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Pathology > Hemodynamic disorders > Flashcards

Hemodynamic disorders Flashcards

1
Q
  • increased fluid in the interstitial tissue spaces and body cavities
A

edema

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2
Q

the abnormal accumulation of fluid in the pleural cavity

A

hydrothorax

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3
Q

or ascites in the peritoneal cavity

A

hydroperitonium

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4
Q

pericardial sac

A

hydropericardium

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5
Q

scrotal sac

A

hydrocele

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6
Q

is severe and generalized edema with profound subcutaneous tissue swelling

A

anasarca

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7
Q

low protein content and specific gravity of less than 1.012

A

noninflammatory edema or transdute

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8
Q

in the arterial end drives fluid from the lumen of blood vessel into the interstitial space

A

normal hydrostatic pressure

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9
Q

absorbs back the fluid in the venous end of capillary

A

plasma colloid osmotic pressure

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10
Q

small amount of extra fluid in the interstitial space is absorbed by the ___ brought to the thoracic duct then to the left subclavian vein to the blood circulation.

A

lymphatic

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11
Q

any disturbance in the hydrostatic pressure, osmotic pressure and obstruction of the lymphatic flow will promote ___

A

edema

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12
Q

result from impaired venous outflow

A

local increases

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13
Q

localized edema of the lower extremity involved

A

deep vein thrombosis in lower extremities

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14
Q

example is a mass causing pressure on lymphatics

A

external pressure

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15
Q
  • Generalized increases causing systemic edema
  • most common
A

congestive heart failure

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16
Q

Reduced plasma osmotic pressure

A

hypoproteinemia

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17
Q

decreased cardiac output

A

constrictive pericarditis

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18
Q

increased permeability of glomerulus of kidney resulting to escape of proteins to the urine

A

nephrotic syndrome

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19
Q

proteins in urine

A

proteinuria

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20
Q

decreased protein synthesis

A

liver cirrhosis

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21
Q

decreased protein intake

A

malnutrition

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22
Q

results from excessive loss or reduced synthesis of albumin

A

Hypoalbuminemia

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23
Q

most commonly encountered in subcutaneous tissues, lungs and brain

A

edema

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24
Q
  • dependant parts: legs, sacrum
  • loose connective tissue matrix: periorbital edema
A

subcutaneous edema

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25
Q
  • occurs in the following clinical conditions: left ventricular failure, renal failure, adult respiratory distress syndrome, pulmonary infections, hypersensitivity reactions
  • lungs 2 – 3x their normal weight; on sectioning reveals a frothy fluid (mixture of air and fluid)
  • microscopic examination shows alveolar spaces filled with fluid
A

pulmonary edema

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26
Q
  • localized : abscess, neoplasms or tumors
  • generalized: encephalititis, hypertensive crisis, obstruction to brain’s venous outflow
  • local or generalized: trauma
  • grossly swollen, narrowing of the sulci and flattening of the gyri
  • dreaded complications: brain herniation
A

brain edema

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27
Q
  • an active process resulting from increased tissue blood flow because of arteriolar dilatation
  • affected tissue is red because of engorgement with blood
  • Ex. Skeletal muscle during exercise sites of acute inflammation
A

hyperemia

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28
Q

a passive process resulting from impaired outflow from tissue
- closely related to development of edema
- Ex. Cardiac failure, venous obstruction

A

congestion

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29
Q

blue-red color congestion

A

cyanosis

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30
Q

– alveolar capillaries engorged with blood
- intra-alveolar hemorrhage

A

acute pulmonary congestion

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31
Q

– numerous heart failure cells in the alveolar spaces (or hemosiderin-laden macrophages)

A

Chronic pulmonary congestion

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32
Q
  • central vein and sinusoids are distended with blood
A

Acute hepatic congestion

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33
Q

– central regions of hepatic lobules are grossly red-brown against the surrounding zones of uncongested tan liver (nutmeg liver)

A

Chronic passive congestion of liver

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34
Q
  • extravasation of blood because of vessel rupture
A

hemorrhage

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35
Q
  • hemorrhage may be external or enclosed with a tissue, the accumulation is ___
  • (Ex. bruise)
A

hematoma

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36
Q

minute 1 – 2 mm hemorrhage into skin, mucous membranes or serosal surfaces are called ___

A

petechiae

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37
Q

petechiae is associated with

A

increased intravascular pressure to rupture to decreased platelet count and clotting factor defects

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38
Q

decreased platelet count

A

thrombocytopenia

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39
Q

slightly larger hemorrhages (> 3 mm) are called

A

purpura

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40
Q
  • larger (> 1- 2 cm) subcutaneous hematomas are called
  • typical after trauma and degraded erythrocytes that are phagocytosed by macrophages is responsible for color change
A

ecchymoses

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41
Q

red to blue

A

hemoglobin

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42
Q

blue to green

A

biliverdin, bilirubin

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43
Q

gold to brown

A

hemosiderin

44
Q

larger accumulations of blood in body cavities

A
  • hemothorax, hemopericardium, hemoperitoneum, hemarthrosis (joint cavity)
  • hemocele (scrotal sac)
45
Q

Clinical significance of hemorrhage

A
  • depends on: volume and rate of blood loss
    site
    iron loss
46
Q

Process of thrombus (clot) formation

A
  1. Vascular wall (endothelium)
    2. platelets
    3. coagulation cascade
47
Q

coagulation cascade

A

injury to endothelium to platelet adhesion and aggregation at site of endothelial injury to activation of coagulation cascade

48
Q

series of conversions of inactive proenzymes to activated enzymes to thrombin to fibrinogen to fibrin (clot)

A

coagulation cascade

49
Q

3 types of anticoagulants

A
  • antithrombins
  • proteins C and S
  • plasmin
50
Q
  • inhibit activity of thrombin,
  • Ex.antithrombin III
A

antithrombins

51
Q

inactive factors Va and VIIIa

A

proteins C and S

52
Q

breaks down fibrin

A

plasmin

53
Q

3 main factors predispose to thrombus formation

A

Virchow’s triad
- endothelial injury
- alterations in normal blood flow
- hypercoagulability of blood

54
Q

as in trauma or inflammation

A

endothelial injury

55
Q

stasis and turbulence

A

alterations in normal blood flow

56
Q

concentration of fibrinogen

A

hypercoagulability of blood

57
Q
  • can occur at any place in the circulatory system: cardiac chambers, heart valves, arteries, veins, capillaries
  • has point of attachment to the vessel wall
  • composed of platelets, fibrin, degenerating leukocytes, and entrapped RBC
A

thrombosis

58
Q

thrombosis are arranged in a laminated pattern called ___ which are produced by alternating pale layers of platelets admixed with some fibrin and darker layers of more RBC.

A

lines of Zahn

59
Q

usually occlusive

A

arterial thrombi

60
Q

most common sites in descending order of thrombosis

A

coronary, cerebral, femoral arteries

61
Q
  • most occlusive thrombosis
  • most commonly affects the veins of lower extremities (90%)
A

venous thrombosis or phlebothrombosis

62
Q

accumulate more platelets and fibrin to enlarge to vessel obstruction

A

propagation

63
Q

thrombi may dislodge or fragment to carried to the other sites

A

embolization

64
Q

thrombi may be removed by fibrinolysis

A

dissolution

65
Q

ingrowth of granulation tissue from vessel wall

A

organization

66
Q

development of new vascular channels, restablishing blood flow

A

recanalization

67
Q

clinical importance of fate of thrombus

A
  1. cause obstruction of arteries and veins
    1. sources of emboli
68
Q

– a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin
- 99% represent some part of a disloged thrombus
- rare forms of emboli include droplets of fats, bubbles of air or nitrogen, tumor fragments, bits of bone marrow

A

emobolus

69
Q

disloged thrombus

A

thromboembolism

70
Q
  • more than 95% originate from deep, vein thrombi of lower extremities
    - most are clinically silent but if massive any may cause sudden death
A

pulmonary thromboembolism

71
Q
  • fat globules in the circulation after fractures of long bones
A

Fat embolism

72
Q
  • gas bubbles within circulation may be due to chest wall injuries or during obstetric procedures
  • when air is breathed at high pressure (deep sea), increased amounts of gas (nitrogen) become dissolved in blood and tissues, if divers ascend too rapidly the nitrogen expands in the tissues and bubbles out of solution in the blood to form gas emboli.
A

air embolism

73
Q
  • decompression sickness
  • occurs when individuals are exposed to sudden changes in atmospheric pressure
    ex. Scuba or deep sea divers
A

Caisson disease

74
Q
  • In the lungs, edema, hemorrhages & focal atelectasis or emphysema may appear leading to respiratory distress.
  • Treatment: requires placing the individual in a compression chamber barometric pressure may be raised, thus forcing gas bubbles back into solution. Subsequent slow decompression permits gradual resorptoin & exhalation of gases so that obstructive bubbles, do not reform.
A

chokes

75
Q
  • a more chronic form of decompression sickness
    - persistence of gas emboli in skeletal system leads to multiple foci of ischemic necrosis.
    - the more common sites are: heads of femur, tibia & humeri.
A

caisson disease

76
Q

– a grave but uncommon (1:50,000 deliveries) complications of labor & the immediate postpartum period caused by infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins.
- The onset is char. By sudden severe dysprea, cyanosis & hypotensive shock affected by seizures & coma. If survive the initial crisis, pulmonary edema & DIC (in ½ the pts.) owing to release of thrombogenic substances from amniotic fluid.
- Classic findings: presence in pulm, microcirc. Of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa & mucin from fetal R.T., GIT, there is also pulm. edema, changes of DAD & systemic fibrin thrombi indicative of DIC.

A

amniotic fluid embolism

77
Q

Where are thrombi formed?

A

A. Arterial or Cardiac thrombi usu. Begin at a site of endothelial injury, turbulence in vessel bifurcation (e.g. atherosclerotic plaque)
B. Venous thrombi occur in sites of stasis.

78
Q

What is characteristics of all thromboses?

A

An area of attachment to the underlying vessel or heart wall, freq. firmest at the point of origin.

79
Q

How do these thrombi propagate?

A

A. Arterial thrombi tend to grow in a retrograde direction from the point of attachment.
B. Venous thrombi extend in the direction of blood flow (e.g., toward the heart)

80
Q
  • Thrombi formed in the heart or aorta may have grossly & microscopically apparent laminations. These are produced by alternating pale layers of platelets admixed w/ some fibrin & darker layers containing more red cells
  • Significance: they imply thrombosis at a site of blood flow.
A

lines of zahn

81
Q

At autopsy, postmortem clots maybe confused for ___

A

venous thrombi

82
Q
  • Are gelatinous with a dark red dependent portion where red cells have settled by gravity & a yellow chicken fat supernatant resembling melted & clotted chicken fat.
  • Are usu. Not attached to the underlying wall.
A

postmortem clots

83
Q
  • formed in a relatively static environment, tend to contain more enmeshed erythrocytes.
    • are firmer.
    • almost always, have a point of attachment.
    • on transection reveal vague strands of pale gray fibrin.
A

venous thrombi (red thrombi or stasis thrombi)

84
Q

usu. Adhere to the wall of cardiac chambers or the aorta & are termed Mural thrombi. Precursors of Cardiac Mural thrombi: Abn. Myoc contraction (Arrhythmias, Dilated CMP, or MI). Precursors of Aotic thrombus: Ulcerated atherosclerotic plaque, aneurysmal dilation.

A

Arterial thrombi

85
Q
  • an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue.
  • 99% result from arterial occlusion
A

infarction

86
Q

Types of infarcts

A
  • red (hemorrhagic) infarct
  • white (anemic) infarct
  • septic infarctions
87
Q

ovarian torsion

A

with venous occlusions

88
Q

lungs

A

in loose tissues

89
Q

in the lungs and small intestine

A

in tissues with dual circulations

90
Q

occur with arterial occlusions or in solid organs (heart, liver, spleen, kidneys)

A

white (anemic) infarct

91
Q

when embolization occurs by fragmentation of a bacterial vegetation from a heart valve or when microorganisms seed an area of necrotic tissue; infarct is converted into an abscess

A

septic infarctions

92
Q

tend to be wedge-shaped, with occluded vessel at apex and the periphery of the organ forming the base

A

Infarcts

93
Q
  • Final common pathway for a number of clinical conditions like severe hemorrhages, extensive trauma or burns, large myocardial infarction, massive pulmonary embolism or microbial sepsis
  • Constitutes systemic hypoperfusion owing to reduction either in cardiac output or in the effective circulating blood volume; the end results are hypotension, followed by impaired tissue perfusion and cellular hypoxia.
A

shock or cardiovascular collapse

94
Q

3 Major types of shock:

A

cardiogenic
hypovolemic
septic

95
Q
  • myocardial infarction, rupture of the heart, arrythmias, cardiac tamponade, oulmonary emoblism
  • failture of myocardial pumo due to intrinsic myocardial damage or extrinsic pressure obstruction of flow
A

Cardiogenic

96
Q
  • Hemorrhage, Fluid loss
  • Inadequate blood or plasma, volume
A

Hypovolemic

97
Q
  • Overwhelming bacterial inf: with gram (-) or gram (+) septicemia, fungal sepsis
  • Peripheral vasodilation and pooling, pooling of blood: endothelial injury; activation of cytokine cascade
A

septic

98
Q

Less common types of shock

A

Neurogenic Shock
Anaphylactic Shock

99
Q

shock:
occurs in anesthetic accident or spinal cord injury

A

neurogenic shock

100
Q

shock:
allergy

A

Anaphylactic Shock

101
Q

cellular and tissue changes induced by shock are those of ___; characterized by failure of multiple organ systems

A

hypoxic injury

102
Q

Clinical manifestations are the same regardless of the cause:

A

Hypotension
weak rapid pulse
tachypnea
cool, clammy, pale or cyanotic skin

103
Q

congestive heart failure to
decreased cardiac output to
decreased arterial blood volume to
decreased renal perfusion to
triggers renin, angiotensin, aldosterone axis will cause
sodium & water retention by kidneys and will temporarily increase intravascular volume to
if failing heart cannot increase cardiac output
extra fluid results in increased venous pressure to
increased transudation to
EDEMA

A

systemic edema

104
Q

elephantiasis

A

inflammatory - filariasis

105
Q

due to scarring of lymphatic channels

A

postsurgical and post irradiation

Pathology (3 decks)

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