Lab 7 - Hemodynamics & Coagulation Flashcards

1
Q

Causes of Inflammatory Edema

A
  • a swelling due to effusion of fluid in the soft parts surrounding a focus of inflammation
  • due to vasodilation & immune resonse
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2
Q

What is the role of lymphatics in hydrostatic edema

A
  • lymphedema: edema due to lymphatic obstruction
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3
Q

Edema

A

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

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4
Q

Ascites

A

fluid accumulation on the abdomen/in peritoneal cavity

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5
Q

Difference between hyperemia & congestion

A

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)

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6
Q

Anasarca

A

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

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7
Q

Transudate

A

extravascular fluid with low protein content and a low specific gravity

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8
Q

Exudate

A

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).

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9
Q

Pitting edema

A
  • subcutaneous edema
  • points to cardiac/renal disease
  • suggests Right sided heart failure
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10
Q

Pulmonary Edema

A
  • fluid backs up into lungs due to lack of pulmonary venous return
  • left ventriculat heart failure
  • frothy (albumin + edema) pink (RBC) sputum
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11
Q

Pulmonary HTN

A

dues to recurring microemboli in lungs

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12
Q

ALT

A
  • 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
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13
Q

AST

A

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
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14
Q

Nutmeg Liver

A

red brown - associated with cell loss & congestion
paler - normal unaffected hepatocytes
-seen iwth CHF & obstructed IVC/hepataic vein

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15
Q

Virchow’s triad

A

1) abnormal blood flow (sluggish = venous/turbulent = art)
2) endothelial injury
3) hypercoagulable state

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16
Q

Lines of Zahn

A

laminations in thrombi consisting of alternating pale (platelets
/fibrin) and dark (red blood cells) layers

17
Q

Vegetations

A

Thrombi composed of infectious agents on heart valves

-ex. endocarditis

18
Q

Thrombi - Arterial vs Venous

A

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

19
Q

Thrombus vs embolus

A

Thrombus: a clot/plaque
-can embolyze, propagate, dissolve or become organized (integrated & vasculature grows around)

Embolus: DISLOGED substance that causes obstruction downstream

20
Q

Rheumatic heart disease

A

an inflammatory disease that occurs following a Strep infection

21
Q

Fat emboli

A

originate in bone marrow, presents as fatty clot

Causes: long bone fxs, burns, soft tissue trauma

22
Q

Major factors in determining the clinical/pathological outcome of infarctions:

A

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)

23
Q

Infarctions

A

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)
24
Q

Stroke

A

Acute onset neurologic syndrome due to vascular event

hemorrhagic - no TPA
occlusion - push TPA

extensive loss initially with very slow/no restoration

25
Q

Volvulus

A

bowel twists on its own messentary axis; can compromise the messenteric artery

26
Q

Intussusception

A

bowel telescopes into itself; can compromise the messenteric artery

27
Q

von Willebrands Disease

A
  • lacking important platelet adhesion molecule that links exposed subendothelial collagen/GP1b
  • PT, PTT & platelet counts are normal
28
Q

Vasculitis

A

a group of disorders that destroy blood vessels by inflammation

inflammation of veins = phlebitis (think phlebotomist)
inflammation of arteries = arteritis

29
Q

Arteriosclerosis

A
arterio = artery
sclerosis = thickening/hardening
  • the thickening, hardening and loss of elasticity of the walls of arteries
30
Q

Disseminated Intravascular Coagulation (DIC)

A
  • 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
31
Q

Atherosclerosis

A

athera = “gruel” or porridge

  • a specific form of arteriosclerosis caused by the buildup of fatty plaques and cholesterol in the artery