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HAEMODYANAMICS FLASH POINTS

DR EJAZ WARIS - PROFESSOR OF HISTOPATHOLOGY , ASMDC

1. An abnormal increase in interstitial fluid within tissues is called edema, while


fluid collections in the different body
2. cavities are variously designated hydrothorax, hydropericardium, and
hydroperitoneum (the last is more commonly called ascites). Anasarca is a severe
and generalized edema with widespread subcutaneous tissue swelling.
3. Edema caused by increased hydrostatic pressure or reduced plasma protein is
typically a protein-poor fluid called a transudate
4. In contrast, inflammatory edema is a protein-rich exudate that is a result of
increased vascular permeability.
5. Reduced plasma osmotic pressure occurs when albumin, the major plasma
protein, is not synthesized in adequate amounts or is lost from the circulation. An
important cause of albumin loss is the nephrotic syndrome
6. Hyperemia is an active process in which arteriolar dilation (e.g., at sites of
inflammation or in skeletal muscle during exercise) leads to increased blood flow.
7. Congestion is a passive process resulting from reduced outflow of blood from a
tissue. It can be systemic, as in cardiac failure, or local, as in isolated venous
obstruction
8. In chronic pulmonary congestion the septa are thickened and fibrotic, and the
alveoli often contain numerous hemosiderin-laden macrophages called heart
failure cells
9. In chronic passive hepatic congestion the centrilobular regions are grossly red-
brown and slightly depressed (because of cell death) and are accentuated against
the surrounding zones of uncongested tan liver (nutmeg liver) .Microscopically,
there is centrilobular hemorrhage, hemosiderin-laden macrophages, and
degeneration of hepatocytes
10. Minute 1- to 2-mm hemorrhages into skin, mucous membranes, or serosal
surfaces are called petechiae
11. Slightly larger hemorrhages (3 mm) hemorrhages are called purpura.
12. Larger hemorrhages (>1 to 2 cm) subcutaneous hematomas (i.e., bruises) are
called ecchymoses.
13. three primary abnormalities that lead to thrombus formation (called Virchow's
triad): (1) endothelial injury, (2) stasis or turbulent blood flow, and (3)
hypercoagulability of the blood
14. Of the inherited causes of hypercoagulability, point mutations in the factor V gene
and prothrombin gene are the most common.
15. Elevated levels of homocysteine contribute to arterial and venous thrombosis, as
well as the development of atherosclerosis
16. Antiphospholipid antibody syndrome(previously called the lupus anticoagulant
syndrome). This syndrome has protean clinical manifestations, including recurrent
thromboses, repeated miscarriages, cardiac valve vegetations, and
thrombocytopenia.
17. Thrombi often have grossly and microscopically apparent laminations called lines
of Zahn; these represent pale platelet and fibrin deposits alternating with darker
red cellrich layers.
18. Arterial thrombi are frequently occlusive; the most common sites in decreasing
order of frequency are the coronary, cerebral, and femoral arteries
19. Postmortem clots can sometimes be mistaken for antemortem venous thrombi.
However, postmortem clots are gelatinous with a dark red dependent portion
where red cells have settled by gravity and a yellow chicken fat upper portion;
they are usually not attached to the underlying wall. In comparison, red thrombi
are firmer and are focally attached, and sectioning typically reveals gross and/or
microscopic lines of Zahn
20. Fate of thrombus include : propogation ,embolization , dissolution and
organization / recanalization
21. Microthrombi of fibrin are seen in DIC.
22. An embolus is a detached intravascular solid, liquid, or gaseous mass that is
carried by the blood to a site distant from its point of origin ( Word literally
means bottle stopper)
23. Rarely, an embolus can pass through an interatrial or interventricular defect and
gain access to the systemic circulation (paradoxical embolism)
24. epending on the size of the embolus, it can occlude the main pulmonary artery,
straddle the pulmonary artery bifurcation (saddle embolus
25. Microscopic fat globules ( fat emboli)with or without associated hematopoietic
marrow elementscan be found in the circulation and impacted in the pulmonary
vasculature after fractures of long bones (which have fatty marrow) or, rarely, in
the setting of soft tissue trauma and burns
26. A particular form of gas embolism, called decompression sickness, occurs when
individuals experience sudden decreases in atmospheric pressure.
27. The rapid formation of gas bubbles within skeletal muscles and supporting tissues
in and about joints is responsible for the painful condition called the bends
28. in the lungs, gas bubbles in the vasculature cause edema, hemorrhage, and focal
atelectasis or emphysema, leading to a form of respiratory distress called the
chokes
29. A more chronic form of decompression sickness is called caisson disease (named
for the pressurized vessels used in the bridge construction; workers in these
vessels suffered both acute and chronic forms of decompression sickness
30. An infarct is an area of ischemic necrosis caused by occlusion of either the
arterial supply or the venous drainage.
31. Infarcts are classified according to color and the presence or absence of infection;
they are either red (hemorrhagic) or white (anemic) and may be septic or bland.
32. Shock is characterized by systemic hypotension due either to reduced cardiac
output or to reduced effective circulating blood volume. The consequences are
impaired tissue perfusion and cellular hypoxia.
33. Cardiogenic shock results from low cardiac output due to myocardial pump
failure. This can be due to intrinsic myocardial damage (infarction), ventricular
arrhythmias, extrinsic compression , or outflow obstruction (e.g., pulmonary
embolism).
34. Hypovolemic shock results from low cardiac output due to the loss of blood or
plasma volume, such as can occur with massive hemorrhage or fluid loss from
severe burns.
35. Septic shock results from vasodilation and peripheral pooling of blood as part of a
systemic immune reaction to bacterial or fungal infection. Its complex
pathogenesis is discussed in further detail below.
36. Toll-like receptors (TLRs) recognize microbial elements and trigger the responses
that initiate sepsis.