Lab 7 - Hemodynamics & Coagulation Flashcards
Causes of Inflammatory Edema
- a swelling due to effusion of fluid in the soft parts surrounding a focus of inflammation
- due to vasodilation & immune resonse
What is the role of lymphatics in hydrostatic edema
- lymphedema: edema due to lymphatic obstruction
Edema
def: accumulation of excess fluid in interstitial spaces
Causes: increased Hydrostatic pressure (HTN/gravity); decreased plasma oncotic pressure, lymphatic obstruction, sodium retention, inflammation (swelling -> osmotic pressure due to inflammatory proteins)
To summarize, the four major causes of edema are:
1) increased hydrostatic pressure => transudate; edema may be localized or generalized
2) increased vascular permeability => exudate; edema may be localized or generalized
3) decreased plasma osmotic pressure => transudate; generalized edema
4) lymphatic obstruction => transudate; edema may be localized or generalized
S/S: dyspnea, LV failure, MI, Pericarditis, infections, etc
Ascites
fluid accumulation on the abdomen/in peritoneal cavity
Difference between hyperemia & congestion
Congestion = passive, from impaired venous return; tissue is cyanotic (pathologic - flow of blood backs up passively)
Hyperemia = active process from increased flow & arteriolar dilation (redder tissue); increased blood supply (physiological)
Anasarca
generalized whole body edema
when in fetus = “hydrops”
Hypoproteinemia (fluid doesn’t get pulled back in due to decreased plasma osmotic pressure) - due to renal disorders, GI loss, malnutrition
Transudate
extravascular fluid with low protein content and a low specific gravity
Exudate
extravascular fluid due to vessel alteration during inflammation (increased permeability, vascular constriction then dilation). This results in an extracellular fluid of high protein content, with cell debris present and high specific gravity (>1.020).
Pitting edema
- subcutaneous edema
- points to cardiac/renal disease
- suggests Right sided heart failure
Pulmonary Edema
- fluid backs up into lungs due to lack of pulmonary venous return
- left ventriculat heart failure
- frothy (albumin + edema) pink (RBC) sputum
Pulmonary HTN
dues to recurring microemboli in lungs
ALT
- Alanine transaminase
- an enzyme found in the highest amounts in the liver that tests for the presence of liver damage
- elevated with death of hepatocytes
- evidence of liver damage
AST
Aspartate Aminotransferase
- an enzyme found in high amounts in liver, heart, and muscle cells
- elevated with death of hepatocytes/heart/muscle cells
- evidence of liver damage/MI
Nutmeg Liver
red brown - associated with cell loss & congestion
paler - normal unaffected hepatocytes
-seen iwth CHF & obstructed IVC/hepataic vein
Virchow’s triad
1) abnormal blood flow (sluggish = venous/turbulent = art)
2) endothelial injury
3) hypercoagulable state
Lines of Zahn
laminations in thrombi consisting of alternating pale (platelets
/fibrin) and dark (red blood cells) layers
Vegetations
Thrombi composed of infectious agents on heart valves
-ex. endocarditis
Thrombi - Arterial vs Venous
Arterial = dislodged & moved downstream - lodged in legs
Left sided heart -> brain & body
Venous = dislodged & go to lungs
Right sided heart -> lungs
-more common in veins
Causes: DVT (popliteal & below), CHF, neoplasia, pregnancy, immobilization, burns, fractures
Thrombus vs embolus
Thrombus: a clot/plaque
-can embolyze, propagate, dissolve or become organized (integrated & vasculature grows around)
Embolus: DISLOGED substance that causes obstruction downstream
Rheumatic heart disease
an inflammatory disease that occurs following a Strep infection
Fat emboli
originate in bone marrow, presents as fatty clot
Causes: long bone fxs, burns, soft tissue trauma
Major factors in determining the clinical/pathological outcome of infarctions:
1) nature of vascuclar supply (i.e liver = 2 blood supplies)
2) rate of occulsion (reorganization)
3) tissue resistance to hypoxia
4) oxygen content of blood (art/venous)
Infarctions
area of ischemic necrosis caused by occlusion of the arterial supply
Anemic (pale)
- solid organs
- end arterial circulations
Hemorrhagic (red)
- venous occlusions
- loose architecture tissue
- reperfusion of ischemic zone
- dual bloods supply (lung, SI - 2nd supply isn’t enough to save necrotic tissue - jsut cause hemorrhage)
Stroke
Acute onset neurologic syndrome due to vascular event
hemorrhagic - no TPA
occlusion - push TPA
extensive loss initially with very slow/no restoration
Volvulus
bowel twists on its own messentary axis; can compromise the messenteric artery
Intussusception
bowel telescopes into itself; can compromise the messenteric artery
von Willebrands Disease
- lacking important platelet adhesion molecule that links exposed subendothelial collagen/GP1b
- PT, PTT & platelet counts are normal
Vasculitis
a group of disorders that destroy blood vessels by inflammation
inflammation of veins = phlebitis (think phlebotomist)
inflammation of arteries = arteritis
Arteriosclerosis
arterio = artery sclerosis = thickening/hardening
- the thickening, hardening and loss of elasticity of the walls of arteries
Disseminated Intravascular Coagulation (DIC)
- AKA “consumptive coagulopathy”
- a pathological process characterized by the widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body
- consumption of clotting factors and platelets disrupts normal clotting -> severe bleeding can occur from various sites & lead to multiple organ damage
Atherosclerosis
athera = “gruel” or porridge
- a specific form of arteriosclerosis caused by the buildup of fatty plaques and cholesterol in the artery
