5. CHEMOTAXIS
• MICROBES RELEASE CHEMICALS
• THEY ATTRACT THE CELLS TO THEIR SITE
• NEUTROPHILS RESPOND MOST QUICKLY
• RELEASE ENZYMES TO DESTROY PATHOGENS
• MONOCYTES,EOSINOPHILS,LYMPHOCYTES ALL
FOLLOW
6.
7. HEMOSTASIS
• SEQUENCE OF RESPONSE TO STOP BLEEDING
WHEN BLOOD VESSELS ARE DAMAGED
• VASOSPASM –CONTRACTION OF SMOOTH
MUSCLES OF BLOOD VESSEL WALL
– BY SUBSTANCES RELEASED FROM DAMAGED
PLATELETS
– NERVE STIMULATION
• PLATELET PLUG FORMATION
8. HEMOSTASIS
• PLATELET PLUG FORMATION
– Platelets contain ADP;ATP;Calcium ;Serotonin
Thromboxane A2; Fibrin stabilizing factor
– Platelets stick together to damaged wall with
increased stickiness, release substances which
cause aggregation & plug formation
• BLOOD CLOTTING
– CLOT IS NETWORK OF PROTEIN CALLED FIBRIN
– Cells are caught in them
• FIBRINOLYSIS—plasminogen is responsible for
this
9.
10. BLOOD CLOTTING
• COMPLEX CASCADE OF ENZYMATIC
REACTIONS TO PRODUCE AN INSOLUBLE
PROTEIN
• 3 STAGES
• FORMATION OF PROTHROMBINASE
– EXTRINSIC & INTRINSIC PATHWAYS
• THROMBIN FROM PROTHROMBIN
• FIBRINOGEN TO FIBRIN
11.
12.
13.
14.
15. BLOOD GROUP
• Glycoproteins on plasma membrane have
antigen
• A antigen—40%
• B antigen -11%
• AB antigens -4%
• O no antigens -45%
• Rh antigen -85%
19. ANAEMIA
• INSUFFICIENT OXYGEN CARRYING CAPACITY
• C/F TACHYCARDIA
– PALPITATIONS
– BREATHLESSNESS ON EXERTION
– GENERAL WEAKNESS
– RECURRENT INFECTIONS
• CAUSE
– IMPAIRED RBC PRODUCTION
– INCREASED DESTRUCTION
20. REDUCED PRODUCTION OF RBC
• DEFICIENCY
– IRON-MICROCYTIC HYPOCHROMIC
• IRON REQUIRMENT 2-3mg /DAY MCH <27 picograms
• IRON ABSORPTION MAY BE AFFECTED WITH OTHER
FOOD IN STOMACH
– FOLIC ACID –MALABSORPTION,COELIAC DISEASE
– VITAMIN B 12 –PERNICIOUS ANEMIA WHEN IF IS
DESTROYED BY AUTOANTIBODIES
• GASTRECTOMY,CHRONIC GASTRITIS,MALABSORPTION
21. HYPOPLASTIC ANEMIA
• BONE MARROW FAILURE
– ASSOCIATED WITH LEUKOPENIA &
THROMBOCYTOPENIA—PANCYTOPENIA
• CAUSES
– IDIOPATHIC-UNKNOWN
– DRUGS
ANTIBIOTICS,ANTICONVULSANTS,CYTOTOXIC
– IONISING RADIATION
– CHEMICALS-BENDENE & DERIVATIVES
– VIRAL INFECTION
– SECONDARY DEPOSIYS IN BONE MARROW
22. INCREASED DESTRUCTION OF RBC
• HEMOLYTIC ANEMIAS
• CONGENITAL
• GENETICALLY TRANSMITTED
• ABNORMAL HEMOGLOBIN & FRIABILITY OF
RED CELL MEMBRANE
23. SICKLE CELL DISEASE
• HEMOGLOBIS S BECOMES SICKLE SHAPED
WHEN DEOXYGENATED
• SICKLING MAY BE PERMANENT IF Hb S IS
MORE
• LIFE SPAN IS REDUCED
• THEY DO NOT MOVE SMOOTHLY THROUGH
SMALL BLOOD VESSELS
• INCREASES VISCOSITY OF BLOOD & CAUSES
THROMBOSIS,ISCHEMIA & INFARCTION
24.
25. COMPLICATIONS
• SICKLE CELL CRISIS
• PREDISPOSED BY
PREGNANCY,INFECTION,DEHYDRATION
• INTRAVASCULAR CLOTTING & ISCHEMIA
• SEVERE PAIN IN LONG BONES CHEST &
ABDOMEN
• GALL STONE FORMATION & CHOLECYSTITIS
28. POLYCYTHEMIA
• LARGE NUMBER OF ERYTHROCYTES IN BLOOD
• HIGH VISCOSITY & SLOWS THE SPEED OF
BLOOD FLOW-CLOTTING,INFARCTION
• PHYSIOLOGICAL-HIGH ALTITUDE,SMOKING
• PATHOLOGICAL-MALIGNANCY
31. HAEMORRHAGIC DISEASE
• THROMBOCYTOPENIA-<1.5L
• BLEEDING DOES NOT OCCUR TILL<30,000
• REDUCED PRODUCTION
– PART OF PANCYTOPENIA
– LEUKEMIA,RADIATION,DRUGS
• INCREASED DESTRUCTION-DIC
• AUTOIMMUNE TP
• MAY BE CONGENITAL,VIRAL INFECTION
32. VITAMIN K DEFICIENCY
• REQUIRED FOR CLOTTING FACTOR
PRODUCTION
• NEW BORN-HEMORRHAGIC DISEASE OF THE
NEWBORN
• ADULTS-LIVER DISEASEVITAMIN K IS FAT
SOLUBLE & BILE SALTS ARE REQUIRED FOR
ABSORPTION
33. DIC
• THE COAGULATION SYSTEM IS ACTIVATED
WITHIN THE BLOOD VESSELS (CONSUMPTIVE
COAGULOPATHY)
• CAUSES
– SHOCK ,SEPSIS
– TRAUMA
– ACUTE PANCREATITIS
– ABRUPTIO PLACENTAE
– MALIGNANCY
34. HEMOPHILIAS
• INHERITED CLOTTING DISORDER CARRIED ON
X CHROMOSOME
• FACTOR 8 & CHRISTMAS FACTOR
• REPEATED EPISODES OF SEVERE PROLONGED
BLEEDING
• WON WILLEBRANDS DISEASE
