequently Relapsing Disease

Frequently relapsing disease is the one with more than 2 relapses in 6 months or more than 4 relapses in 1 year.

Steroid Dependent Disease

Steroid dependent nephrotic syndrome is defined as relapse of disease on either switching to alternate therapy or within 15 days of stopping steroid therapy.


Nephrotic syndrome results from impaired permeability across the glomerular basement membrane resulting in loss of albumin in urine. There is decreased oncotic pressure resulting in edema. Reduced blood volume triggers renin angiotensin 2 aldosterone axis. There is an increased hepatic production of TGs and lipoprotein carriers resulting in hyperlipidemia.


95 percent of the kids report with complaints of edema and weight gain. Edema usually appears first in areas of low tissue resistance. It then progresses rapidly or slowly to become generalized and massive.

Other complains include frothy urine, breathlessness secondary to ascites and plueral effusions. Some kids also have a history of respiratory tract infections or a hypersensitivity event like bee sting.

Physical Exam

On physical examination the edema is pitting and typically dependent in nature. Blood pressure is usually normal in minimal change disease. Many children have significant respiratory distress secondary to ascites and pleural effusions. Abdominal tenderness might indicate peritonitis.


Various urine and blood studies are performed to confirm the diagnosis of nephrotic syndrome.

Urine Studies

First morning urine protein/creatinine ratio is more easily obtained than 24-hour urine studies and is more reliable as well. Other urinary investigations include urine dipstick test, urine microscopy and culture.

Blood Studies

Serum albumin levels are low. Pateints have an elevated total cholesterol, triglycerides and LDL levels.

Serum sodium and calcium levels are typically low. In addition there is marked hemoconcentration due to intravascular volume depletion.

Complement levels and renal function tests are normal in minimal change disease.

Some investigations to rule out secondary causes include serology for hepatitis B and C, blood screening for malaria, ASO titres and throat swab to check for poststreptococcal glomerulonephritis and anti nuclear antibodies to rule out SLE.

Imaging Studies

Kidney ultrasonographic findings are usually nonspecific. CXR may show pleural effusions and pulmonary edema.

Kidney Studies

Indications to perform renal biopsy in a patient of nephrotic syndrome are:

  • Age < 1 Year or > 10 Years at Presentation
  • Gross or Persistent Microscopic Hematuria
  • Low Complement Levels
  • Hypertension
  • Impaired Renal Function
  • Steroid Resistant Nephrotic Syndrome

Differential Diagnosis

Differential diagnosis includes acute glomerulonephritis and other entities causing generalized edema like hereditary angioedema, protein losing enteropathy, heart failure and malnutrition if supported by  history and physical examination.


Treatment of nephrotic syndrome aims at providing supporting and specific relief to patients.


Upper respiratory tract infections are treated with appropriate antibiotic therapy.


Patient is advised to use no added salt diet, diuretics and albumin infusions  are advised only when there is significant respiratory distress due to massive ascites or bilateral plueral effusions.


Hyperlipidemia goes away on its own mostly.

Specific Treatment for Minimal Change Nephrotic Syndrome

Oral corticosteroids are mainstay in the treatment of minimal change disease. One must exclude active infections, tuberculosis and other contraindications before prescribing steroid therapy. Patients are also checked for their vaccination status against Pneumococci, Meningococci and Hemophilus influenzae.

Longer regimens of steroids are preferred because of lower relapse rates. Total duration of this regimen is 4.5 months. We start by giving 60mg/m2/day prednisolone until proteinuria is gone. The same dose is continued for 30 days and then switch to alternate day therapy for another 2 months. After 2 months steroids are tapered off by 15mg/m2 every 2 weeks.

Steroid Resistant Nephrotic Syndrome

For steroid resistant disease steroid intake duration is prolonged and steroid sparing agents are added.

Frequently Relapsing and Steroid Dependent Nephrotic Syndrome

To tackle frequently relapsing nephrotic syndrome and to treat steroid dependent disease low dose steroid therapy is given for an increased duration.

Congenital Nephrotic Syndrome

For congenital nephrotic syndrome unilateral nephrectomy is carried out for the control of hypoalbuminemia, followed by dialysis for renal failure until the child is large and fit for renal transplantation.

Secondary Nephrotic Syndrome

Secondary nephrotic syndrome is managed by identifying and treating the underlying cause.

Complications of Nephrotic Syndrome

Various complications of nephrotic syndrome include

  • Peritonitis
  • Thromboembolism and CVS Disease
  • Pleural Effusion and Ascites
  • Anasarca
  • Renal Insufficiency
  • Vitamin D deficiency
  • Hypothyroidism
  • Impaired Growth

Complications of Medical Therapy

Prolonged steroid therapy may lead to

  • Cushing Syndrome
  • Growth Suppression
  • Decreased Bone Mineral Density
  • Peptic Ulceration
  • Increased Risk of Infections
  • Impaired Glucose Tolerance
  • Cataracts
  • Depression


Histopathology Images: Adenocarcinoma Prostate


The histopathology image below depict adenocarcinoma prostate.

Classification of Primary Tumors Involving Bones

bone tumor

Primary tumors involving bones may be classified into benign and malignant tumors. Benign and malignant tumors of bones may be further classified as follows:

Benign Tumors


  • Osteochondroma
  • Chondroma
  • Chondrobastoma
  • Chondromyxoid fibroma


  • Osteoid osteoma
  • Osteoblastoma


  • Fibroma
  • Non-ossifying fibroma
  • Fibrous histiocytoma
  • Desmoplastic fibroma

Unknown Origin

  • Giant cell tumor
  • Unicameral cyst
  • Aneurysmal bone cyst


  • Benign notochordal cell tumor

Malignant Tumors


  • Myeloma
  • Malignant lymphoma


  • Chondrosarcoma
  • De differentiated chondrosarcoma
  • Mesenchymal chondrosarcoma


  • Osteosarcoma


  • Fibrosarcoma


  • Ewing Sarcoma


  • Chordoma