Disorders of cardiovascular system-part one Dr. Zainab Sajid Al-Shimmari

1. Disorders of cardiovascular system-part one Dr. Zainab Sajid Al-Shimmari

2. Ante- mortem clot = thrombus or thrombosis :- Clot formed in the following blood during the life. Microscopic App. :- 1- fibrin , WBC , RBC , + platelets ( it is the primary constituent ) . 2- Platelets adhere to each other and to the B.V wall to give amorphous pink or gray staining masses that alternate with layers of fibrin , WBC , RBC , i.e it is laminate. 3- Area of attachment to the B.V wall. 4- Fibrin fibrils are heavy and thick. GROSS App :- 1- Friable, dull with rough and stringy surface. 2- Color is mixture of red and grey . 3- Layers of lamination. 4- Find the attachment.

3. Types of thrombus :- 1- Occluding thrombus:- is one that closes the B.V lumen entirely. 2- Canalized thrombus:- is one that closes the B.V lumen but one or more openings. The canals are lined by endothelium. 3- Obturating thrombus:- is one that trails down of the free end of thrombus that may attain good length.

4. Causes:- 1- Injury to the endothelium  release of thromboplastin  initiate the clotting and platelets adhere. Causes of injury :- a- phlebitis due to infection b- contusion or ligation c- hypodermic needle injection 2- Heart :- as common due to infection ex. Streptococcus 3- Roughened vessel lining ex. after healing of an early lesion . 4- Blood flow slowing or stasis of flow. Very important

5. Ex. a- cardiac insufficiency. b- extensive inflammation  chronic venous congestion . 5- Disruption of laminar blood flow . 6- Changes in blood composition :- ex. ^ number and adhensiveness of platelets ex. A- After surgery . B- After parturition. C- After trauma D- Poly cythemia  ^ blood viscosity ( ^ # of RBc ) . E- ^ catecholamines and epinephrine  hasten coagulation.

6. Significance :- or fate 1- Lead to partial or complete obstruction to B.V. lead to necrosis . 2- Edema due to retarded out flow fluid from area drained by the thrombosed B.V . 3- Embolus formation due to fragmentation . emboli stop at narrow bifurcation. 4- Thrombus could be slowly liquefied by plasmin or enzymes of W.B.C 5- C.T. Organization :- replacement by C.T , it is permanent. 6- Calcification:- Ca replaces decomposed fibrin and dead cells. 7- C.T encapsulation . 8- Canalization .

8. dark red thrombus is apparent in the lumen of the coronary. The yellow tan plaques of atheroma narrow this coronary significantly, and the thrombus occludes it completely.

9. This section of coronary artery demonstrates remote thrombosis with recanalization to leave only two small, narrow channels

10. There is a pink to red recent thrombosis in this narrowed coronary artery. The open, needle-like spaces in the atheromatous plaque are cholesterol clefts.

11. Emboli It is a foreign body floating in the blood. Types : 1- Simple emboli = thrombo emboli = fibrinous emboli = piece of broken thrombus . 2- Fatty emboli : little of patient's fat circulate in his own blood. Stays as separate bodies . Causes : of fatty emboli 1- Sudden release of fat from adipocytes ex. bone fracture. 2- Sever subcutaneous trauma. 3- Metabolic failure ex. diabetes . 4- Deficiency of cystine, methionine, choline  fatty change 5- Over loaded hepatocyte with fat  rupture  release of fat in to blood .

12. Gas emboli :- there are air bubbles in the blood Causes 1- Lowering of ambient pressure. 2- Air sucked into venous circulation through gaping wound. 3- Experimental . Injection of air in the air vein rabbits. 4- Bacterial emboli :- They comes from tissues heavily infected with bacteria .

14. Their effects :- 1- Interface with blood supply. 2- Cause metastasis = provide another focus on infection . #This metastasis depend on : 1- Amount of blood flowing in that organ. 2- Extent of capillaries through which blood is filtered in that organ . Most frequent site of Bacterial emboli are liver, kidney and lungs, because flowing amount of blood and capillaries are high.

15. 5- parasitic emboli :- These are fragments of adult parasites circulating in the blood. 6- Neoplastic cell emboli : Clumps of tumor cells carried in the blood . 7- Spodogenous emboli : Are clumps of agglutinated R.B.C due to immunologic process or injection of incompatible blood. 8- other types : Ex. foreign body ( piece of broken needle ) Amniotic fluid emboli Hepatic emboli flowing trauma to liver . Clotting failure It is partial or complete failure.

16. Causes:- 1- Septicemic disease. The expected clotting in the vessels after death may not ex. anthrax. 2- Liver destructive lesion. Ex. severe acute or chronic hepatitis. Because liver synthesize prothrombin & fibrinogen & other factor needed clotting. 3- Hypocalcemia : decrease level of ca in blood. 4- Vit. K deficiency ( 2-methyl – 1,4 naphthaquinone ) needed for synthesis of prothrombin. Vit. K is synthesized by bacterial action in the intestin in all animals except primates. 5- Thrombocytopenia ( decrease # of platelets ) results in an interference with clotting.  certain poisoning. 6- Hemophilia. In heredite defect of clotting mechanism .

17. Here is a larger area of infarction produced by a medium-sized thromboembolus to the lung. This infarction has begun to organize at the margins.It is also possible to have multiple small pulmonary thromboemboli that do not cause sudden death and do not occlude a large enough branch of pulmonary artery to cause infarction. However, if there are lots of small emboli, particularly if they are showered to the lungs over a period of time, then they collectively may block enough small arteries to produce pulmonary hypertension.

18. Pulmonary thromboembolus in a large pulmonary artery. There are interdigitating areas of pale pink and red.These lines represent layers of red cells, platelets, and fibrin which are layed down in the vessel as the thrombus forms.

19. Hyperemia and congestion Excess of blood in the vessel in a given part of organ due to too much blood brought in by artery or too little drained out by vein ( congestion ) Hyperemia: excessive arterial flow. Congestion : interference with venous exit . Active hyperemia:- Microscopic App:- 1- Capillaries are dilated and filled with blood. 2- Capillaries look more numerous. Gross: 1- The organ take bright red color . 2- During life: organ is warmer and may feel pulsating artery.

20. The alveoli in this lung are filled with a smooth to slightly floccular pink material characteristic for pulmonary edema. Note also that the capillaries in the alveolar walls are congested with many red blood cells. Congestion and edema of the lungs is common in patients with heart failure and in areas of inflammation of the lung.

21. Causes: 1- Inflammation : since it is the first step . 2- Heat locally applied as therapeutic. 3- ^ physiological activity ex:- in muscles, lactation . 4- Psychologic : human blushing . Passive congestion = venous congestion. Can be acute or chronic and may be seen in any part of the body Microscopic App:- of acute passive congestion 1- Capillaries and veins are dilated and filled with blood . 2- Sinusoidal spaces ( liver & spleen ) are dilated & filled with blood . 3- If chronic ( c-v-c ) : slight ^ in C-T in veins wall is seen . 4- Liver : if a cute passive congestion : sinusoidal & central veins dilated. 5- Liver: if Chronic passive congestion : centrilobular necrosis.

22. Gross App:- 1- Congested part is swollen and bluish red color . 2- During live temperature is lower. 3- After death color get darker . 4- Cut surface : large amounts of blood can be squeezed. Causes :- 1- Decrease blood pressure due to failing heart . 2- Vasodilation seen in shock which is seen in late stages of infections disease in the case death is due to congestion heart failure . The gross of veins in case of congestion heart failure : A- Large veins of abdominal and thoracic cavities are larger, dark and blood filled . B- Mesentery and intestinal wall veins are dark and prominent C- Liver and lungs filled with blood .

23. Chronic Venous Congestion (C.V.C) Its causes are : I- Valvular Disease C.V.C of the lungs For ex., if there is hindrance to blood-,flow from the pulmonary to systemic circulation* i*e, interferance with the proper blood flow on heart left side as occurs in ; (A) Mitral insufficiency: When valves are Leaking back due to failure of cusps of valves to seat well* The failure is caused by : 1-Thickenned surface of valves cusps by inflammatory granulation tissue of fibrinous exudate. 2-Contraction of cusp due to shrinkage of scar. In both cases,when left ventricle contracts $ some of the blood is forced back through leaky valves and so impedege ; incoming flow in the pulmonary vein and so, blood accumulates in the lungs.

24. , — (B) Mitral stenosis Here„ there is narrowing of the total size of the lumen of the mitral valve. The cause of the narrowed lumen is shrinkage of fibrous tissue formed around the base of cusps. Result; Lesser amount of blood is able to pass. Note: Both (A) & (B) are due to inflammation caused by infection. The inflammation is called valvular endocarditis (C) Aortic semilunar valve disorder :This is also subject to the same .disorders. i.e. insufficiency or stenosis. In either cases, it will cause left ventricle hypertrophy (Compensatory). This may lead to distortion of the mitral valve and there forits insufficiency and hence pulmonary congestion which is secondary to the case.

25. (D) Tricuspid valvular disorder : Is also subject to insufficiency and stenosis, and is more common than the mitral defects The result: blood is thrown back into vena cava and its branches 'especially that of the liver leading to hepatic C.V.C.-The latter could result from severe pulmonary flow obstruction that may causes retardation of the flow to the heart right side.Therefor, blood will go back to the liver. II- Liver Cirrhosis ; Here blood can't go through the liver and the result is C.V.C of portal venous system, C.V,C of the spleen::, intestine and ascites .

29. lII- Large size vein obstruction : i.e, Obstruction of drainage of a particular area. Causes of the obstruction: 1- Thrombi. 2- Stenosis , due .to outside pressure & shrinkage of scared vein. ( seen after phlebitis IV- Late Pregnancy . Here fetus pressure over femoral vein as it passes over the pubic anterior border causing C.V.C of hind legs & edema of the hind legs. V- Gravity : Causes hypostatic congestion of organs at lower side of a recumbent.

30. Significance : 1- Anoxia :- necrosis Impaired function on the organ ( quantity of milk from breast with c-v-c will gets lower ) 2- Thrombosis due to stagnation of blood . 3- Edema because anoxia of the endothelial in B.V. 4- C.T Proliferation - In liver : thickened walls of central veins and of the sinusoids. - In spleen: fibrosis of red pulp, there is hemosidrein pigment due to hemolysis of R.B.C. - In lung : there is brown induration. ( brown color + it is very tough in consistency ) . - Causes of toughness : due to too much C.T in alveolar septa. - Cause of brown color due to hemosidrin pigment, there is engulfed by macrophages called heart failur cells )

31. Edema It is excessive accumulation of fluid in inter cellular spaces and body cavity. Types According to the causes either general or local or inflammatory & non inflammatory 1- Inflammatory edema:- occurs in response to irritant . 2- Non inflammatory edema:- transudate. according to site 3- Localized edema:-is seen in most organs and tissue due to local causes. 4- Generalized edema ( Anasarca ): affects the body as whole but due to gravity it seen mostly in the ventral parts .

32. Microscopic App:- 1- There is larger space between cells, fibrils and other structure of the organ 2- Space has a faint pink staining residue of precipitated protein ( albumin ). 3- Few R.B.C , WBC or fibrin threads are seen especially in inflammatory edema . 4- In brain:- there are perivascular & perineuronal space . 5- In lung:- alveoli are filled with fluids Gross App:- 1- Edematous part is swollen , delineated. 2- Edematous tissue is firm & doughy in consistency . it pits on pressure. 3- Cut surfaces pale yellowish fluid oozes. 4- During life, cool, painless & swollen . 5- Lungs, blood stained watery fluid exudes if lung is congested, the lung is distended & firm. 6- Serous cavities are distended with fluid. 7- Brain watery , flattening of swollen gyri .

33. The surface of the brain with cerebral edema demonstrates widened gyri with a flattened surface.

34. Transudate :- it is the fluid of non inflammatory edema. Exudate :- it is the fluid of inflammatory edema and characterized the inflammation . Differences between transudate & exudates

35. Causes of transudate : 1- Decrease plasma colloidal osmotic pressure due to hypoproteinemia Causes of hypoproteinemia A- Nephritis  albuminura  decrease osmotic pressure  hypoproteinemia edema B- Starvation and cachexia. C- Protein deficiency D- Liver diseases ( cirrhosis )  decrease plasma protein synthesis. E- Parasitic infestation. 2- ^ capillary blood pressure due to venous stasis . Causes of this A- ^ hydro static pressure (B.P ) in veins & venous end of capillaries B- Anoxia of the capillary endothelium & nutrient  weakening of capillary wall  leakage of albumin and other molecules ( globulin ) .

36. 3- Obstruction to lymphatic drainage. Ex. lymph node invaded by neoplasm. 4- Na & H2O retention * causes due to failure to excreted Na in urin H20 Retention—generalizel edema. * causes of failure to excrete Na in urin. a- congestive heart failure . b- Nephritis ( Na retained , K will be excreated ) C- Adrenal cortical hormones. ( ACH) *Mechanism of Na retention . 1- ^ renal tubular Na reabsorbtion. 2- decrease glomerular filtration

37. Significance of edema : - 1- Diagnostic :- tell me about other causes ( parasitic , cardiac, nutritional, renal disease ) 2- Fluid gets organized by C.T ( clotted first ) 3- If causes is removed  edema subsides. Term - Ascites :- accumulation of fluid in the peritoneal cavity. - Hydrothoracic: accumulation of fluid in the thoracic cavity . - Hydro pericardium : accumulation of fluid in the pericardium. - Hydrocele : accumulation of fluid in the scrotal sac. -Anasarca : generalized s/c edema .

39. Pulmonary edema Acute pulmonary edema is the most important form of local edema as it causes serious functional impairment but has special features. It differs from edema elsewhere in that the fluid accumulation is not only in the tissue space but also in the pulmonary alveoli.

42. I. Elevation in pulmonary hydrostatic pressure (Haemodynamic edema). 1-In heart failure, there is increase in the pressure in pulmonary veins which is transmitted to pulmonary capillaries. This results in imbalance between pulmonary hydrostatic pressure and the plasma oncotic pressure so that excessive fluid moves out of pulmonary capillaries into the interstitium of the lungs.

43. II. Increased vascular permeability (Irritant edema). 1-The vascular endothelium as well as the alveolar epithelial cells (alveolo-capillary membrane) may be damaged causing increased vascular permeability so that excessive fluid and plasma proteins leak out, initially into the interstitium and subsequently into the alveoli.

44. Shock : Its circulatory disturbance characterized by decrease total blood volume, by decrease blood flow and by hemo concentration Gross App:- 1- Sever Congestion of B.V ( lung , liver , and especially intestine ). 2- Ischemia of peripheral parts. 3- Blood – tinged fluid in the peritoneal , pleural & pericardial cavities. 4- Spleen is empty  blood less. 5- If patient lives ( 1- 2 days ) degeneration is seen in kidney, liver, heart , adrenal cortex. Significance :- fate 1- Death due to cerebral & myocardial ischemia . 2- Regain normal circulation by fluid.

45. Causes :- 1- Blood loss  hemorrhagic shock 2- Trauma, painer psychic = Neurogenic shock . 3- Surgery  surgical shock . 4- Fluid loss  burns shock. 5- Bacterial toxins  septic or endotoxic shock . Mechanism of shock :- 1- There is an inaquality between blood volume and the capacity of the vascular system  reduction of the blood flow to the tissue. 2- Anoxia :- complete reduction of O2 concentration to the organ or tissue.

46. Infarction Localized area of necrotic tissue due to sudden loss of blood supply. The necrosis is coagulative type and the area is supplied by an end artery and so it is well delineated. Mechanism of Formation: 1-If tissue dies, its capillaries will die. 2-Blood will diffuses from adjacent living tissue capillaries. 3-So recent infarcts are red. Type of infarcts: 1-Hemorrhagic = red infarct: are infarcts seen before blood hemolysed. 2-Anemic = pale infarcts: escaped blood accumulate in the periphery and the rest of the area is pale.

50. Why pale or red infarcts: 1-Depends on the time between death of the tissue and its examination 2-3 days red infract. 2-Depends on denseness of tissue. Kidney (solid dense)  pale infarct. Lung (less dense)  red infarct. Microscopic App: 1-Area of coagulative necrosis may or may not be filled with blood. 2-Its shape depends on the shape of the part supplied by the closed artery. Usually it is triangular with apex at site of obstruction and base at capsule of the organ. 3-Has inflammatory zone (congested B.V. WBC) at its border. 4-Fibrous tissue replacement. 5-If it has certain structures that are still getting blood, these structures stay alive. Ex. glomeruli