1.] Hepatitis – B virus [HBV] the cause of ”serum hepatitis” is the most versatile of the hepatotropic viruses.

2.] It has an longer incubation period of about 30 – 180 days and is basically transmitted such as in recipient of blood and blood products.

3.] HBV can produce severe form of illness that includes :-

• acute hepatitis B
• chronic hepatitis
• progression to cirrhosis
• fulminate (severe and sudden in onset) hepatitis
• asymptomatic carrier stage

4.] HBV plays role in the development of hepatocellular carcinoma (most common primary malignant tumor of the liver).

MODE OF TRANSMISSION :-

• HBV is an hardy virus and can withstand extremes of temperature and the humidity.
• HBV can spread primarily through blood and body fluids.
• Virus may also spread through contact with body secretion, such as semen, saliva, sweat, tears, breast milk and pathologic effusions.
• During the active acute chronic hepatitis, HBV is present in all physiologic and pathologic body fluids with the exception of stool.

HEPATITIS – B VIRUS [HBV] :-

1.] HBV shows three forms of viral particles of 2 sizes :-

• Small (spheres and tubules/filaments)
• Large (spheres)

2.] Small particles are numerous and exist in two forms – as 22 nm sphere, and as tubules 22 nm in diameter and 100 nm long.

3.] Large particles, 42 nm in diameter, are double – shelled spherical particles, also called dane particles.

4.] The genomic structure of HBV is quite compact and complex. The HBV DNA consist of 4 overlapping genes which encode for multiply proteins :-

• S gene code for the surface envelope protein, hepatitis B surface antigen (HBsAg) this protein in the major  protein. Pre S -1 and Pre S – 2 region of genome are the upstream of S – gene and code for pre – S gene protein products that include receptor on the HBV surface and for hepatocyte membrane protein.
• P gene is the largest and codes for the DNA polymerase.
• C gene codes for two nucleotide protein HBeAg and a core protein termed as HBcAg.
• X gene codes for HBxAg which is a small non – particulate protein. HBxAg has a role in transactivation of the transcription of both viral and cellular genes.

Expression of HBxAg and its antibodies associated with enhanced HBV DNA replication has been implicated in a hepatocellular carcinoma in patients of chronic hepatitis.

PATHOGENESIS :-

There are certain evidence which links immune pathogenesis with the hepatocellular damage :-

• When HBV is not directly cytopathic (refers to structural change in host cell that are caused by viral invasion) that means a carrier state of hepatitis B without the hepatocellular damage exists.
• It has been observed that individuals with defect or deficiency of the cellular immunity have more persistent, hepatitis B diseases.
• In support of cell mediated mechanism in  hepatocellular damage by HBV comes from the observation that viral antigens are attacked by host cytoxin CD8+T lymphocytes.
• The host response of CD8+T lymphocytes by elaboration of antiviral cytokines is variable in different individuals, that determines whether an HBV – infected person recovers, develops mild or severe disease, or progresses to chronic disease.

TREATMENT :-

A.] Oral Antiviral drugs for Hepatitis – B :

Tenofovir disoproxil (Viread)

Tenofovir alafenamide (Vemlidy)

Entecavir (Baraclude)

Telbivudine (Tyzeka or Sebivo)

Adefovir Dipivoxil (Hepsera)

Lamivudine (Epivir-HBV, Zeffix, or Heptodin)

B.] Immune modulators (Interferon) for Hepatitis – B :

Pegylated Interferon (Pegasys)

Interferon Alpha (Intron A)

MULTIPLE CHOICE QUESTIONS :-

1.] Which of the following hepatitis virus is not RNA virus ?

a. Hepatitis – A virus

b. Hepatitis – B virus

c. Hepatitis – E virus

d. Hepatitis – G virus

2.] Which of the following nucleic acid is present in hepatitis – B virus ?

a. dsDNA

b. ssRNA

c. ssDNA

d. dsRNA

3.] The most serious infection is ?

a. super infection of an HBsAg carrier by HDV

b. infection with HBV and HDV

c. coinfection of HBV and HDV

d. None of the above

4.] Which of the following specimen contains hepatitis B virus in an infected person ?

a. Blood

b. Semen

c. Saliva

d. All of the above

5.] Which of the following antigenic type of hepatitis B virus is present in the envelope ?

a. HbsAg

b. HBcAg

c. HBeAg

d. HBxAg

6.] The development of hepatocellular carcinoma is associated with ?

a. ground squirrel hepatitis virus

b. hepatitis B virus

c. woodchuck hepatitis virus

d. all of the above

7.] Which of the following antigenic type of hepatitis B virus is prevalent in India ?

a. Adw

b. Adr

c. Ayw

d. Ayr

8.] Which of the following virus can be transmitted by parental route ?

a. HBV

b. HCV

c. HDV

d. All of the above

9.] Incubation period of HBV virus ?

a. 30 – 180 days

b. 2 days

c. 1 week

d. 10 days

10.] The tubule of small viral particle has a diameter of about ?

a. 23 nm

b. 30 nm

c. 22 micro meter

d. 22 nm

SOLUTIONS :-

1.] (b) hepatitis – B virus

2.] (a) dsDNA

3.] (a) super infection of an HBsAg carrier by HDV

4.] (d)

5.] (a) HbsAg

6.] (d)

7.] (c) Ayw

8.] (d)

9.] (a) 30 – 180 days

10.] (d) 22 nm

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REFERENCES :-

1.] Textbook Of Pathology By Harsh Mohan; 7th edition; Page no. 591 – 592.

2.] Robbin’s Basic Pathology; 5th edition; Page no. 844 – 846.

The post Hepatitis-B : Mode of Transmission, HBV, Pathogenesis, Treatment And MCQs for NEET, GPAT, appeared first on Gpatindia: Pharmacy Jobs, Admissions, Scholarships, Conference,Grants, Exam Alerts.

1.] Hepatitis – A is an long known ” Infectious Hepatitis ” is an benign self – limited disease with an incubation period of about 14 – 45 days.

2.] Hepatitis – A is responsible for 20 – 25 % of clinical hepatitis in the developing countries of the world but the incidence of this disease in much lower in the developed countries.

SPREAD OF THE HAV/ HEPATITIS – A :-

• It is exclusively spread by faeco – oral route.
• It is also related to close personal contact such as in over crowding, poor hygienic and sanitary conditions.
• Frozen and stored contaminated food and water have been blamed in many epidemics.
• Most frequently affected age group is 5 – 14 years, adults are often infected by spread from children.
• Because the viremia (presence of virus in blood) of acute HAV is transient (during the relatively short incubation period and the first day of symptom) this agent is rarely implicated in transfusion-acquired hepatitis.

HEPATITIS – A VIRUS (HAV) :-

• The etiologic agent of hepatitis – A, HAV is an small 27nm diameter, isosahedral (a type of polyhedron with 20 faces), non – enveloped single stranded RNA virus.
• HAV infection can be transmitted to primates and the virus can be cultivated in – vitro.
• HAV replicates and is released from the infected cell without having any adverse affect on them.
• The virus is present in the liver cell, bile, stool and blood during the incubation period.
• Inactivation of viral activity can be achieved by boiling it for about 1 min., by ultraviolet radiation, or by contact with formaldehyde and chlorine.

PATHOGENESIS :-

Evidences that hepatitis caused by HAV has an immunologic basis comes from demonstration of following antibodies acting as serum makers for the hepatitis – A infection.

• IgM anti – HAV antibody appears in the serum at the onset of symptoms of acute hepatitis – A.
• IgG anti – HAV antibody is detected in the serum after acute illness and remains detectable indefinitely. It provides lifetime protective immunity against reinfection with HAV.

TREATMENT :-

No specific treatment exists for hepatitis A. Your body will clear the hepatitis A virus on its own. In most cases of hepatitis A, the liver heals within six months with no lasting damage.

Hepatitis A treatment usually focuses on keeping comfortable and controlling signs and symptoms. You may need to:

• Rest. Many people with hepatitis A infection feel tired and sick and have less energy.
• Manage nausea. Nausea can make it difficult to eat. Try snacking throughout the day rather than eating full meals. To get enough calories, eat more high-calorie foods. For instance, drink fruit juice or milk rather than water. Drinking plenty of fluids is important to prevent dehydration if vomiting occurs.
• Avoid alcohol and use medications with care. Your liver may have difficulty processing medications and alcohol. If you have hepatitis, don’t drink alcohol. It can cause more liver damage. Talk to your doctor about all the medications you take, including over-the-counter drugs.

Certain drugs which are used in the treatment of hepatitis A are GamaSTAN S/ D and immune globulin intramuscular

MULTIPLE CHOICE QUESTIONS :-

1.] In 2012, the hepatitis – A burden in the U.S. includes ?

a. 1,562 illnesses

b. 1,562 hospitalizations

c. 1,562 deaths

d. $ 1,562

2.] If you are infected with hepatitis – A virus, you will most likely become sick ?

a. Within few hours

b. Within 1 week

c. Within 2 – 7 weeks

c. Within 1 year

3.] Which of the following statement is true about hepatitis – A ?

a. A person infected with hepatitis – A can spread the disease before symptom begin and up to 1 week after onset of jaundice

b. A person infected with hepatitis – A cannot spread the disease to others

c. A person infected with hepatitis – A can spread the disease only while experiencing symptoms.

d. Children are very rarely infected with hepatitis – A and do not spread disease to others.

4.] Clinical diseases (hepatitis – A infection) symptom include sudden onset of ?

a. Diarrhea

b. Fever, Tiredness, Loss of appetite and Nausea

c. Jaundice, Diarrhea and Vomiting

d. Dark – colored urine, light colored feces and jaundice

5.] A few days after the first symptom begins, person suffering from hepatitis – A may begin to experience ?

a. Diarrhea

b. Jaundice, Diarrhea and Vomiting

c. Dark – colored urine, light colored feces and jaundice

d. Fever, Tiredness, Loss of appetite and Nausea

6.] Hepatitis – A is transmitted through ?

a. Fecal – oral route, contaminated food, water of ice

b. Causal contact

c. Contact with infected animal

d. Temperature/ time  abused food where the virus was able to grow and multiply

7.] What is diameter of HAV virus ?

a. 27 nm

b. 27 mm

c. 26 nm

d. 28 nm

8.] HAV virus is which type of virus ?

a. small, isosahedral, non – enveloped, double stranded RNA virus

b. small, isosahedral, non – enveloped, single stranded RNA virus

c. large, isosahedral, enveloped, single stranded RNA virus

d. none of the above

9.] Which antibody appears in the serum at the onset of symptom of acute hepatitis – A ?

a. IgG

b. IgA

c. IgM

d. IgE

10.] Most frequently affected age group are ?

a. Adults

b. 5 – 14 years

c. Both (a) and (b)

d. None of the above

SOLUTIONS :-

1.] (a) 1,562 illnesses

2.] (c) within 2 – 7 weeks

3.] (a) a person infected with hepatitis – A can spread the disease before symptom begin amd up to 1 week after onset of jaundice

4.] (b) fever, tiredness, loss of appetite and nausea

5.] (c) dark – colored urine, light colored feces and jaundice

6.] (a) fecal – oral route, contaminated food, water and ice

7.] (a) 27 nm

8.] (b) small, isosahedral, non – enveloped, single stranded RNA virus

9.] (c) IgM

10.] (b) 5 – 14 years

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REFERENCES :-

1.] Textbook Of Pathology By Harsh Mohan; 7th edition; Page no. 590.

2.] Robbin’s Basic Pathology; 5th edition; Page no. 843 – 844.

The post Hepatitis-A Spread, Symptoms, Causes, Pathogenesis, Treatment And MCQs for NEET, GPAT, CSIR NET JRF appeared first on Gpatindia: Pharmacy Jobs, Admissions, Scholarships, Conference,Grants, Exam Alerts.

1.] Initially, in previous times Hepatitis – C was designated as non – A and non – B [ NANB ] hepatitis. But, now it has been characterized and is called Hepatitis – C.

2.] Hepatitis – C infection is acquired by the blood transfusion, blood products, haemodyialysis, parental drug abuse and accidental cuts and Needle pricks in health workers.

3.] About 90% of post – transfusion hepatitis is of hepatitis – C type.

4.] About 1 – 2% of volunteer blood donor and upto 5% of professional blood donors are the carrier of HCV.

5.] It has an incubation period of about 20 – 90 days ( mean 50 days ).

6.] Persistent of infection and chronic hepatitis are the key features of HCV.

7.] Currently, HCV is considered more important cause of chronic liver disease worldwide than HBV.

HEPATITIS – C VIRUS [ HCV ] :-

1.] HCV is a single – stranded, enveloped RNA virus, having a diameter of 30 – 60 nm.

2.] HCV genome has about 3000 amino acids.

3.] The genomic organization of HCV shows a 5’ terminal end, C (caspid) region and the envelope region E1 and E2 in the exons.

4.] The viral protein results in corresponding serologic and virologic markers of HCV infection as under :-

A.) ANTI HCV ANTIBODIES :

• 1st generation antibodies are against C 100 – 3 region protein and appear 1 – 3 months after infection.
• 2nd generation antibodies are against C 200 and C 33c protein appear about 1 month earlier than the 1st generation.
• 3rd generation antibodies are against C22 – 3 and NS – 5 region proteins and are detected even earlier.

B.) HCV RNA : HCV infection is, however confirmed of HCV – RNA employing PCR technique which can be detected within a few days after the exposure of the HCV infection.

PATHOGENESIS :-

HCV induces hepatocellular injury by cell – mediated immune mechanism is supported by the following :-

• It is possible that the host lymphoid cell are infected by HCV.
• Natural killer cell [NK] cells also seem to contribute to containment ( the limitation of something harmful ) of HCV infection.
• HCV activated CD4+ lymphocytes stimulate CD8+ T lymphocytes via cytokines elaborated by CD4+ helper T – cells.
• The stimulated CD8+T lymphocytes, in turn, elaborate antiviral cytokines against various HCV antigen.
• This may seriously hamper efforts to develop an effective HCV vaccine, particularly because HCV appears to be a relatively unstable virus, with continued alteration in envelope antigen expression.

TREATMENT :-

Hepatitis C virus (HCV) infection causes liver inflammation that can lead to liver problems, including cancer. People who have chronic hepatitis C need medication to treat it. These drugs can ease symptoms of HCV.

Ribavirin works by stopping viruses from replicating and spreading. It’s an oral medication that comes as a capsule, tablet, or solution and is available in several strengths. It’s used in combination with other drugs.

Brand names of ribavirin include:

• Copegus
• Moderiba
• Rebetol
• Ribasphere
• Ribasphere RibaPak

Ribavirin may cause birth defects if a woman takes it during pregnancy. It can also cause birth defects if a man fathers a child during his treatment with this drug.

B.] DIRECT – ACTING ANTIVIRALS ( DAAs )

C.] Protease inhibitor antiviral medications (NS3/4A inhibitors)

• paritaprevir, for genotype 1
• simeprevir (Olysio), for genotypes 1 and 4
• grazoprevir, for genotypes 1 and 4

D.] Protease inhibitors (NS5A inhibitors)

Examples of directed inhibitors include:

• ledipasvir (a component of the combination drug Harvoni)
• ombitasvir (a component of the combination drug Viekira Pak)
• elbasvir (a component of the combination drug Zepatier)
• daclatasvir (Daklinza)

E.] Nucleotide/nucleoside and nonnucleoside polymerase inhibitors (NS5B inhibitors)

Examples of these drugs include:

• sofosbuvir (Sovaldi)
• dasabuvir

MULTIPLE CHOICE QUESTIONS (MCQs) :-

1.] Hepatitis – C causes an infection of the ?

a. Brain

b. Liver

c. Kidney

d. Blood

2.] Is hepatitis – C contagious ?

a. True

b. False

3.] In most people, what are the symptoms of hepatitis – C when they are initially infected ?

a. Itching

b. Jaundice

c. Back pain

d. Most people do not experience symptom

4.] What are cirrhosis ?

a. Scarring of the liver

b. Liver pain

c. Early – stage liver cancer

d. All of the above

5.] There is a vaccination against Hepatitis – C ?

a. True

b. False

6.] Hepatitis – C virus has how many amino acids ?

a. 1000 amino acids

b. 2000 amino acids

c. 1500 amino acids

d. 3000 amino acids

7.] Hepatitis – C virus is which type of virus ?

a. Single stranded, enveloped, having diameter of 30 – 60nm

b. Double stranded, non – enveloped with a diameter of 30 – 60nm

c. Both the above statements are incorrect

d. None of the above

8.] Incubation period for HCV are ?

a. 10 – 15 days

b. 20 – 90 days

c. 2 days

d. 1 week

9.] Which of the following is the most important goal of treating chronic viral hepatitis – C infection ?

a. Normalize ALT and AST

b. Improve symptoms

c. Reverse cirrhosis

d. Eliminate the HCV RNA from serum

10.] What specific treatment do you recommend for chronic hepatitis – C infection for TAS ?

a. Interferon – α + ribavirin

b. Lamivudine

c. None; he is likely to respond to interferon – α

d. None; the risk of adverse effect of interferon – α is too great in TAS

SOLUTIONS :-

1.] (b) liver

2.] (a)

3.] (d) most people do not experience symptoms

4.] (a) scarring of the liver

5.] (b)

6.] (d) 3000 amino acids

7.] (a) single stranded, enveloped, having diameter of 30 – 60nm

8.] (b) 20 – 90 days

9.] (d) eliminate the HCV RNA from serum

10.] (a) interferon – α + ribavirin

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REFERENCES :-

1.] Textbook Of Pathology By Harsh Mohan; 7th edition; Page no. 593 – 594.

2.] Robbin’s Basic Pathology; 5th edition; Page no. 846 – 848.

The post Hepatitis-C HCV, Symptoms, Causes, Pathogenesis, Treatment and MCQs for NEET, GPAT, NET JRF Exam appeared first on Gpatindia: Pharmacy Jobs, Admissions, Scholarships, Conference,Grants, Exam Alerts.

1.] Also called “delta agent” and “hepatitis delta virus”.

2.] Hepatitis – D virus [HDV] is an unique RNA virus that is replication defective, causing infection only when it is encapsulated by HBsAg.

3.] Thus, taxonomically distinct from HBV, HDV is absolutely dependent on the genetic information provided by HBV for multiplication and causes hepatitis only in the presence of HBV.

4.] Delta hepatitis thus arises in two settings :-

• Acute coinfection occurs following exposure to serum containing both the HDV and HBV.
• Superinfection of a chronic carrier of HBV with a new inoculum of HDV results in disease about 30 – 50 days later. The carrier may have been previously “healthy” or may have had underlying chronic hepatitis.

5.] Endemic region for HDV are Southern Europe, Middle – East, South India and parts of Africa.

6.] The high risk individuals of HDV infection are the same as for HBV infection i.e. intravenous drug abusers, homosexuals, transfusion recipient and health care workers.

HEPATITIS DELTA VIRUS [HDV] :-

1.] It is small single stranded RNA particle with a diameter of 36nm.

2.] It is double – shelled – the outer shell consist of HBsAg and the inner shell consist of delta antigen provided by a circular RNA strand.

3.] It is highly infectious and can induce hepatitis in any HBsAg – positive host.

4.] HDV replication and proliferation takes place within the nuclei of the liver cell.

5.] Markers of HDV infection include the following :-

• HDV identification in the blood and in the liver cell nuclei.
• HDAg detectable in the blood and on the fixed liver tissue specimens.
• Anti – HD antibody in acute hepatitis which is initially IgM type and is later replaced by IgG type anti – HD antibody which persist for life to confer immunity against reinfection.

PATHOGENESIS :-

1.] HDV, unlike HBV, is thought to cause direct cytopathic effect on hepatocytes.

2.] There are some example of transmission of HDV infection from individuals who themselves have not suffered from any attack of hepatitis, suggesting that it may not be always cytopathic.

Treatment :-

There are no known treatments for acute or chronic hepatitis D. Unlike other forms of hepatitis, antiviral medications don’t seem to be very effective in treating HDV.

You may be given large doses of a medication called interferon for up to 12 months. Interferon is a type of protein that may stop the virus from spreading and lead to remission from the disease. However, even after treatment, people with hepatitis D can still test positive for the virus. This means that it’s still important to use precautionary measures to prevent transmission. You should also remain proactive by watching for recurring symptoms.

If you have cirrhosis or another type of liver damage, you may need a liver transplant. A liver transplant is a major surgical operation that involves removing the damaged liver and replacing it with a healthy liver from a donor. In cases where a liver transplant is needed.

MULTIPLE CHOICE QUESTIONS [MCQs] :-

1.] Hepatitis – D virus is also called ?

a. Delta virus

b. Hepatitis delta virus

c. Both (a) and (b)

d. None of the above

2.] The most serious infection is ?

a. Superinfection of and HBsAg carrier by HDV

b. Infection with HBV alone

c. Coinfection of HBV and HDV

d. None of the above

3.] The defective satellite virus is ?

a. Hepatitis – B

b. Hepatitis – C

c. Hepatitis – D

d. Hepatitis – E

4.] What is the diameter of HDV ?

a. 36 µm

b. 40 nm

c. 36 nm

d. 35 µm

5.] Which of the following viruses can be transmitted by the parental route ?

a. HBV

b. HCV

c. HDV

d. All of the above

6.] HDV virus is an ?

a. Single stranded DNA particle

b. Double stranded RNA particle

c. Single stranded RNA particle

d. Double stranded DNA particle

7.] Hepatitis – D is which type of virus ?

a. Small, single stranded RNA with diameter of 36 nm

b. Large, single stranded DNA with diameter of 36 nm

c. Small,double stranded RNA with diameter of 36 µm

d. Large, double stranded DNA with diameter of 36 µm

8.] HDV has how many layers ?

a. Double layered

b. Single layered

c. Their is no layer

d. May be double layered or single

9.] Incubation period for hepatitis – D is ?

a. 1 week

b. 10 – 15 days

c. Approx. 35 days

d. 2 – 3 days

10.] The outer shell of HDV virus consist of ?

a. HDsAg

b. HCsAg

c. HAsAg

d. HBsAg

SOLUTIONS :-

1.] (c)

2.] (a) superinfection of an HBsAg carrier by HDV

3.] (c) hepatitis – D

4.] (c) 36 nm

5.] (d)

6.] (c) single stranded RNA particle

7.] (a) small, single stranded RNA with diameter of 36 nm

8.] (a) double layered

9.] (c) approx. 35 days

10.] (d) HBsAg

For More Standard and Quality Question Bank you can Join Our Test Series Programme for GPAT, NIPER JEE, Pharmacist Recruitment Exam, Drug Inspector Recruitment Exams, PhD Entrance Exam for Pharmacy

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REFERENCES :-

1.] Textbook Of Pathology By Harsh Mohan; 7th edition; Page no. 592 – 593.

2.] Robbin’s Basic Pathology; 5th edition; Page no. 848.

The post Hepatitis D: Symptoms, Causes, Pathogenesis, Treatment and MCQs for NEET, GPAT, Nursing Exam appeared first on Gpatindia: Pharmacy Jobs, Admissions, Scholarships, Conference,Grants, Exam Alerts.

Urine formation takes place in three steps:-

• Filtration:- takes place through the semi permeable walls of Glomerulus and Glomerular capsule. Water and other small molecules pass through it easily but blood cells, plasma proteins and molecules which are larger in size so they do not take part in filtration process and remain in blood capillaries, some of the small molecules and water are later reabsorbed. Filtration takes place due to the difference in the blood pressure in the glomerulus and the pressure of filtrate in the glomerular capsule.
Since the efferent arteriole is narrower that afferent arteriole, a pressure develops in the glomerulus known as capillary hydrostatic pressure( 55 mmHg);this pressure is opposed by two pressures, first is the osmotic pressure of blood(30 mmHg) and second is the filtrate hydrostatic pressure(15 mmHg) in glomerular capsule, so the net filtrate pressure is
55-(30+15)=10 mmHg
The volume of filtrate formed by each kidney is known as glomerular filtration rate which is about 125ml/min in a healthy adult. Nearly about 8 liters for filtrate is formed in a day but only 1-1.5 liter is excreted in form of urine because of re absorption and secretion process.

• Selective re absorption:- mostly the reabsorption from the filtrate takes place in the proximal convoluted tubules(PCT) because it has increased surface area for reabsorption . many substances are reabsorbed here including water electrolytes and nutrients such as glucose. some substances are reabsorbed passively while glucose is reabsorbed through active transport mechanism, from here only 60-70% of filtrate passes ahead and much of water, Na and Cl are reabsorbed in the medullary loop, so at last only 15-20% of the filtrate reaches the DCT. Electrolytes are mainly absorbed in PCT and DCT because of which the filtrate that reaches the ducts is very diluted and the main function of the duct is to reabsorb as much as water as the body needs.
Some ions like Na and Cl are reabsorbed by both active and passive ways while some constituent of the filtrate like glucose are completely reabsorbed unless its level is high in the body while the nitrogenous waste products like urea and uric acid are reabsorbed very limitedly.
The maximum capacity of the kidney for reabsorption is known as transport maximum or renal threshold. For example If glucose level in the body rises above its transport maximum than glucose is found in the urine. The transport maximum for some substances is regulated by the body needs while for some constituents it is regulated by hormones

1. parathyroid hormone – regulates the reabsorption of Ca and phosphate
2. antidiuretic hormone ADH – it increases water reabsorption in DCT and in collecting ducts.
3. aldosterone – increases reabsorption of sodium and water and excretion of potassium.
4. atrial natriuretic peptide ANP – it decreases the reabsorption of sodium and water from PCT and collecting ducts.

• Tubular secretion:- filtration takes place when the blood flows through the glomerulus, substance which are not required and foreign particles like drugs example penicillin and asprin may not be completely filtered in that small duration , that’s why such substances are cleared by secretion from the tubular capillaries within the convoluted tubules. Tubular secretion of hydrogen ions is important for maintaining normal blood Ph level.

Multiple choice questions(MCQs)

1. What are the 3 steps of urine formation?
A. formation, selective reabsorption and tubular secretion
B. filtration, selective absorption and tubular secretion
C. filtration, selective reabsorption and tubular secretion
D. formation, selective absorption and tubular secretion

2. Why do filtration takes place?
A. difference between the BP in glomerulus and the pressure of filtrate
B. similarity between the BP in glomerulus and the pressure of filtrate
C. difference between the pressure in glomerulus and the BP of filtrate
D. similarity between the pressure in glomerulus and the BP of filtrate

3. Where do capillary hydrostatic pressure builds up?
A. glomerulus                                        B. PCT
C. DCT                                                    d. collecting ducts

4. Match the following-
a. parathyroid hormone               1. Increases excretion of potassium
b. atrial natriuretic peptide         2. Decreases reabsorption of Na and water
c. aldosterone                                 3. Reabsorption of Ca
d. antidiuretic hormone               4. Increases water reabsorption

5. Which of the following products is reabsorbed very limitedly?
A. urea                                               B. uric acid
C. creatinine                                     D. all of the above

6. Why there is difference in the volume of filtrate formed and the concentration of urine excreted?
A. due to selective reabsorption and tubular secretion of the constituents
B. due to low transport maximum of some constituents
c. due to higher net filtration pressure
D. the difference is not constant so no particular reason for it

7. Which of the following statement is NOT true?
A. ADH is secreted by posterior pituitary
B. filtrate hydrostatic pressure is found in glomerular capsule
C. the kidney’s maximum capacity is known as glomerular filtration rate
D. ANP is secreted by atria of the heart

8. What factor maintains the normal blood pH?
A. tubular secretion of hydrogen ions
B. tubular secretion of Ca ions
C. tubular secretion of potassium ions
D. tubular secretion of Na ions

9. Which of the following hormones decreases reabsorption?
A. ADH                                             B. parathyroid hormone
C. aldosterone                                 D. none of the above

10. Out of the given options which one is not constituent of glomerular filtration?
A. amino acids                                    B. glucose
C. some drugs (large molecule)       D. some drugs (small molecules)

ANSWERS:-

1. filtration, selective reabsorption and tubular secretion
2. difference in the BP in glomerulus and the pressure of filtrate.
3. glomerulus
4. a – 3 b – 2 c – 1 d – 4
5. all of the above
6. due to selective reabsorption and tubular secretion of constituents
7. the kidney’s max capacity is known as glomerular filtration rate
8. tubular secretion of hydrogen ions
9. none of the above
10. some drugs( large molecules

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REFRENCES:- 1. Ross and Wilson-Anatomy and physiology in health and illness; 12th edition; page no.-:
2. Gerard J. Tortora -Principles of anatomy and physiology; edition twelfth ; page no.-: 1030-1034.

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1.) It is caused either due to excessive formation of uric acid, or inability to excrete it.

2.) It get deposited in joints as monosodium salt.

3.) Gout is a disorder of purse metabolism manifested by the following features occurring singly or in combination :

• Increased serum uric acid concentration ( hyperuricamia ).
• Recurrent attacks of characteristic type of acute arthritis in which the crystals of monosodium urate monohydrate may be demonstrated in the leukocytes present in the synovial fluid.
• Aggregated deposits of monosodium urate monohydrate ( tophi ) in an around the joints.
• Renal disease involving interstitial tissue and blood vessels.
• Uric acid nephrolithiasis ( the process of forming kidney stone ).

4.) This disease affect men more often than women.

CLASSIFICATION OF GOUT :-

A.] PRIMARY GOUT : Enzymes defects are unknown in 85 – 90% of primary gout. Overproduction of uric acid, normal excretion, increased excretion, underexcretion of uric acid with normal production, overproduction of uric acid are some of the metabolic defects. Primary gout is 90% of all cases.

B.] SECONDARY GOUT : 10% of all cases. It is associated with increased nucleic acid turnover and inborn error of metabolism. Overproduction of uric acid with increased urinary exertion, reduced excretion of uric acid with normal production, overproduction of uric acid with increased urinary excretion are some metabolic defects.

PATHOGENESIS :-

1.] Many factors play a role in the conversion of asymptomatic ( producing or showing no symptoms ), hyperuricemia ( excess uric acid in blood ) into primary gout. Some of these are :-

• Age of the individual and the duration of the hyperuricemia.
• Genetic factor.
• Heavy alcohol consumption.
• Obesity.
• Predisposition of certain drugs. Fir example : Thiazides.

2.] Central to the pathogenesis of the arthritis is precipitation of monosodium urate ( MSU ) crystals into the joints.

3.] Synovial fluid is a poorer solvent of MSU than plasma, and so with the hyperuricemia the urates in the joint fluids become supersaturated, particularly in the peripheral joint where the temperature is as low as 20°C in the ankle.

Fig : 1

CLINICAL COURSE :-

1.] The natural history of gout passes through four stages :-

• Asymptomatic hyperuricemia.
• Acute gouty authorities.
• Intercritical gout.
• Chronic tophaceous gout.

2.] Certain medicines like analgesics, uric acid reducers, non steroidal – inflammatory drugs are also given.

• Colchicine
• Corticosteroids
• Probencid
• Sulfinapyrazone
• Allopurinol
• Febuxostat

MULTIPLE CHOICE QUESTIONS :-

1.] Which of the following is not a first – line option for the pharmacological treatment of gout gout ?

a. NSAIDS

b. Corticosteroids

c. Oral colchicine

d. Aspirin

2.] How long after the onset of an acute gout attack should pharmacologic therapy be initiated ?

a. Within 1 hour

b. Within 24 hour

c. After 24 hour

d. After 48 hour

3.] Ice packs can be effective adjuncts to the management of an acute gout attack ?

a. True

b. False

4.] Which if the following is the recommended first – line therapy to consider ?

a. Febuxostat

b. Allopurinol

c. Probenecid

d. Benzbromarone

5.] Gout is caused by the buildup of what substance in the body ?

a. WBC

b. Synovial fluid

c. Uric acid

d. Blood plasma

6.] Uric acid is usually eliminated from the body by way of ?

a. Breathing

b. Urine

c. Metabolization of liver

d. Sweat

7.] People with gout should avoid consuming ?

a. Alcohol

b. Dairy products

c. Both (a) and (b)

d. None of these

8.] Symptoms of gout may include ?

a. Warmth, severe pain and swelling in the joint

b. Red or purple skin

c. Peeling, itching skin at the site of gout attack

d. All of the above

9.] What is most common site of gout attack ?

a. Big toe

b. Foot

c. Knee

d. Ankle

10.] What increases a person risk for developing gout ?

a. Family  history ( genetics )

b. High – salt diet

c. Asthma

d. All of the above

SOLUTIONS :-

1.] (d) aspirin

2.] (b) within 24 hours

3.] (a)

4.] (b) allopurinol

5.] (c) uric acid

6.] (b) urine

7.] (a)alcohol

8.] (d)

9.] (a) big toe

10.] (a) family history ( genetics )

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REFERENCES :-

1.] Textbook Of Pathology By Harsh Mohan.

2.] Robbin’s Basic Pathology.

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1.) Rheumatoid arthritis [RA] is a chronic systemic inflammatory disorder that may affect many tissues and organs.

2.) Although, the cause of rheumatoid arthritis [RA] remains unknown.

3.) Women are three to five times are more vulnerable towards this disease.

4.) The onset of this disease is insidious ( developing in a gradual and the harmful way ), beginning with prodrome ( an early symptom indicating the onset of a disease or illness ) of fatigue, weakness, joint stiffness, vague arthralagies and myalgias. This is followed by pain and swelling of  joints, especially involving the joints of hands, wrist and feet.

5.) Also, extra – articular manifestations infrequently produces symptoms, but when present complicate the diagnosis.

ETIOPATHOGENESIS :-

1.) It is believed that rheumatoid arthritis is triggered by exposure of an immunogenetically susceptible host to an arthriogenic microbial antigen.

2.) Therefore, causes involved in rheumatoid arthritis are :-

• Genetic susceptibility.
• Primary exogenous arthritogen.
• An autoimmune reaction within synovial membrane.
• Mediators of the joint damage.

3.) Genetic predisposition is a clearly a major determinant of susceptibility to rheumatoid arthritis.

4.) Moreover, the majority of ( 65 to 80% ) individuals who develop rheumatoid arthritis are HLA – DR4 or DR – 1 or both.

5.) It is generally belived that the initiator of the disease is a microbial agent,  but the identity of microbial agent is always elusive.

6.) An autoimmune reaction in which T cells plays the pivotal role is widely held to be responsible for the chronic destructive nature of rheumatoid arthritis, once an inflammatory synovitis has been initiated by an exogenous agent.

7.) T cells, mainly CD4+ memory cells, appear within the affected area that is in affected joints early in the development of rheumatoid arthritis.

8.) IgM antibodies mostly are generated in the joints. About 80% of individuals with rheumatoid arthritis have auto antibodies to the Fc portion of autologous IgG.

Fig : 1

CLINICAL COURSE :-

1.) The clinical course of rheumatoid arthritis is extremely variable.

2.) Initially there is a malaise ( feeling of discomfort ), fatigue and generalized musculoskeletal pain.

3.) The involved joints are swollen, warm, painful and particularly stiff on arising or following inactivity.

4.) Symptoms, usually develops in the small joints of the hand ( proximal interphalangeal joint and metacarpophalangeal joint ) and frets, followed by the wrist, knees, ankles and elbows.

5.) Thus, there are no specific laboratory test diagnostic of rheumatoid arthritis.

DIAGNOSIS :-

The diagnosis is made primarily on the clinical features and requires the presence of four of following criteria :-

• Morning stiffness
• Arthritis in three or more joint areas.
• Arthritis of hand joints.
• Symmetric arthritis.
• Rheumatoid nodules.
• Serum rheumatoid factor.
• Typical radiographic changes.

MULTIPLE CHOICE QUESTIONS :-

1.] What are the early signs and symptoms of rheumatoid arthritis ?

a. Joint pain, tenderness, redness and swelling

b. Loss of joint range of motion

c. Limping

d. All of the above

2.] Rheumatoid arthritis [RA] is different from some other forms of arthritis because it ?

a. Is more painful than other forms

b. Occur below the waist

c. Is symmetrical, affecting the right and left side of the body

d. Generally occur above the waist.

3.] Rheumatology is the branch of medicine that involve the study of ?

a. The immune system

b. Musculoskeletal ( muscle and bone ) system

c. Rheumatic disease

d. All of the above

4.] The sudden appearance or worsening of RA symptom is referred to as an ?

a. Outbreak

b. Flare

c. Burst

d. Eruption

5.] The term arthritis refers to ?

a. Stiffness in joint

b. Inflammation of the joints

c. Both (a) and (b)

d. None of the above

6.] Rheumatoid arthritis is more severe in ?

a. Men

b. Women

c. Both (a) and (b)

d. None of the above

7.] People with rheumatoid arthritis experience the most stiffness at night ?

a. True

b. False

8.] Rheumatoid arthritis can be treated by ?

a. Medication

b. Exercise

c. Surgery

d. All of the above

9.] Which test cannot be used to aid in the diagnosis or monitoring of progression of rheumatoid arthritis ?

a. ESR

b. RF Test

c. Anti – CD

d. Heterophile AB

10.] The cause of rheumatoid arthritis is ?

a. Heterophile antibodies

b. EBV

c. IgM

d. IgG

SOLUTIONS :-

1.] (d)

2.] (c) is symmetrical, affecting in right and left side of body

3.] (d)

4.] (b) flare

5.] (b) inflammation of the joints

6.] (b) women

7.] (b)

8.] (d)

9.] (d) heterophile AB

10.] (c) IgM

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REFERENCE :-

1.] Textbook Of Pathology By Harsh Mohan.

2.] Robbin’s Basic Pathology.

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1.) Osteoporosis is also called osteoarthrosis or degenerative joint disease.

2.) Osteoporosis teem denotes increased porosity of the skeleton resulting in a reduction of bone mass.

3.) It is characterized by progressive degenerative changes in the articular cartilages over the year, particularly in weight – bearing joints.

TYPES OF OSTEOPOROSIS :-

A.] PRIMARY OSTEOPOROSIS :

• It occur more in elderly people, more in women than men.
• The condition of primary osteoporosis may show longevity.
• The primary osteoporosis, wear and tear with repeated minor trauma, heredity, obesity, gaining all contribute to focal degenerative change in the articular cartilage of the joint.
• Genetic factor favoring susceptibility to develop osteoporosis have also been observed.

B.] SECONDARY OSTEOPOROSIS :

• Secondary osteoporosis can occur at any age.
• Secondary osteoporosis is the result of any previous wear and tear phenomena involving the joint such as previous injury, fracture, inflammation, loose bodies and congenital dislocation of the hip.

Fig : 1

PATHOGENESIS :-

1. Age related changes in bone cells and matrix have a strong impact on bone metabolism.
2. Osteoblasts from elderly individuals have reduced reproductive and the biosynthetic potential when compared with osteoblasts from younger individuals.
3. The end result will be skeleton populated by bone – forming cells that have a diminished capacity to make bones.
4. This form of osteoporosis also known as senile osteoporosis, is categorized as a ” low turnover variant “.
5. Reduced physical activity increase the rate of bone loss in experimental animals and humans.
6. The decreased physical activity that is associated with aging contribute to sensile osteoporosis ( condition of significantly diminished bone mass due to long standing imbalance between bone resorption and bone formation ).
7. Postmenopausal osteoporosis is characterized by a hormone – dependent acceleration of bone loss.
8. In postmenopausal osteoporosis the yearly reduction in bone mass may reach upto 2% of cortical bone and 9% of cancellous bone.
9. No surprise that 1 out of every 2 women suffers an osteoporotic fracture in contrast to 1 in40 men. Estrogen deficiency is belived to play the major role in this phenomenon.
10. Decreased estrogen level result in increased secretion of interleukin – 1 by blood monocytes. Interleukin – 1 is the most potent known stimulator of osteoclast recruvitment and activity.

Fig : 2

CLINICAL COURSE :-

1. Vertebral fractures, which frequently occur in the thoracic and lumbar region, are potentially very painful.
2. Femoral neck and wrist fractures are common.
3. Osteoporosis cannot be readily detected in plain radiographs until 30 to 40% of the bone mass is loss.
4. Osteoporosis is a difficult situation to be diagnosed because it remains asymptomatic until skeleton fragility is well advanced, it is only one of a group of osteopenic skeletal disorders characterized by “too little” bone, which can be difficult to differentiate and there is no easy, sensitive, and specific method to determine the degree of bone loss.
5. Currently, the best methods or procedure that accurately estimate the amount of bone loss are single – energy photon absorptiometry, dual energy absorptiometry and quatitative computed tomography (CT).

MULTIPLE CHOICE QUESTIONS ( MCQs ) :-

1.] At what age do we have the most bone density ?

a. Your 20s

b. Your 30s

c. Your 40s

d. Your 50s

2.] Which of these activities could cause a broken bone in someone with osteoporosis ?

a. Coughing

b. Bending

c. Sneezing

d. All of the above

3.] Which of these makes it more likely that you’ll get osteoporosis ?

a. Drinking too much alcohol

b. Family history

c. Smoking

d. All of the above

4.] Which test is used to do screening for osteoporosis ?

a. Blood test

b. Special type of X – rays

c. Urine test

d. All of the above

5.] What causes a “dowager’s hump” or stooped posture ?

a. Spinal bone spurs

b. Inflexible spine

c. Broken vertebrae

d. None of the above

6.] Which kind of exercise can help to prevent osteoporosis ?

a. Swimming

b. Running

c. Weightlifting

d. Both (a) and (c)

7.] How can osteoporosis be prevented ?

a. Eat a low fat diet

b. Exercise every day

c. Get enough calcium and vitamin – D throughout your lifetime

d. Both (b) and (c)

8.] How is osteoporosis treated ?

a. Medicines

b. Surgery

c. X – ray treatment

d. It can’t be treated

9.] Which of these medications causes rapid bone loss in the first three to six months of treatment – placing the individual at higher risk of osteoporosis and fractures ?

a. Beta blockers

b. Corticosteroids

c. Acetaminophen

d. Benzodiazepines

10.] Calcium is a key mineral that help maintain bone health. Which of this essential vitamins is needed to ensure that enough calcium is absorbed by the body ?

a. Vit. A

b. Vit. B

c. Vit. C

d. Vit. D

SOLUTIONS :-

1.] (b) Your 30s

2.] (d)

3.] (d)

4.] (b) Spinal type of X – ray

5.] (c) Broken vertebrae

6.] (d)

7.] (d)

8.] (a) Medicines

9.] (b) Corticosteroids

10.] (d) Vit. D

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REFERENCES :-

1.] Textbook Of Pathology By Harsh Mohan.

2.] Robbin’s Basic Pathology.

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