Saturday 10 June 2017

Lets Play wid Clotting Factors

Mnemonic for clotting factors
Fresher’s Party Tonight, Come Let’s Sing And Call Seniors, Please Have Fun”

I Fibrinogen
II Prothrombin
III Tissue factor
IV Calcium
V Proaccelerin, Labile factor
VI  Unassigned – Old name of Factor Va
VII Stable factor, proconvertin
VIII Antihemophilic factor A
IX Antihemophilic factor B or Christmas factor
X Stuart-Prower factor
XI Plasma thromboplastin antecedent
XII Hageman factor
XIII Fibrin-stabilizing factor

All about immunoglobulins
1.Smallest Ig- IgG
 2. Largest Ig- IgM
 3. Maximum serum concentration- IgG 
4. Minimum serum concentration- IgE 5.Heat Labile- IgE 
6. Earliest to be Synthesised (primary immune response)- IgM
 7. Secondary immune response- IgG 8. Crosses Placenta- IgG 
9. Minimum half Life- IgE 
10. Maximum half life- IgG 
11. Protects Surfaces- IgA 
12. Warm Antibodies- IgG
 13. Cold Antbodies- IgM 
14. Present in Milk- IgG and IgA 
15. Fix complements via classical pathway- IgM & IgG 
16. Fix complements via alternative pathway- IgA & IgD 
17. Primary allergic response- IgE 
18. Maximum sedimentation cofficient- IgM 
19. Reagin activity – IgE
 20. Antigen recognition by B cells – IgD 
21. Prausnitz kustner reaction – IgE 22. Homocytotropism – IgE
 23. Present in milk – IgA & IgG
 24. Highest carbohydrate – IgE
 25. Lowest carbohydrate – IgG
Important 
CD Markers
1-5 , 7 , 8 , 28TCR (T cell Marker)
19-23 , 10 (CALLA)BCR (B cell Marker)
16 , 56NK cell Marker
68Macrophage (histocyte) marker
31Adhesion Molecule (PECAM -1àon both endothelium and neutrophil)
11/18Integrin Beta2 (LFA-1/MAC-1) (on neutrophil)
117 = c-KitGIST
44
Needed for hematological spread (metastasis),
Hyaluronic acid receptor
45= LCALymphoma Marker
99Ewing’s Sarcoma marker
1aLangerhan’s Cell marker
15,30RS cell Marker
16Fc receptor of NK cells
34Stem Cell Marker
55 = DAFInhibit C3 and C5 convertase
59 = MIRLInhibits MAC
20Hodgkin’s –Lymphocytic Predominant
95FAS
71
Mesangial IgA1 receptor
Enhanced expression in Berger Disease(IgA nephropathy) and Henoch-Schönlein Nephritis





Important Bodies


1)  Asteroid  bodies  -  Sporotrichosis   2)  Councillman  bodies  -  Yellow  fever  
3)  Torries  bodies  -  Yellow  fever  
4)  Leishmans  Donovans  bodies  -  Kala  Azar  
5)  Halbersteadter-Prowazeke's  bodies  -  Trachoma  
6)  Miyagava's  bodies  -  Lymphogranuloma  venereum  
7)  Levinthal-Cole-Lillie  bodies  -  Psittacosis  
8) Negri bodies (intracytoplasmic, intraneuron,hippocampus)  -  Rabies   9)  Guarnieri's  bodies  -  Vaccinia  (intracytoplasmic)  
10)  Bollinger's  bodies  -  Fowl  pox  (inrtacytoplasmic)
11)  Henderson-Peterson's  bodies  -  Mollascum  cantagiosum  
12)  Cowdry  type-A  bodies  -  Yellow  fever,  Herpus  virus  infection  
13)  Cowdry  type-B  bodies  -  Adenovirus,  Poliovirus(code-BAP)   14)  Aschoff's  bodies  -  Rheumatic  fever  
15)  Rusell's  bodies  -  Multiple  myeloma  
16)  Schauman's/Conchoid  bodies(calcium  &  iron  complexes)  -  Sarcoidosis  &  Beryliosis  
17)  Asteroid  bodies(eosinophilic  inclusions)  -  Sarcoidosis  
18)  Call-Exner  bodies  -  Granulosa  cell  tumour  of  ovary  
19)  Verrocy  bodies  -  Neurilemmoma  
20)  Civette(colloid)  bodies  -  Lichen  planus  
21)  Michelis-Guttmann's  bodies  -  Malakoplakia  
22)  Lewy  bodies  -  Parkinson's  disease  
23)  Lafora  bodies  -  Familial  myoclonus  
24)  Hirano  bodies  -  Alzhemer's  disease  
25)  Weibel-Palade  bodies  -  storage  organeles  of  vonWillebrands  factor  in  platelets  & endothelium  
26)  Papperheimer  bodies  -  nonheame  iron  pigments  in  siderocytes  
27)  Howell-Jelly  bodies  -  spleenectomy  ,  Megaloblastic  Anaemia,  Hemolytic  anaemia  
28)  Hectoid  bodies  -  Sickle  cell  anemia  
29)  Heinz  bodies  -  thalasemia  
30)  Dohle  bodies  -  cytoplasmic  inclusion  bodies  in  neutrophils  seen  in  bacterial  infection  
31)  Histocytosis-X(HX)(Birbeck's  granules)  -  Histocytosis-X  
32)  Gamma-Gandy  bodies  -  Congestive  spleenomegaly  
33)  Mallory's  bodies  -  hyaline  inclusions  in  heapato  cytes  seen  in  alcoholic,  indian  childhood cirrhosis  etc...  
34)  Apoptotic  bodies  -  membrane  bound  spherical  sturctures  in  Apoptosis
35)  Psammoma  bodies  -  dystrophic  calcification  in  meningioma,  papillary  serous  cystadenoma of  ovary  &  papillary  carcinoma  of  thyroid,  papillry  type  of  RCC.  
36)  LE  bodies  (haematoxylin  bodies)  -  SLE  
37)  Dumbell  shaped  Asbestos  bodies  -  asbestos  fibres  coated  with  glycoprotien  &  hemosiderin. stained  with  Prussian  blue  stain  
38)  Luys  body  -  subthalamic  nucleus  
39  )Davidson's  body  -  sex  chromatin  in  neutrophils  (dumbell  shaped)  
40)  Herring  bodies  -  pars  nervosa  of  pituitary  gland  

41)  Donovan  body  -  Granuloma  inguinale  
42)  Nissels  bodies  -  cytoplasmic  inclusions  in  neurons  
43)  Mooser's  bodies  -  Typhus  fever   44)  Lipschutz'  bodies  -  intra  nuclear  inclusions  in  herpes  simplex  infection  
45)  Zebra  bodies  -  cytoplsmic  inclusions  in  schwaan  cell  degeneration  
46)  Babes-Ernest  metachromatic  granules  -  Diphtheria  
47  )Reilly's  bodies  -  Hurler's  syndrome  
48)  Gamma-Favre  bodies  -  LGV  
49)  Winkler's  &  Ross's  bodies  -  Syphilis  
50)  Sandstrom's  bodies  -  Parathyroid  gland  
51.  COUNCILLMAN  BODIES  =  HEP  B  (  dying  hepatocytes  )  
52.  FERUGINOUS  BODIES  =  ASBESTOSIS  
53.  HEINZ  BODIES  =  G6PD  DEF  
54.  PICK  BODIES  =  PICKS  D/S  
55.  CREOLA  BODIES  =  ASTHMA  
56.  ODLAND  BODIES  =  KERATINOSOME  
57.  RUSHTON  BODIES  =  ODONTOGENIC  CYSTS  
58.  ZEBRA  BODIES  =  METACHROMATIC  LEUKODYSTROPHY  ,  NEIMANN  PICK'S  DISEASE.  
59.  BRACHY  WACHTER  BODIES  =  INFECTIVE  ENDOCARDITIS  
60.  GLOBOID  BODIES  =  KRABBES  DISEASE  
61.  ALDER  -  REILLY  BODIES  =  coarse  azurophilic  granules  in  the  leukocytes  in  ALDER  - REILLY  SYNDROME.  
62.  BODIES  OF  ARANTIUS  =  aortic  valve  nodules  
63.  VEROCAY  BODIES  =  schwaanoma  
64.  BALBIANI'S  BODIES  =  yolk  nucleus   
65.  BAMBOO  BODIES  =  asbestos  bodies  
66.  BRASSY  BODY  =  dark  shrunken  blood  corpuscle  found  in  MALARIA  67.  COCCOID  X  BODIES  =  psittacosis  
68.  CYTOID  BODIES  =  in  degenerated  retinal.N  fibres..seen  in  cotton  wool  spots  
69.  HARTING  BODIES  =  calcospheritis  in  the  cerebral  capillaries  
70.  BODY  OF  HIGHMORE  =  mediastinum  testis  
71.  MASSON  BODIES  =  rheumatic  pneumonia  
72.  MOTT  BODIES  =  multiple  myeloma  
73.  DONNES  BODIES  =  colostrum  corpuscles  
74.  OKEN'S  BODY  =  mesonephros   75.  PASCHEN  BODIES  =  variola  or  vaccinia  
76.  SCHILLER  DUVAL'S  BODIES  =  ENDODERMAL  SINUS  TUMOUR  
77.  RESIDUAL  BODIES  =  SARCOID  AND  SARCOID  LIKE  GRANULOMAS   78.  body  of  HIGHMORE  =  medullary  carinoma  of  testis  
79.  ODLAND  bodies  =  flegel  disease  (i.e  hyperkeratosis  lenticularis  perstans)  
80.  Red  Neurons  =  Apoptosis

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Monday 27 February 2017

MALE REPRODUCTIVE DISORDERS

                           Penis Diseases                  

 A. Malformations of the urethral groove of the penis

 1. Hypospadias
a. Abnormal opening on the ventral surface of the penis 
b. Most common malformation of urethral groove
c. Risk factors
(1) Father or previous male sibling with defect
(2) Monozygotic twins
• Insufficient production of human chorionic gonadotropin by single placenta
d. Frequently associated with ventral curvature of penis
• Called chordee
e. Pathogenesis
(1) Due to faulty closure of the urethral folds
(2) Possibly related to abnormal androgen production

 2. Epispadias
a. Abnormal opening on the dorsal surface of the penis
b. Due to a defect in the genital tubercle

 B. Phimosis of the penis
1. Orifice of the prepuce is too small to retract over the head of the penis
2. Commonly associated with infections

 C. Balanoposthitis of the penis

 1. Infection of the glans and prepuce
a. It usually occurs in uncircumcised males with poor hygiene.
b. Accumulation of smegma leads to infection.
• Candida, pyogenic bacteria, and anaerobes

 2. Inflammatory scarring may produce an acquired phimosis.

 D. Miscellaneous disorders of the penis

 1. Peyronie disease
a. Type of fibromatosis 
b. Painful contractures of the penis
• Causes lateral curvature of the penis
c. May cause infertility

 2. Priapism
a. Persistent and painful erection
b. Causes include sickle cell disease, penile trauma

 E. Carcinoma in situ (CIS) of the penis

 1. Bowen disease
a. Leukoplakia involving the shaft of the penis and scrotum
(1) Patients are usually >35 years old
(2) Association with human papillomavirus (HPV) type 16
b. Precursor for invasive SCC (~10% of cases)
c. Association with other types of visceral cancer

 2. Erythroplasia of Queyrat
a. Erythroplakia located on the mucosal surface of the glans and prepuce
b. HPV type 16 association
c. Precursor for invasive SCC

 3. Bowenoid papulosis
a. Multiple pigmented reddish brown papules on the external genitalia
b. Association with HPV type 16
c. Does not develop into invasive SCC
• Only CIS with no predisposition for invasion

 F. SCC of the penis

 1. Epidemiology
a. Circumcision protects against developing SCC of penis.
b. SCC is the most common cancer of the penis.
(1) Usually affects men 40 to 70 years old
(2) Most common sites
• Glans or mucosal surface of prepuce
c. Two-thirds of cases associated with HPV types 16 and 18
• Products from smoking tobacco may act as cocarcinogens with HPV.
d. Risk factors
(1) Lack of circumcision
• Greatest risk factor
(2) Bowen disease, erythroplasia of Queyrat

 2. Metastasizes to inguinal and iliac nodes
  Testis, Scrotal Sac, and Epididymis Diseases

 A. Cryptorchidism of the testes

 1. Normal descent of testes
a. Transabdominal phase
(1) Testes descend to lower abdomen or pelvic brim
(2) Müllerian inhibitory substance (MIS) is responsible for this phase.
b. Inguinoscrotal phase
(1) Descent through the inguinal canal into the scrotum
(2) Androgen- and human chorionic gonadotropin (hCG)-dependent

 2. Cryptorchidism
a. Epidemiology
(1) Incomplete or improper descent of the testis into the scrotal sac
(2) Most common genitourinary (GU) disorder in male children
(3) Occurs in 30% of premature males and 5% of full-term males
(4) Associations
• Androgen insensitivity syndrome, Kallmann syndrome, cystic fibrosis
(5) Locations
(a) Inguinal canal is the most common site (80% of cases)
• Palpable mass; majority are unilateral (90% of cases)
(b) Intra-abdominal (5%–10% of cases)
(6) Many will spontaneously descend by 3 months of age
(a) Due to combination of androgens and hCG
(b) Spontaneous descent is uncommon after 3 months.

 b. Complications if uncorrected
(1) Potential for infertility
(a) Arrest in germ cell maturation
(b) Testicular atrophy
(c) Similar changes occur in the normally descended contralateral testis.
(d) Greatest risk if intra-abdominal or long duration in the inguinal canal
(2) Increased risk for developing a seminoma
(a) Risk for cancer in the cryptorchid testis increases by fivefold to tenfold.
(b) Risk also applies to the normally descended testicle.
(3) Increased risk for the undescended testis to undergo torsion (see later)

 c. Treatment
(1) Orchiopexy may be done as early as 6 months; it should be performed by 2 years
of age.
(2) Hormonal therapy with hCG produces variable results.
(3) Administration of gonadotropin-releasing hormone (GnRH) before orchiopexy
may improve fertility in adult.

 B. Orchitis

 1. Mumps
a. Infertility is uncommon.
b. Most cases are unilateral.
c. Orchitis is more likely to occur in an older child or adult.

 2. Congenital or acquired syphilis
3. HIV
4. Extension of acute epididymitis

 C. Epididymitis

 1. Causes
a. Common pathogens in persons <35 years old
(1) N. gonorrhoeae
(2) C. trachomatis

 b. Common pathogens in persons >35 years old
(1) E. coli
(2) Pseudomonas aeruginosa

 c. Tuberculosis
(1) Begins in the epididymis
• Spreads to the seminal vesicles, prostate, and testicles
(2) Caseating granulomatous inflammation

 d. AIDS
• Association with cytomegalovirus, Toxoplasma, Salmonella

 2. Clinical findings in acute epididymitis
a. Usually unilateral scrotal pain with radiation into spermatic cord or flank
b. Scrotal swelling, epididymal tenderness
c. Urethral discharge
• If it is sexually transmitted
d. Prehn sign
• Elevation of the scrotum decreases pain.

 3. Treatment
a. If <35 years old, ceftriaxone + doxycycline (STD treatment)
b. If >35 years old, ciprofloxacin extended release

 D. Varicocele

 1. Epidemiology
a. Occurs in 15% to 20% of all males
(1) Usually occurs between 15 and 25 years of age
(2) Rarely occurs after 40 years old
b. Occurs in 40% of infertile males
c. Most common cause of left-sided scrotal enlargement in adults
d. Left spermatic vein drains into the left renal vein
(1) Increased resistance to blood flow
(2) Blockage of left renal vein can also produce a varicocele.
• Examples—renal cell carcinoma invading renal vein; superior mesenteric artery
compressing the left renal vein
e. Right spermatic vein drains into the vena cava
(1) Blockage of right spermatic vein produces right-sided varicocele.
(2) Examples—retroperitoneal fibrosis; thrombosis of the inferior vena cava

 2. Pathogenesis
• Incompetent valves in the left spermatic vein from increased pressure

 3. Clinical findings
a. Aching pain in scrotum
b. Dragging sensation in testicle
c. Visible “bag of worms”
d. Infertility (controversial)
• Heat decreases spermatogenesis.

 4. Diagnose by ultrasound

 5. Treatment
a. Varicocelectomy
b. Embolization by an intervention radiologist

 E. Torsion of the testicle

 1. Epidemiology
a. Majority occur between 12 and 18 years old.
b. Predisposing factors
(1) Violent movement or physical trauma
• Most common causes
(2) Cryptorchid testis
(3) Atrophy of testis
c. Twisting of spermatic cord cuts off the venous/arterial blood supply.
• Danger for hemorrhagic infarction of the testicle 

 2. Clinical findings
a. Sudden onset of testicular pain
b. Absent cremasteric reflex (key diagnostic finding)
• Stroking the inner thigh with a tongue blade normally causes the scrotum to retract.
c. Testicle is drawn up into the inguinal canal 

 3. Diagnose with ultrasound

 4. Treatment
a. One-third spontaneously remit.
b. Surgery is imperative within 12 hours for those that do not remit.

 F. Hydrocele

 1. Most common cause of scrotal enlargement in children 
a. The tunica vaginalis fails to close.
b. Fluid accumulates in serous space between the layers of the tunica vaginalis.
c. It is invariably associated with an indirect inguinal hernia.

 2. Diagnosis
• Ultrasound distinguishes fluid versus a testicular mass causing scrotal enlargement.

 3. Other fluid accumulations
a. Hematocele contains blood.
b. Spermatocele contains sperm.

 4. Treatment is surgery.
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URINARY TRACT DISORDERS

I. Common Ureteral Disorders


A. Congenital megaloureter
• May be associated with Hirschsprung disease
B. Ureteritis cystica
1. Disorder is a manifestation of chronic inflammation.
2. Smooth cysts project from the mucosa into the lumen.
• Similar findings may be present in the bladder.
3. Cysts may undergo glandular metaplasia and predispose to adenocarcinoma.
C. Ureteral stones
• Ureters are the most common site for stones to cause obstruction.
D. Retroperitoneal fibrosis
1. Causes
a. Most cases are idiopathic.
b. Known causes/associations include:
(1) Ergot derivatives used in the treatment of migraines
(2) Retroperitoneal malignant lymphoma
(3) Association with other sclerosing conditions
(a) Primary sclerosing cholangitis (PSC)
(b) Sclerosing mediastinitis, Reidel fibrosing thyroiditis

2. Complications
a. Hydronephrosis is the most common complication.
b. It may cause a right scrotal varicocele (see section V).
• Blocks the drainage of the right spermatic vein into the vena cava
E. Ureteral cancers
• Transitional cell carcinoma (TCC) is the most common cancer.

II. Urinary Bladder Diseases

A. Congenital diseases of the urinary bladder
1. Exstrophy of the bladder 
a. Developmental failure of the anterior abdominal wall and bladder
(1) Bladder mucosa is exposed to the body surface.
(2) It is often associated with epispadias (see section IV).
b. Complications
(1) Inflammation predisposes to glandular metaplasia.
(2) The likelihood of developing adenocarcinoma of the bladder is high.


2. Urachal cyst remnants
a. Usually the embryonic allantois (part of the yolk sac) is obliterated to form the fibrous
urachus connecting the apex of the bladder with the umbilicus (called the median
umbilical ligament in adults).
• If the lumen remains patent in the newborn, fistulas may develop between
the bladder and the umbilicus; midline cysts may persist that may drain
urine.
b. Cyst remnants predispose to adenocarcinoma of the bladder
• Most common cause of bladder adenocarcinoma

B. Acute and chronic cystitis

1. Risk factors for lower urinary tract (LUT) infection
a. Female sex
(1) Short urethra
(2) Ascending infection (refer to Chapter 20)

b. Indwelling urinary catheter
(1) Most common cause of sepsis in hospitalized patients
(2) Account for 50% of nosocomial urinary tract infections (UTIs)

c. Sexual intercourse
(1) “Honeymoon cystitis” occurs from trauma to the urethra.
(2) Voiding after intercourse reduces the risk for infection by washing out bacteria in
the urethra.

d. Diabetes mellitus, neurogenic bladder

e. Cyclophosphamide
(1) Produces hemorrhagic cystitis
(2) Prevented with mesna

f. Schistosoma haematobium
(1) Transmission
(a) The fork-tailed cercariae penetrate the skin.
(b) Larvae enter veins in the urinary bladder wall.
(c) Larvae develop into adult worms that deposit eggs.
(d) Host develops an intense inflammatory response consisting of
eosinophils that surround the eggs.
(e) Inflammation causes squamous metaplasia of the bladder
epithelium.
(2) Eggs have a large terminal spine (see Fig. 21-1B).
(3) Treatment is praziquantel.

2. Causes of acute cystitis
a. Escherichia coli
(1) Most common uropathogen (80%–90% of cases)
(2) Gram-negative rod (see Fig. 21-1C)
(3) UTIs account for 40% of hospital-acquired (nosocomial) infections.
(4) Most common cause of sepsis in a hospitalized patient
(5) Treatment is double-strength trimethoprim-sulfamethoxazole.

b. Adenovirus
• Causes hemorrhagic cystitis

c. Staphylococcus saprophyticus
(1) Causes acute cystitis in young, sexually active women
• Accounts for ~10% to 20% of LUT infections
(2) Coagulase negative
(3) Treatment is oral cephalosporin or amoxicillin-clavulanate.

d. Acute urethral syndrome in women
(1) Female counterpart to nonspecific urethritis (NSU) in men
(2) Chlamydia trachomatis is the most common cause of acute urethral syndrome.
(3) Identification of Chlamydia
• Polymerase chain reaction (PCR) testing of voided urine
(4) Treatment is azithromycin

e. Other uropathogens
• Mycoplasma hominis, Ureaplasma urealyticum, Neisseria gonorrhoeae

3. Clinical findings in LUT infections
a. Dysuria (painful urination)
b. Increased frequency, urgency, nocturia
c. Suprapubic discomfort
d. Gross hematuria

4. Laboratory findings in LUT infections
a. Pyuria ≥10 white blood cells (WBCs) per high-power field (HPF) in a
centrifuged specimen
• More than 2 WBCs/HPF in an uncentrifuged specimen
b. Bacteriuria, hematuria
c. Positive dipstick for leukocyte esterase and nitrite (refer to Chapter 20)
d. Culture showing at or above 105 colony-forming units (CFUs)/mL
• Gold standard criterion of infection

5. Asymptomatic bacteriuria in women
a. Two successive cultures with 105 or more CFUs/mL in an asymptomatic
patient
b. Causes
(1) Pregnancy
• Acute pyelonephritis may occur in 1% to 2% of cases.
(2) Elderly women in nursing homes
c. Treatment
(1) Pregnant women
• Amoxicillin
(2) Asymptomatic, healthy elderly women
• No treatment necessary

6. Sterile pyuria
a. Neutrophils in the urine and negative standard culture after 24 hours
• Positive leukocyte esterase, negative nitrite
b. Causes
(1) C. trachomatis
(2) Renal tuberculosis (TB)
(3) Acute tubulointerstitial nephritis (TIN; refer to Chapter 20)

7. Malacoplakia
a. Associated with a chronic E. coli infection of the bladder
b. Microscopic findings
(1) Yellow, raised mucosal plaques
(2) Foamy macrophages filled with laminated mineralized concretions
• Called Michaelis-Gutmann bodies, which are defective phagosomes that cannot
degrade bacterial products


C. Miscellaneous diseases of the urinary bladder

1. Acquired diverticula
a. Most are due to benign prostatic hyperplasia (BPH)
b. BPH causes obstruction of urine outflow and increased intravesical pressure,
predisposing to diverticula formation through areas of weakness.
c. Diverticulitis and stone formation are common complications.

2. Cystocele
a. Common in middle-aged to elderly women
b. Mechanism
(1) Relaxation of pelvic support causes descent of the uterus
(2) Bladder wall protrudes into the vagina
• Creates a pouch that collects residual urine

3. Cystitis cystica and glandularis
a. Bladder analog of ureteritis cystica
b. Increased risk for developing bladder adenocarcinoma


III. Urethral Diseases

A. Infections of the urethra
1. Chlamydial and gonococcal infections in men and women
• Urethra is the most common site for these sexually transmitted diseases (STDs).

2. Nonvenereal diseases causing urethritis
a. Most commonly due to E. coli
b. Complications
(1) Cystitis in women
(2) Prostatitis in men

3. Chlamydial urethritis is a common component of Reiter syndrome in men.
a. Urethritis
b. Sterile conjunctivitis
c. Human leukocyte antigen (HLA)-B27–associated arthritis (refer to Chapter 24)

B. Urethral caruncle
1. Female dominant disease
2. Friable, red, painful mass is present at the urethral orifice.
3. Chronically inflamed granulation tissue causes bleeding.

C. Squamous cell carcinoma of the urethra
• Most common cancer of the urethra

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Saturday 4 February 2017

SAVE YOURSELF FROM " ROAD ACCIDENTS"

THINGS ARE AT FAULT:-


1.Drivers - Over speeding, rash driving, violation of rules, failure to understand sign and fatigue
2.Pedestrian - Carelessness, illiteracy, crossing at wrong places, moving on carriage way
3.Passengers - Projecting their body outside vehicle, by talking to drivers, alighting & boarding vehicle from side travelling on footboards, catching a running bus etc
4.Road Users - Excessive speed and rash driving, violation of traffic rules, failure to perceive traffic situation or sign or signal in adequate time, carelessness, fatigue, alcohol,sleep etc.
5.Vehicle - Defects such as failure of brakes, steering system, tyre burst, lighting system,overloading, projecting etc.
6.Road Condition - Skidding road surface, pot holes, ruts, merging of rural roads with highways, diversion etc.
7.Road design - Defective geometric design like inadequate sight distance, inadequate width of shoulders, improper curve design, improper traffic control devices and improper lighting,.
8.Weather conditions - Fog, snow, heavy rainfall, wind storms, hail storms etc.
9.Environmental factors -Unfavourable weather conditions like mist, snow, smoke and heavy rainfall which restrict normal visibility and makes driving unsafe
10. Other causes - Improper location of advertisement boards, gate of level crossing notclosed when required etc


Measure taken to prevent road accident
*  Adapting the environment
*    Changes to the road environment to reduce traffic volumes and speeds, separate cyclists from other vehicles and improve safety for pedestrians can have a positive impact on levels of RTAs and injuries. 
*    Area-wide traffic calming measures (e.g. speed humps, narrowing roads, 20mph zones or road closures) have been found to reduce traffic speeds and injuries, particularly among children (12-15).
•         The average speed within the zones was 17mph
•         Mean traffic speeds had reduced by an average of 9mph
•          The use of red light cameras (these identify vehicles crossing a junction after a traffic light has turned red). There is some evidence that they can reduce right-angled collisions, but rear-end collisions have been found to increase, suggesting they may not be a successful safety measure
•         Marked pathways for cyclists on roads. Clearly marked lanes for cyclists on the road can reduce injury rates when compared to unmarked roads ;
•         The use of school crossing patrols.an evaluation of their use in the late 1980s suggested that they can reduce the number of accidents occurring to child pedestrians at, or near, crossing sites ;
•         Safe routes to school initiatives. These combine different measures to create safer routes to school for children, including: better pavements; traffic calming measures; safe crossings for pedestrians and cyclists;
•         By-passes that divert traffic out of towns and villages;
•         Improving rural routes for walkers and cyclists;
•         Reviewing and reducing traffic speeds on country lanes;
•         Reducing speeds at problematic junctions or locations (e.g. through the use of vehicle activated signs or rough road surfaces);
•         Removing road markings (e.g. central white lines) from narrow roads;
*  Safety education and skills training
•        Promoting the use of safety equipmen
*    A range of educational and promotional methods have been used to encourage the use of safety equipment, often with the provision of free or discounted equipment. These have included: information and lessons targeting parents and/or children; media campaigns highlighting the importance of their use; and health promotion counselling by clinicians.demonstrations of helmet protection and information about how to wear a helmet properly. Helmets were offered to children at a low cost.
*                    2.2 Safety education programmes for pedestrians
*                      Education programmes have been used to increase an individual’s ability to cope with traffic environments and so reduce pedestrian injuries.
*                    2.3 Driver training / education programmes
*                    Driver education programmes aim to increase the safety behaviours of drivers and reduce driver errors.
*                    2.4 Media education campaigns
*                      In the UK, media education campaigns have been used to increase knowledge, and change attitudes towards, a range of road safety behaviours using television, radio, and printed materials such as newspapers, posters and magazines. For instance, in England and Wales the Government’s THINK! campaigns have promoted: road safety among children and older people; reducing driving speeds in both rural and urban areas; wearing seat belts; and using child restraints.
*                    3.Addressing drink driving
*                    Addressing drink driving is  implemented to reduce levels of drink driving in the community. These include bar server training programmes and designated driver programmes.
*                    3.1 Bar server training programmes
Bar server training programmes train bar staff how to serve alcohol responsibly, with the intention of slowing patron drinking and preventing customers from becoming intoxicated.
3.2 Designated driver programmes
*                      Designated driver programmes promote the use of one person (within a group of friends) abstaining from alcohol during a night out and driving the other individuals home safely. Information on designated driver programmes are either disseminated through media campaigns or through initiatives based in nightlife settings that offer incentives (e.g. free soft drinks).
*  4. Multi-component community interventions
*    Comprehensive interventions that engage the community at large and combine strategies such as education programmes and traffic calming measures can be effective in reducing the incidence of childhood pedestrian injury
*  5. Enforcement of legislation      
*    There is a wide range of legislation relating to roads, vehicles and drivers that protect road users and pedestrians against accidents (see box on road safety legislation).
*  5.1 Speed enforcement detection devices
*    Speed enforcement detection devices (e.g. speed cameras and laser and radar devices) can be effective in reducing traffic speeds and reducing the level of road traffic crashes, injuries and deaths in the vicinity of device sites
*  5.2 Increased policing for drink and drug driving
*  The presence of police on the roads (and the threat of arrest) can act as a deterrent for people considering driving after drinking alcohol or taking drugs. 
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