RENAL FUNCTION TEST

Renal function test:-(kidney function test)  

In general, the kidney performs the following vital functions in the body-

1. Excretion of waste products

2. Regulation of Acid-base balance

3. Regulation of salt-water balance

4. Formation of renin and erythropoietin

 Renal function test are broadly divided into four groups-

1. Urine analysis

2. Concentration and dilution test

3. Blood chemistry

4. Renal clearence test

  In addition renal biopsy is performed to confirmed the diagnosis of renal disease.

Normal constituents of urine:-
Characteristics of normal urine-
1. Color:-
 Normal urine is clear or straw colored. The color is light when large amount of water is consume. It is highly colored in jaundice due to excretion of bile pigment.

2. Odour:-
  Freshly voided urine has a mild aromatic odour.

3. Volume:-
 The average daily output of urine is 1.5 ltr.
The urine output decrease in-
i. Hot climate 
ii. After heavy sweating (perspiration)
iii. After vomiting and diarrhoea

 The urine output increase in-
i. Taking large amount of water
ii. Cold climate
iii. After taking alcohal

4. Specific gravity:-
 The specific gravity of normal urine is 1.010-1.030.

5. Reaction (Ph):-
 Normal urine is slightly acidic with Ph of 6. It is acidic after a heavy protein diet and in fever.

Characteristics of abnormal urine:-
 The various characteristics of abnormal urine are as follow-
1. Color:-
 Various chemical constituents imparts different color to urine-
i. Colorless- dilute urine (polyuria)
ii. Dark amber color- Concentrated urine (oliguria)
iii. Yellow color:- bile pigment (jaundice)
iv. Orange-red color- (rifanpicin)
v. Red to reddish brown- hemoglobin with urine (hematouria)
vi. Milky - Presence of fat (chyluria)
vii. Cloudy (turbid)- Pus cells with urine
viii. Black on standing- Alkaptonuria

2. Volume:-
i. Urine output more than 2 ltr per day is called polyuria.
ii. Urine output between 300ml-500ml per day is called oliguria.
iii. Urine output between 30ml-50ml per day called anuria.

3. Odour:-
i. Smell of acetone indicates uncontrolled diabetes or starvation.
ii. Smell of burned sugar or maple sugar indicates urinary disease.

4. Specific gravity:-
  High specific gravity indicates diabetes mellitus and also in excessive fluid loss. Eg- Dehydration low specific gravity occurs in diabetes insipidus or CRF.

5. Ph:-
 Acidic urine indicates metabolic acidosis. Alkaline urine indicates metabolic alkalosis.

Normal constituents of urine:-
Inorganic constituents-

Sodium- 4gm
Potassium- 2gm
Calcium - 0.1-0.2gm
Magnesium - 0.05-0.2gm
Sulphur - 1gm
Phosphorus - 2-2.5gm
Chlorine- 9-16gm

Organic nitrogenous constituents-
Urea - 30gm
Uric acid- 0.5-0.8gm
Creatinine - 1.2-1.8gm
Ammonia-  0.3-1gm

Organic non-nitrogenous constituents-
Oxalic acid - 15-20gm
Citrate -  0.2-1 or 2 gm
Ketone bodies - 3-15gm

Abnormal constituents of urine-
Substance like protein, sugar, ketone bodies and blood and not excreted in normal urine. They are excreted in urine in pathological conditions. So they are called abnormal constituents of urine. 
The presence of abnormal constituents in urine helps in diagnosis of various systemic and renal disease.

Abnormal constituents ---- Disease

Protein        -         Proteinuria
Albumin     -         Albuminuria
Pentose      -         Pentosurea 
Ketone bodies -   Ketosis
Bile salts    -         Jaundice
Blood     -             Haematouria 
Pus       -               Pyurea
Glucose    -         Glycosurea


PROTEIN:-
Normally urine virtually has no protein of all the proteins, albumin is readily excreted because of its smaller size. So, urinary excretion of protein is referred as albuminuria.
Cause-
1. Violent exercise 
2. Pregnancy
3. High fever
4. Renal disease like nephritic and nephrotic 
5. Ascites and abdominal tumour

NEPHRITIS (BRIGHT's DISEASE):-

It is the inflammation of the kidney. It is also known as glomerulonephritis.
It is convenient to classify glomerular disease in two broad groups-
1. Primary glomerulonephritis
2. Secondary glomerulonephritis

1. Primary glomerulonephritis :-
It is condition in which the glomerulus are predominent site of involving.

2. Secondary glomerulonephritis:-
It includes certain systemic and hereditary which secondarily affects the glomerulus.

Clinical feature:-
i. Proteinuria
ii. Haematouria
iii. Hypertension 

The following are 6 major glomerular syndrome commonly found in glomerular disease-
Nephritic and nephrotic syndrome
Acute renal failure and chronic renal failure
Asymptomatic proteinuria and haematouria

1. Acute nephrotic syndrome:-
This is acute onset of haematouria, proteinuria, hypertension, oedema and oliguria.

2. Nephrotic syndrome:-
It is characterized by massive proteinuria, hypoalbuminaemia, oedema, hyperlipidaemia, lipidouria and hypercoagulability of blood.

Difference between Acute nephritic and nephrotic syndrome:-

Glucose:-
Normal urine does not contain glucose. The abnormal condition in which glucose is excreted in urine is called glycosuria.

Causes of glycosuria:-
1. Diabetes mellitus
2. Renal glucosuria
3. Alimentary glycosuria
4. Glycosuria of pregnancy
5. Advanced glomerulonephritis

1. Diabetes mellitus: (DM)
 It is defined as hetrogeneous metabolic disorder characterized by common features of chronic hyper glycaemia with disturbance of carbohydrate, protein and fat metabolism.
Classification-
 It is of two types-
i. Insulin dependent diabetes mellitus (IDDM)- (juvenile onset diabetes)(JOD) - Type 1 deabetes mellitus

ii. Non-Insulin dependent diabetes mellitus (NIDDM)Type 2 diabetes mellitus

Cause of diabetes mellitus:-
i. The basic phenomena in type 1 diabetes mellitus is distruction of β-cells mass, usually leading to absolute insulin deficiency.
ii. The basic metabolic defect is either a delayed insulin secretion related to glycose secretion. (Impaired insulin secretion) or the peripheral tissues are unable to respond to insulin. (Insulin resistance)

Clinical feature:-
1. Polyuria (increased urination)
2. Polydypsia (increased thirst)
3. Polyphagia  (increased appetite)
4.Weight loss
5. Patient may be asymptomatic

Complication:-
1. Diabetic retenopathy
2. Diabetic nephropathy
3. Diabetic neuropathy

Normal glucose level-
Fasting -      70-110mg/dl

Postprandial    120-150mg/dl



Pentosuria:-
It is abnormal defect of sugar metabolism, causing abnormal excretion pentose in urine.


Ketone bodies:-
Ketone bodies are-
1. Acetoacetic acid
2. 𝞫-hydroxy-butyric acid
3. Acetone

Cause of ketone bodies:-
1. Diabetes mellitus
2. Starvation

Ketosis:-
It is also known as diabetes ketoacidosis (DKA).
It is complication of Type-1 diabetes mellitus.
A metabolic state resulting from a profound lack of insulin which leads to inability in glucose production from the liver. Result in hyperglycaemia to conversion of fatty acid into ketone.


Jaundice:- (Icterus)
It refers to the yellow pigmentation of the skin sclera be increase in the bilirubin level in blood. Which results in Hyper bilirubinaemia.
Normal bilirubin level in blood is 0.3-1.3 mg/dl. The presence of bile salt in urine indicates jaundice.
Bile salts are sodium taurocholate, sodium glycholate, pattasium taurocholate, pattasium glycolate.

Haematouria:-
Excretion of blood in urine is called haematouria. It indicates hemorrhage in urinary tract.
Cause of haematouria:-
1. Injury to the kidney or urinary tract
2. Infection of urinary tract 
3. Tumour in urinary tract
4. Parasitic infection

Renal function test result example-

LYMPHATIC FILARIASIS

Lymphatic filariasis:-

Causative organism-  wucheria bancrofti

   Lymphatic filariasis is also known as Elephantiasis or filariasis. Infection are transmitted to man by the bite of infective mosquito. Man is a definitive host and mosquito is the intermediate host. Adult worms are usually find in lymphatic system.

Vector- culex mosquito

The mosquito cycle begins when the micro filarae are picked up by the vector mosquito during feedie.
 The following stages of development takes place in the vector-

1.Exsheathing stage:-
The larva comes out of the sheath in which it is enclosed with in 1-2 hours of ingestion. This is known as exsheathing which take place in the stomach of mosquito.

2. First stage larva:-
 The larva is able to penetrate the stomach wall of the mosquito which takes place in 6-12 hours and migrate into the thoraxic muscle, Where it grow and develop into sausage shape. (short and thick)

3. Second stage larva:-
  Larva moults or infective larva (long and thin form). It is highly active and motile. When it is migrate to the mouth of the mosquito it is ready to transmit to the new host. Mosquito is ready to be infective.

Mode of transmission:-
 Filariasis is transmitted by the bite of a infected vector. The parasite is deposited near the site of puncture. It penetrate the skin and reach the lymphatic system.

Incubation period- 8-16 months

Clinical features-
Acute inflammation in lymph glands and vessels.
Filarial fever
lymphangitis
lymphadenitis

DYSPNOEA

Dyspnoea

Introduction:-

  The term dyspnoea refers to sudden and some shortness of breath or difficulty in breathing. Breathlessness may be normal after exercise or exertion. They usually resolve itself. Breathlessness that comes on suddenly and unexpectidy may be a warning sigh of underlined disease.

Cause:-

Bronchial asthma

Chronic asthma

Emphysema

Bronchieteatis

NOTE:-

COPD (Chronic obstructive pulmonary disease) are commonly used clinical term for a group of pathological condition in which there is chronic, partial or complete obstruction to the airflow at any level from trachea to the smallest air ways results in functional disability of lungs. The following Four entities are included in COPD.

1. Chronic bronchitis:-

    It is a common condition defined clinically as persistent cough with expectoration on most days for at least 3 months of the year for 2 or more consecutive years. The cough is caused by over secretion of mucus.

Cause-

Cigarette smoking

Atmospheric pollution

Occupational Disease

Family and genetic factors

Clinical features:-

i. Paroxysms of cough

ii.Dyspnoea

iii. Wheezing respiration

iv. It typically last for a few minutes to hours.

2. Emphysema:-

   It is defined as combination of permanent delatation of air base distal t the terminal bronchioles and the distructions of the walls of dilated air base (Alveolei)

Thus, Emphysema is defined morphologically, while chronic bronchitis is defined clinically.

Etiology-

Smoking

Air pollution

Occupational disease

Family and genetic factors

Clinical features-

  The age at time of diagnosis is often a decate later (about 60 years). Then the age for the predominent bronchitis(about 50 years).

It is a common condition defined clinically as persistent cough with expectoration on most days for at least 3 months of the years. The cough is caused by over secretion of mucus.

3. Bronchial asthma:-

   Asthma is a disease of air base ie characterized by increased responsiveness of the tracheobronchial tree to a variety of stimulus resulting in wide spread spasmodic narrowing of air passage which may be relieved spontaneously or by air therapy. It is manifest as paroxysms of dyspnoea cough and wheezing.

Etio-pathogenesis:-

  The two main types are -

1. Atopic, allergic asthma or Extrinsic asthma

2. Intrinsic asthma

3. Mixed type

1. Extrinsic asthma:-

  It is usually begins in childhood or early adulthood life. Hypersensitivity to various extrinsic antigenic substance or allergens is usually present in this case. Allergens eg- house dust, pollen grains, animal danders (fur, scales etc) etc.

2. Intrinsic asthma:-

   This type of asthma develops laters in adult life with or without family history of adult. Most of these patients develops symptoms after upper respiratory tract infection by virus. Associated with nasal palyp or chronic bronchitis is possible.

3. Mixed type:-

    Many patients do not clearly fit into either of the above 2 categories. Those patients who develops asthma in early life have strong allergic component, while those who developed the disease later tend to be non-allergic.

Clinical feature-

Paroxysms of dysnoea

Cough

Wheezing

         Most attack last for a few minute to hours. When attack occur continuously, it result in more serious condition called "status asthmaticus".

4. Bronchiectasis :-

   It is defined as abnormal irreversible dilation of the bronchi and bronchioles(greater than 2mm) in diameter, developing secondary to the inflammatory weakening if the bronchial walls. The most characteristic clinical manifestation is persistent cough with expectorations of copious amount of foul smelling, purulent sputum.

Clinical features-

Chronic cough with foul smelling sputum production, hemoptysis (bloody sputum) and recurrent pneumonia sinusitis may be present.

FEVER

Fever

 Fever is an ancient term means raised body temperature. Feverish is synonyms for fever. Pyrexia is come from greece word which means increased body temperature.

Normal body temperature- 98.6℉ or 37℃.

Apyrexia:-

  Absence of fever, normal temperature is below the normal body temperature.

Hyper pyrexia:-

  Elevation of body temperature above 106℉ produced by infection caused by micro-organisms.

 Highest temperature recorded - 114℉

 lower temperature recorded- 75℉

Cause:-

i. Infection (viral, bacterial, fungal, parasite)

ii. Infraction

iii. Severe hemorrhage (trauma)

iv. Inflammatory disease

v.  Occasionally a patient has an increased temperature continuously or intermittently called habitual hyperthermia.

vi. Heat stroke

vii. Injury to brain stem may produce fever

Mechanism-

  Fever is the result of breakdown of bacterial toxins liberated by the disease organism that affects the heat regulatory centers. (hypothalamus)

 Heat stroke is caused when heat or humidity are so extreme that the body can no longer cool itself sweating. Which is a major mechanism for loosing heat usually stopped.

         

                    Bacterial virus

                            ⬇release toxins

                  Exogenous pyrogen

                             ⬇ stimulate

                    Macrophages

                             ⬇ secrete

                 Endogenous pyrogen

                             ⬇

             carried in the blood to brain

                             ⬇acts on

           Heat regulatory center in hypothalamus

                             ⬇ 

             Temperature increased (pyrexia)

Symptoms:-

     Flushed face (redness), anorexia (loss of appetite), hot and dry skin, nausea and vomiting, constipation and diarrhoea, scanty and highly colored urine. Delirium is possible if temperature is over 105 degree F. Delusion (disturbed state of mind as restlessness illusion, incoherence)

Clinical representation:-

Clinically fever has 3 stages- Chill, heat, sweat.

   First is chill stage, as the temperature begins to rise, the body conserve the heat, the patient feels the cold. Cutaneous vasoconstriction reduces the loss of heat. The skin is dry often shivering or chill. The teeth chatters.

   Then comes the heat stage, this is peak stage of fever fall in the morning and rise in the evening. After cutaneous vasodilation develops it allows loss of excess heat, though sweating is uncommon the patient feels warm.

   Finally comes the sweat stage, it is also known as the stage of resolution. The heat center is reset, the excess of heat is lost mainly from skin. The patient feels not throws off the covering. 

 Cutaneous vasodilation and sweating is profuse.

Type of Fever:-

i. Intermittent fever

ii.Recurrent fever

iii Remittent fever

iv. Continuous fever

v . Undulent fever

i. Intermittent fever:-

    Any fever characterized by intervals of below normal temperature or touches the normal. Changeable temperature with great chill followed by heat and sweat with in 24 hours. Eg- Malaria.

ii. Recurrent fever:-

     Recurrent fever is also known as "Suppressive fever" or "Replacing fever". After 1-7days or week or a month again temperature rises. Normal person feels better but after a week or a month temperature rises. ie inflammatory conditions, typhoid.

iii. Remittent fever:-

   Fever is always above normal temperature cannot touch the normal level in 24 hours. eg- septicaemia, TB.

iv. Continuous fever:-

   Where the temperature remains above the normal temperature throughout a 24 hour period and do not fluctuate more than 1 ℃.

v. Undulent fever:-

    In this temperature rises after a month, 6 month, a year toxins does not suddenly removed. Eg- Malaria.

THROMBOSIS

THROMBOSIS

   Thrombosis is the process of formation of solid mass in circulation from the constituents of flowing blood, the mass itself is called thrombus.

NOTE-

   Hemostatic plughs are the blood clot formed in healthy individual at the site of bleeding. It is helpful as they stop the escape of blood and plasma. Where as thrombi developed in the unruptured cardiovascular system may be life threatening by causing one of the following harmful effect-

1. Ischemic injury:-

     Thrombi may decrease the blood supply to part of an organ or tissue and cause ischemia which may subsequently resulting in infraction.

2. Thrombo embolism:-

  The thrombus or its part may get dislodged and be carried along in the blood stream as embolus to lodge in a distant vessel.

Pathophysiology:_

  The factor which predisposes to thrombus formation are-

1. Endothelial injury

2. Altered blood flow

3. Hyper coagulability of blood 

   These events are described as-

1. Endothelial injury-

    The integrity of blood vessel wall is important for maintaining normal blood flow.

Number of factors and condition may cause vascular injury and predispose to the formation of thrombi.

 These are as under -

i. Endocardial injury in myocardial infraction, myocarditis

ii. Ulcerated plaques in advance atheroscalrosis 

iii. Hemodynamic stress in hypertension 

iv. Arterial diseases

v. Diabetes mellitus

2. Role of platelets :-

   Platelets comes to play a central role in normal hemostasis as well as thrombosis. 

The sequence of events is as under-

i. Platelets adhesion:-

  The platelets in circulation recognize the site of endothelium injury and adhere to exposed subendothelium collagen.

ii. Platelets release reaction:-

  The activated platelets then undergo release reaction by which the platelets granules are released to the exterior.

iii. Platelets aggrigation:-

  This result in formation of temporary hemostatic plough. 

3. Role of coagulation system:-

  Coagulation mechanism is the conversion of the plasma fibrinogen into solid mall of fibrin. The coagulation system is involved in both hemostatic process and thrombus formation. 

4. Alteration of blood flow:-

  Turbulence and stasis occur in thrombosis.

5. Hyper coagulability of blood:-

   The effect of hypercoagulability on thrombosis is formed by advance age, smoking and obesity.

6. Predisposing factor:-

   The number of primary and secondary factors favour thrombosis.

i. Primary factor-

   a. Deficiency of antithrombin

   b. Defect in fibrinolysis

ii. Secondary factor-

   a. Cigarette smoking

   b. Immobilization 

   c. Prolonged bed rest

Origin of thrombi:-

    Thrombi may arise from the heart, arteries, veins or in micro circulation.

1. Cardiac thrombi:-

  Thrombi may form in any of the chambers of the heart and on the valcusps.

2. Arterial and venous thrombi:-

  Arterial thrombi-  Arota, coronary arteries, arteries of limbs, renal artery, cerebral artery

Venous thrombi-  veins of lower limb, pulmonary veins renal vein

 Capillary thrombi- minute thrombi composed mainly of packed red cell are formed in the capillary in acute inflammatory lesions.

Fate of thrombus:-

  The possible fate of thrombi can be as under-

1. Resolution:-

  Thrombus activates the fibrinolytic system with consequent release of plasmin which may dissolve the thrombus completely resulting in resolution.

2. Organization:-

  If the thrombus is not remove, its start getting organized. Fibrocytic cells appear and begin to phagocytes fibrin and cell debris.

Proteinetic enzyme liberated by lucocytes and endothelial cell start digesting coagulent.

Capillaries grown into the thrombus from the site of its attachment and fibroblast start invating the thrombus.

3. Propogation:-

    The thrombus may enlarge in size due to more and more deposition from the constituents flowing blood. In this way, it may ultimately cause obstruction of some important vessels.

4. Thrombo embolism:-

  The thrombi in early stage and infected thrombi are quite friable and may get detached from its vessel wall. These are released in part or completely in blood stream as emboli which produces in effect at the site of there lodged.

HEMORRHAGE

HEMORRHAGE

    Hemorrhage is the escape of blood from a blood vessels. The bleeding may occur externally or internally into the serous cavity. Eg: Hemothorax, hemoperitonium, hemopericardium or into the hollow viscous.

  Extra vassation of blood into the tissue with resultant swelling is known as hematoma.

 Large extravassation of blood into the skin and mucus membrane are called Icchymosis. 

  Purpura are the small area of hemorrhage up to 1cm into the skin and mucus membrane.

  Petechiae hemorrhage are minute pin head size hemorrhage.

Condition of hemorrhage:-

1. Trauma to the vessel wall

2. Sponteneous hemorrhage

3. Inflammatory lesions of vessel wall. Eg:- ulcers

4. Neoplastic invasion 

5. Vascular disease.  Eg:- Atheroscalrosis 

6. Elevated pressure with in the blood vessel

Effect:-

  The effects of blood loss depend upon three main factors-

1. The amount of blood loss

2. Speed of blood loss

3. Site of hemorrhage

OEDEMA

OEDEMA

  Oedema may be defined as abnormal and excessive accumulation of free fluid in interstitial tissue space and serous cavities.

1. Free fluid in tissue cavity or body cavity:-

     Depending upon the body cavity in which the fluid accumulates, it is corresponding known as ascites, hydrothorax and hydropericardium.

2. Free fluid in interstitial space:-

      The oedema fluid lies free in the interstitial space between the cells and can be displaced from one place to another.

 In the case of oedema in the subcutaneous oedema is divided into two parts-

a. Pitting oedema:-

      In case of oedema in the subcutaneous tissue, momentry pressure of finger produces a depression known as pitting oedema.

b. Non-pitting oedema or solid oedema:-

  In which no pitting is produce on pressure. Ex- elephanticis, myxoedema.

The oedema may be of two main type-

1. Localized

2. Generalized 

1. Localized:-

     When limited to an organ or limb. Ex: lymphatic oedema, inflammatory oedema, allergic oedema.

2. Generalized oedema:-

     When it is systemic in distribution particularly noticible in the subcuteneous tissue. Ex: renal oedema, cardiac oedema, nutritional oedema.

      Besides, there are few special forms of oedema. Ex- pulmonary oedema, cerebral oedema.

Depending upon fluid composition oedema fluid may be -

1. Transudate

2. Exudate

1. Transudate:-

      Which is more often the case (low protein content and few cells are present) such as in oedema of cardiac and renal disease.

2. Exudate:-

    Such as in inflammatory oedema (High protein content and presence of WBC and RBC cells).

Pathogenesis of oedema:-

     Oedema is caused by mechanism that interfere with normal fluid balance plasma, interstitial fluid and lymph fluid.

Note:-

Normal fluid exchange:-

     At the arterioler end  of the capillaries the balance between the hydrostatic pressure 32mm Hg and plasma oncotic pressure 25mmHg is the hydrostatic pressure of 7mmHg. Which is the outward riding force so that the small quantity of fluid and solute leave the vessel to enter the interstitial space.

  At the venular end of the capilary the balance between the hydrostatic pressure 12 mmHg and plasma oncotic pressure 25mmHg is the osmotic pressure of 13mmHg which is the inward force. so that the fluid and solute re-enters the plasma.

  Tissue tension is the hydrostatic protein of interstitial fluid and is lower then the hydrostatic pressure in the capilary at the end.

  Effective hydrostatic hydrostatic pressure. That drives fluid through the capilary wall into to interstitial space.

Pathogenesis of oedema:-

1. Decreased plasma oncotic pressure:-

       The plasma oncotic pressure exerted by the total amount of plasma protein tends to draw fluid into the vessels normaly.

  A fall in the total plasma protein level (Hypoproteimnia) of less than 5gm per dl) result in lowering plasma oncotic pressure in a way that it can no longer counter act effect of hydrostatic pressure of blood. This result in increase outward movement of fluid from the capilary wall and decreased invert movement of fluid from the interstitial space causing oedema. 

 Hypoproteinmia usually produces generalized oedema. Eg- Oedema of renal diseased -- nephrotic syndrome, acute glominulo nephritis, ascitis of liver disease- (cirosis).

2. Increased capillary hydrostatic pressure:-

        The hydrostatic pressure of the capillary is the force that normally tends to dry fluid from the capillary wall into the interstitial space by counter acting the force of plasma oncotic pressure.

    A rise in the hydrostatic pressure at the venular end of the capillary which is normally low to a level more than the plasma, oncotic pressure results in minimal or no reabsorption of fluid at eh vennular end. Consequently leading to oedema.

Eg:-  Oedema of the cardiac disease--  congestive cardiac failure, constructive pericarditis,

Postular oedema-- transient oedema of feet and ankles due to increased venous pressure seen in individual who remain erect for long time.

3. Lymphatic obstruction:-

       Nonmally the interstitial fluid in the tissue spaces escapes by way to lymphatic. obstruction to outflow of these channel causes localized oedema, also known as lymphoedema.

Eg-= filaria

4. Tissue factor:-

      In some situation the tissue factor in combination with other mechanism play a role causation of oedema.

 Eg:- Elevation of oncotic pressure of interstitial fluid due to incresed vascular permeability and inadequate removal of protein by lymphatics.

5. Increase capillary permeability:-

      An intact capillary endothelium is semi permeable membrane which permits the free flow of water and crystalloids but allow minimum passage of plasma protein.

However when the capillary endothelium is injured such as toxin and there products, capillary permeability to plasma protein is inhenced due to development of gaps between the endothelium cells leading to leakage of plasma protein into interstitial space which may lead to oedema.

6. Sodium and water retention:-

        Normally about 80% of sodium is reabsorbed by PCT while retentionof water is affected by release of Anti-diuretic harmone. 

Intrinsic renal mechanism :-

    It is activated in response to sudden reduction in effective arterial blood volume Hypovolemia. As a result of this renal ischemia occur which causes reduction in glomerular filtration rate, decreased excretion of sodium in the urine and consequent retention of sodium which can lead to oedema.

Anti- diuretic harmone mechanism:-

      Retention of sodium leads to retention of water secondarily under the influence of ADH or vaso pression.

INFLAMMATION

 INFLAMMATION

Brief understanding of the common terms used in pathology:-

Inflammation:-

     Inflammation is defined as the local response of a living mammalian vascular tissue to injury due to any agent. It is a body defense reaction in order to eliminate or limit the spread of injurious agent, followed by removal of the necroced cell or tissue.

     The agents causing inflammation may be as under-

1. Inffective agents-  Bacteria, virus and their toxins, fungi, parasites.

2. Immunological agents-  cell mediated and antigen-antibody reaction.

3. Physiological agents-  heat, cold, radiation, mechanical trauma

4. Chemical agents- organic and inorganic poison

5. Inert material-  Foreign body

Sign of inflammation:-

                                       Celsius has given four sign of inflammation-

1. Rubor- redness

2. Tumor - swelling

3. Calor- heat

4. Dolor- pain

given by verchow-

5. Funtio loesa- loss of function

Type of inflammation:-

                                       Depending upon the defense capacity of the host and duration of response, inflammation can be classified as acute and chronic.

1. Acute inflammation:-

          Acute inflammation is of short duration (lasting less than 2 weeks) and represents the early body reaction, resolves quickly and is usually followed by healing.

2. Chronic inflammation:-

             Chronic inflammation is of longer duration and occur either after the causative agent of acute inflammation persist for a long time or the stimulus is such that it induces chronic inflammation from the begining.

Morphology of Acute inflammation:-

Inflammation of an organ is usually named by adding the suffix "Itis".

ex: Meningitis, hepatitis, cholecystitis, phlebitis etc.

  A few morphological varieties of acute inflammation are-

1.Pseudo membranous inflammation:-

       It is a inflammatory response of mucus membrane to toxins of diphtheria or irritant gases. As a result of epithelium plasma exudes on the surface where it coagulates and together with necrosed epithelium forms false membrane.

2. Ulcer:-

Ulcer are local defect on the surface of an organ produced by inflammation. Common site for ulceration are the stomach, duodenum, intestine, etc.

In acute stage there is infiltration of polymorph with vasodialation. while long standing ulcer developed infiltration by lymphocytes, plasmacells and macrophages with associated fibroblastic prolifiration and scarring.

3. Suppuration:-

   When acute bacterial infection is accompanied by intense neutrophilic infiltration in the inflammed tissue. It result in tissue necrosis. A cavity is formed which is called an abscess and contain purulent exudate or pus and the process formation is called suppuration. The bacteria formation is called suppuration. The bacteria which cause suppuration is called pyogenic bacteria. 

4. Cellulitis:-

      It is a defuse inflammation of soft tissue resulting from spreading effect of substance like Hyaluronidase enzyme by some bacteria.

5. Bacterial infection of the blood:-

      This include following three condition-

a. Bacteremia:-

   It is defined as a presence of small numbers of bacteria in the blood which do not multiply significantly. Ex- Salmonella typhi, escherichia etc.

b. Septicemia:-

   It means presence of rapidly multiplying, highly pathogenic bacteria in the blood. It is generally accompanied by systemic effect.

c. Pyramia:-

  It is the dissemination of small septic thrombi in the blood which cause their effect at the site where they are lodged.

Systemic effect of Acute inflammation:-

  Acute inflammation is associated with systemic effects as -

1. Fever

2. Leucocytosis

3. Lymphangitis

4. Shock

1. Fever:-

     Fever occurs due to Bacteraemia.

2. Leucocytosis:-

     It is commonly accompanies the acute inflammatory reaction usually in the range of 15000-20000 per cubic mm.

3. Lymphangitis:-

  It is one of the important manifestation of localize inflammatory injury. The lymphatics and lymphnodes that drain the inflammed tissue show reactive inflammatory changes in the form of lymphangitis and lymphadenitis.

4. Shock:-

  Shock may occur in severe cases. Shock is the clinical syndrome of cardiovascular collapse.

Fate of Acute inflammation:-

   The acute inflammatory process can in one of the following outcomes-

1.Resolution:-

   It means complete return to normal tissue following acute inflammation. It occurs when tissue changes are slight and the cellular changes are reversible.

2. Healing:-

   Healing by fibrosis take place when the tissue distraction in acute is inflammation is extensive so that there is no tissue regeneration. But when tissue loss in superficial, it is restored by regeneration.

3. Suppuration:-

    When the pyogenic bacteria causing acute inflammation results in severe tissue necrosis, The process progress of suppuration, the abscess may drained, if not may get organised by dense fibrous tissue, and in time get calcified.

4. Chronic Inflammation:-

   Persisting or recurrent acute inflammation may progress to chronic inflammation in which the process of inflammation and healing proceed by site.

CHRONIC INFLAMMATION:-

  Chronic inflammation is defined as prolonged process in which tissue distraction and inflammation occur at the same stage.

  Chronic inflammation can be caused by one of the following three ways-

1. Chronic inflammation following acute inflammation:-

     When the tissue distraction is extensive or the bacteria servive and persist in small number at the site of acute inflammation. Ex- osteomollitis

2. Recurrent attack of acute inflammation:-

     When repeated attack of acute inflammation occur in chronicity of the process. Ex:- recurrent UTI

3. Chronic inflammation starting de novu:-

    When the infection with organism of low pathogenicity is chronic from the begining. ex:- TB

General features of chronic inflammation:-

   Following general features characterize any chronic inflammation-

1. Mono nuclear cell infiltration:-

    Chronic inflammatory lesions are infiltrated by mono nuclear inflammatory cell. like phagocytes and lymphoid cell.

   Phagocytes are represented by circulating monocytes, tissue macrophages, epithiloid cells and some times multinucleated giant cell. The macrophages comprises the most important cell in chronic inflammation. 

2. Tissue distruction or necrosis:-

   Tissue distruction and necrosis are central feature of most form of chronic inflammatory lesions. This is brought by activated macrophages, which release a variety of biological active substance like protiase, elastiase, lipase.

3. Proliferated changes:-

      As a result of necrosis, proliferation of small blood cells and fibroblast stimulated resulting in formation of inflammatory granulation tissue.

Systemic effect of chronic inflammation:-

 Chronic inflammation is associated with following systemic feature-

1. Fever-

               There is a mild fever, often with loss of weight and weakness.

2. Anemia-

                 Chronic inflammation is accompanied by anemia of varrying degree.

3. Leucocytosis-

                    As in acute inflammation, chronic inflammation also has leucoctosis but generally there is lymphocytosis.

4. ESR-

            ESR is elevated all cases of chronic inflammation.

5. Amylotosis-

                Long term cases of chronic suppurative inflammation may developed systemic amylotosis.

Types of chronic inflammation:-

     Chronic inflammation is subdivided into two type-

1. Chronic non-specific inflammation:-

       It is characterized by non-specific inflammatory cell infiltration. ex- chronic osteomollitis, lung abscess.

2. Chronic granulomatous inflammation:-

        It is characterized by formation of granuloma. Ex- TB, leprosy, sarcoidis etc.

Note:-

     Granuloma is defined as circumscribed, tiny lesion about 1mm of diameter, composed predominatly of collection of modified macrophages called epitheloid cells and rimmed at the periphery by lymphoid cell.