Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology I > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

what does circulation do

A

delivers oxygen and nutrients to tissues
- removes wastes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is hemostasis

A

blood clotting that prevents excess bleeding after blood vessel damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is thrombosis

A

inappropriate clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is embolism

A

migration of clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is hyperemia

A

-active process
- arteriolar dilation and increased blood flow
- occurs at site of inflammation or skeletal muscle movement
-red in color: oxygenated hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is congestion

A

-passive process
- impaired outflow of venous blood from a tissue
- blue/red color - deoxygenated hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what percentage of the body weight is water

A

60%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where is 2/3 of water in body located

A

intracellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what percentage of water is in blood plasma

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is edema

A

accumulation of ISF in tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are effusions

A

extravascular fluid that collects in body cavities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is an effusion in pleural cavity called

A

hydrothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is an effusion of the pericardial cavity called

A

hydropericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is an effusion of the peritoneal cavity called

A

hydroperitoneum or ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is anasarca

A

severe generalized edema due to fluid retention in tissues and cavities
- seen in systemic disease such as kidney disease and severe malnutrition
- causes weight gain and multiple organ failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what diseases is ascites seen in

A

severe liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

when is hydrothorax seen

A

in CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what makes pulmonary edema distinct in a histo slide

A

fluid collects between the alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what determines capillary fluid movement

A

vascular hydrostatic pressure and colloid osmotic pressure (plasma proteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

where is arterial outflow is normally balanced by inflow at

A

the venous end

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

why is arterial outflow balanced by inflow at the venous end

A

results in small net outflow of fluid in interstitial spaces -> drained by lymphatics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what pressures cause edema

A

increased hydrostatic pressure or plasma colloid osmotic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is increased hydrostatic pressure caused by

A

disorders that impair venous return such as deep venous thrombosis and CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what caused reduced plasma osmotic pressure

A

reduced plasma albumin concentration from loss in circulation or reduced synthesis
- nephrotic syndrome
- severe liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how does heart failure lead to edema- mechanism

A
  • increased capillary hydrostatic pressure -> edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how does renal failure cause edema - mechanism

A
  • retention of Na+ and H2O
  • increase in blood volume
  • edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how does malnutrition, decreased hepatic synthesis and nephrotic syndrome cause edema

A
  • decreased albumin-> decreased plasma osmotic pressure -> edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how does lymphatic obstruction cause edema

A
  • compromises resorption of fluid from interstitial spaces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what causes lymphatic obstruction

A
  • inflammatory conditions: bacterial/ parasitic infections
  • neoplastic conditions: breast cancer
  • congenital lymphedma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the stages of lymphedema

A
  • stage 1: asymptomatic, abnormal lymph flow but no build up
  • stage 2: swelling, due to accumulation of lymph fluid that may subside when elevated
  • stage 3: permanent swelling that cannot be relieved through elevation accompanied by fibrosis
  • stage 4: lymphostatic elephantiasis or the deformation of a limb due to extensive swelling, skin thickening and scarring
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is a hemorrhage

A
  • extravasation of blood from vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what causes a hemorrhage

A
  • defective clot formation
  • trauma
  • atherosclerosis
  • inflammatory
  • neoplastic conditions
  • inherited/acquired defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the hemorrhage manifestations

A
  • hematoma
  • ecchymoses
  • purpura
  • petechiae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is a hematoma

A

large collection of hemorrhage in a tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is ecchymoses

A

1-2cm of subcutaneous hemorrage - bruises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is purpura

A

3-5mm hemorrhages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are petechiae

A

1-2mm minute hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are petechiae caused by

A

-thrombocytopenia
- vitamin C deficiency
- mononucleosis
- trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the steps in clot formation

A
  • vasoconstriction
  • platelet plug forms
  • fibrin deposition
  • clot stabilization and resorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are the primary regulators of hemostasis and how

A

endothelial cells through changes in expression of procoagulant or anticoagulant factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

describe vasoconstriction step in clot formation

A

occurs immediately to decrease blood flow
- endothelin causes the vasoconstriction

42
Q

describe platelet activation and aggregation step of clot formation

A
  • initial formation of platelet plug from endothelial cell disruption
  • vWF promotes platelet adherence and causes conformational change and activates them
43
Q

describe the activation of clotting factors and formation of fibrin step in clot formation

A
  • secondayr hemostatsis
  • activation of cotting factors and formation of fibrin
  • exposes tissue factor expressed on subendothelial cells
    -activates clotting cascade which ends in thrombin formation
  • thrombin converts fibrinogen into fibrin
  • forms mesh work of clot
44
Q

describe the clot resorption step in clot formation

A
  • permanent plug
  • t-Pa limits clotting to site of injury
45
Q

describe platelets

A

disk shaped
- anucleate fragments of megakaryocytes

46
Q

what are platelets derived from

A

megakaryocytes

47
Q

what is platelet adhesion mediated by

A

vWf

48
Q

what is the coagulation cascade

A

a series of amplifying enzymatic reactions that lead to the deposition of an insoluble fibrin clot
- secondary hemostasis

49
Q

what is the intrinsic pathway activated by

A

spontaneous, internal injury to vascular endothelium

50
Q

what is the extrinsic pathway activated by

A

external trauma

51
Q

what is involved in the intrinsic pathway

A
  • factor 12
  • factor 11
  • factor 9
  • factor 10
52
Q

what is involved in the extrinsic pathway

A
  • factor 7
  • factor 10
  • tisssue factor
53
Q

what do the extrinsic pathway and intrinsic pathway form

A
  • common pathway
  • prothrombin converted into thrombin
  • thrombin converts fibrinogen to fibrin
54
Q

what does partial prothrombin time (PTT) evaluate

A

intrinsic pathway factors

55
Q

what does prothrombin time (PT) evaluate

A

the extrinsic pathwya factors

56
Q

what is the role of vitamin K

A
  • regulation of coagulation, plays key role in synthesis of factors 2,7,9,10
  • helps synthesize protein C and S: important for negative feedback regulation of clotting cascade
  • vitamin K deficiency- increased bruising and bleeding
57
Q

what is warfarin

A

-anticoagulant medication
- antagonist for vitamin K
- inhibits clotting

58
Q

what is the most important coagulation factor

A

thrombin

59
Q

what does thrombin do

A
  • converts fibrinogen into fibrin
  • activates platelets
  • pro inflammatory effects
  • anti coagulation effects
60
Q

what factors limit coagulation

A
  • dilution of blood past the site of injury
  • negatively charged phospholipids required - activated platelets
  • regulation by neighboring intact endothelium
  • fibrinolytic cascade limits size of clot
61
Q

decsribe endothelium and coagulation limitation

A
  • serves as barrier to platelets
  • anticoagulant effects
  • fibrinolytic effects
62
Q

how does endothelium serve as a barrier to platelets

A
  • lack of access to vWF and collagen
  • release of NO, prostacyclin, adenosine diphosphate
63
Q

what do anticoagulant effects do

A

expresses factors that inactivate thrombin

64
Q

what are fibrinolytic effects

A

synthesis of tissue plasminogen activator (tPA)

65
Q

what does thrombosis cause

A
  • endothelial injury
  • abnormal blood flow
  • hypercoagulability
66
Q

what is endothelial injury caused by

A

-coronary artery disease
- MI
- chronic inflammation - physical injury, infectious agents, abnormal blood flow, inflammatory mediators, toxins

67
Q

what is abnormal blood flow caused by

A
  • promotes endothelial procoagulant activity
  • stasis allows platelets and leukocytes to associate with endothelial cells
  • stasis slows removal of activated clotting factors and impedes inflow of clotting factor inhibitors
68
Q

what is hypercoagulability

A
  • abnormally high tendency for blood to clot
  • important risk factor for venous thrombosis
69
Q

what are the types of hypercoagulability

A

-primary (genetic)
- secondary (acquired)

70
Q

what are the common primary hypercoagulable states caused by and what percentage of population is affected

A
  • less than 1%
  • factor V mutation
  • prothrombin mutation
  • increased levels of factor 7,9 or 11 or fibrinogen
71
Q

what is considered high risk for secondary hypercoagulable staes

A
  • prolonged bed rest or immobilization
  • MI
  • A fib
  • tissue injury
  • cancer
  • prosthetic cardiac valves
  • disseminated intravascular coagulation
  • heparin induced thrombocytopenia
  • anti phospholipid antibody syndrome
72
Q

what is in Virchow’s triad in thrombosis

A
  • endothelial injury
  • abnormal blood flow
  • hypercoagulability
73
Q

where do thrombi occur

A

anywhere in the cardiovascular system

74
Q

where are arterial thrombi located and describe them

A

often at sites of injury
- typically rich in platelets

75
Q

where do cardiac mural thrombi occur

A

in heart chambers or aorta

76
Q

where do venous thrombi occur and describe them

A

at sites of stasis
- contain high volume of RBCs

77
Q

what are lines of Zahn

A
  • lines observed in flowing blood clots
  • differentiates antemortem clots from postmortem clots
78
Q

where do 90% of venous thrombi occur

A

in the legs

79
Q

what are the 4 fates of thrombi

A
  • propagation: clot enlarges
  • embolization: clot dislodges and moved by circulatory system
  • dissolution: activation of fibrinolytic factors
  • organization and recanalization- older thrombi are reorganized to facilitate some function
80
Q

what are superficial venous thrombosis caused by

A

local congestion and swelling from impaired venous flow

81
Q

decsribe deep vein thrombosis

A
  • larger veins
  • may be asymptomatic in 50% of patients
  • may embolize to lungs
82
Q

what is a major cause of arterial and cardiac thrombosis

A

atherosclerosis

83
Q

what does arterial and cardiac thrombosis caused by atherosclerosis result in

A

loss of endothelial integrity and abnormal blood flow
- leads to MI, ischemia to organs especially brain, kidney and spleen

84
Q

descibe disseminated intravascular coagulation (DIC)

A
  • widespread thrombosis within microcirculation
  • consumption of platelets and clotting factors
  • may occur from complications in obstetrics, injuries, cancer and more
  • net result: excessive clotting and bleeding
85
Q

describe an embolism

A

may be a solid, liquid or gaseous matrix carried by the blood from its point of origin to a distant site

86
Q

what is a pulmonary embolism

A
  • most common
  • mostly from upper deep leg veins proximal to popliteal fossa
  • pass through the larger right heart vessels and lodge in them pulmonary artery or arterioles
  • multiple emboli can occur
  • most are small and large ones can cause sudden death
  • multiple emboli over time can cause pulmonary HTN and right ventricular failure
87
Q

describe systemic thromboembolism

A
  • may arise from intracardiac mural thrombi - 80%
  • can embolize to lower extremities most frequently, CNS, intestines, kidneys and spleen
88
Q

describe fat embolism

A
  • injury to bone marrow can cause release of fat globules into circulation but rarely show clinical manifestations, but less than 10% show pulmonary problems, neurologic problems, anemia, thrombocytopenia and petechial rash
88
Q

describe amniotic fluid embolism

A
  • severe post birth complication with 80% mortality rate due to biochemical activation of coagulation system and immune system from entry of amnitoic fluid into circulation system of mother
89
Q

what is air embolism

A

gas in circulation can come together to obstruct vascular flow
- ex: decompression sickness in scuba divers

90
Q

what is an infarction

A

area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue

91
Q

what are the most common infarctions

A

arterial thrombosis or embolism
- involvment of brain or heart

92
Q

what are the 2 classes of infarct and describe each

A
  • red: contain hemorrage. venous occlusion, loose tissue, tissue with dual circulation, previously congested tissue, reperfusion injury
  • white infarct: arterial occlusion in solid organs, heart, liver spleen
93
Q

what is shock

A

a state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia

94
Q

what does prolonged shock lead to

A

irreversible tissue injuryw

95
Q

what are the 3 types of shock

A

cardiac
- hypovolemic
- septic

96
Q

what are the clinical examples and pathogenic mechanisms for cardiogenic shock

A
  • ex: MI, ventricular rupture, arrhythmia, cardiac tamponade, pulmonary embolism
  • mech: failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic pressure or obstruction to outflow
97
Q

what are the clinical examples and pathogenic mechanisms of hypovolemic shock

A
  • ex: hemorrhage, fluid loss
  • mech: inadequate blood or plasma volume
98
Q

what are the clinical examples and pathogenic mechansim of septic shock

A
  • overwhelming microbial infections
  • gram negative sepsis
  • gram positive septicemia
  • fungal species
  • superantigens
  • mech: peripheral vasodilation and pooling of blood, endothelial activation/injury, leukocyte induced damage, disseminated intravascular coagulation, activation of cytokine cascades
99
Q
A

Pathology I (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions