Sites of Anaerobic Glycolysis / EM pathway

• Exercising muscle
• RBC
• Brain
• GIT
• Renal medulla
• Retina
• Skin

Gluconeogenesis at a glance

 Substrate :http://medicalscienceeasy.blogspot.com/2017/12/substrstes-of-gluconeogenesis-at-glance.html

Site: liver 90% , Kidney 10%
Compartment: Mainly cytoplasm ,party in mitochondria
Nature : Anabolic
Rate limiting enzyme : http://medicalscienceeasy.blogspot.com/2017/12/rate-limiting-enzymes-of-gluconeogenesis.html
 ATP needed: 6 ( to produce 1 glucose from substrate)
Source of ATP : Beta Oxydation of fatty acid
 Importance:

• Maintain normal glucose concentration in fasting & starvation
• Disposal of lactic acid & glycerol in normal state

Regulation :http://medicalscienceeasy.blogspot.com/2017/12/factors-regulate-gluconeogenesis.html

Factors regulate Gluconeogenesis

Factors increase / stimulate Gluconeogenesis :

• ATP
• Acetyl CoA
• Cortisol
• Epinephrine
• NADH
• Glucagone

Factors decrease / inhabit Gluconeogenesis :

• AMP
• Fructose -2,6- Bis Phosphate
• Insulin

Rate limiting enzymes of Gluconeogenesis

•  Pyruvate carboxylase

• Pyruvate to Oxaloacetate

• Phosphoenol pyruvate carboxykinase

• Oxaloacetate to Phosphoenol pyruvate

• Fructose -1,6- bis phosphatase

• Fructose -1,6- bis phosphate to  Glucose-6- phosphate

• Glucose Bis phosphatase
• Glucose-6- phosphate to Glucose

Substrstes of gluconeogenesis at a glance

• Glucogenic amino acid
• Lactate
• Glycerol
• Pyruvate
• Propionate
• Alfa keto acid
• Ketone body
• Intermediates of TCA cycle
• Intermediates of Glycolisis

Metabolic Pathway take place both in Mitochondria & cytoplasm

• Urea Cycle
• Gluconeogenesis
• Heme Synthesis

Metabolic Pathway take place only in Mitochondria

1. TCA cycle
2. B-Oxidation  of Fatty Acid
3. Respiratory Chain
4. Ketogenesis
5. Oxidative Deamination
6. Oxidation of pyruvate to acetyl-CoA
7. Carboxylation of pyruvate to OAA ( Oxalo Acetic Acid)

Bacteria which are not seen by Gram Staining

• Bacteria which have thin flexible cell wall
• Treponema pallidum
• Borelia sp.
• leptospira sp.

• Bacteria which have no cell wall 
• Mycoplasma sp.

• Bacteria which are obligate intracellular
• Chlamydia
• Ricketsia

• Bacteria which are Acid fast
• Mycobacterium
• Nocardia

Absolute Methods Of Sterilization at a glance

     Absolute Methods Of Sterilization :

• Dry heat : Hot air oven

• Moist Heat : Autoclave

• Filtration : Membrane Filtration

• Radiation : Ionizing

• Chemical : 
• formaldehyde
• Gluteraldehyde
• Ethylene oxide
• Hydrogen peroxide
• Halogens

Renal stone

 According to Radio-density on X-ray

                1.Radio-opaque stone

•   Calcium phosphate stone (as dense as bone )
•   calcium oxalate stone ( more frequently ,about 80%)

              2.Relatively Radiolucent

•  Cystine stones
•  Struvite stone (Magnesium ammonium phosphate stone)

        

               3.Complete Radiolucent

• Pure Uric acid stone
• Xanthine stone
• Indinavir stone
• Matrix stone
• Triamterene stone

Disseminated intravascular coagulopathy

Disseminated intravascular coagulopathy

It is a disorder arising as a secondary manifestation of various diseases where there are consumption of platelets, clotting factors in wide spread area of circulation as well as secondary activation of plasminogen fibrinolytic system.

Etiology:

1.       Massive tissue trauma

2.       Sepsis

3.       Obstructive complications: abruption placenta,

Dead fetus, amniotic fluid embolism

4.       Incompatible blood transfusion

5.       Fat embolism

6.       Cardio pulmonary bypass surgery

7.       Advance malignancy

8.       Autoimmune diseases

9.       Shock, heatstroke ,burn

10.   Snake venom

Sites: in decreasing order of frequency

1.       Brain

2.       Heart

3.       Lungs

4.       Kidneys

5.       Adrenal glands

6.       Spleen

7.       Liver

Pathophysiology:

Wide spread activation of the inflammatory

Cells due to the predisposing Factor

Causes release of cytokines (IL-1, 6, 8, TNF, Plasminogen

Activator factor, amino acid metabolites)

↓

When there is large amount of cytokines released

Its causes endothelial damage and cytokines

Exposed to sub endothelial matrix

↓

at the same time it causes activation of both arm

of coagulation pathway (intrinsic & extrinsic) in

wide spread area of the body.

↓

Formation of micro thrombi

↓

(A.)Vascular occlusion of various organ-

1. microangiopathic hemolytic anemia(due to fragmentation of red cell )

2. Ischemic tissue damage

(B.)Activision of plasmin

1.       Proteolysis of clotting factors

2.       Fibrinolysis- inhabit thrombin, platelet aggregations, fibrin polymerization

Consumption of clotting factors and platelet ;hence it also called CONSUMPTION COAGULOPATHY

NOTE:

The predisposing factors are often multiple and interrelated

TWO MAJOR MECHANISM TRIGGERED DIC:

1.       Release of tissue factors or thromboplastic substances into the

Circulation

2.       Wide spread injury to the endothelial cell

TWO CONSEQUENCES OF DIC:

1.       Widespread deposition of fibrin within the microcirculation

Leads to ischemia

2.       Consumption of platelet and clotting factors and the activation of

Plasminogen leads to hemorrhagic diathesis.

As there is consumption of platelet so there is increase of  BLEEDING TIME & PT

As there is consumption of clotting factors so there is increase of  CLOTTING TIME & APTT

Factors responsible for descent of the testis

Factors responsible for descent of the testis are:

1. Shortening & traction of gubernaculum testis

2. Differential growth of body wall in relation to a
     relatively immobile gubernaculum

3. Raised intra-abdomenal pressure due to fecal accumulation and
    growth of intra abdominal  viscera.

4. Development and maturation of the epididymis.

5. Higher temperature in the abdomen

6. Hormaonal influence such as HCG,testosterone and DHT.

Factors responsible for maldescent of Testis:

Factors responsible for mal descent of Testis:

1.  Retroperitonial adhesion
2. Obstruction at the deep inguinal ring
3. Short Vas deferans
4. Short Pampiniform plexuses
5. Short Testicular vessels
6. Insufficient pull of gubernaculum testis
7. Abnormal attachment of the gubernaculum Testis
8. Gonadal dysgenesis
9. Deficient hormon stimulation
10. Deficency of gonadotropin & testosterone
11. Deficiency of Mullerian inhibitory factor from fetal      
       Sertilicells
12. Prune-Belly Syndrome .