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IHP 1001 > Ch.3 Hemodynamic Disorder Pt.1 > Flashcards

Ch.3 Hemodynamic Disorder Pt.1 Flashcards

1
Q

the accumulation of fluid in tissues resulting from a net movement of water into extravascular spaces

A

Edema

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2
Q

process of blood clotting that follows blood vessel damage.

A

Hemostasis

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3
Q

(excessive bleeding), which may compromise tissue perfusion and, if massive and rapid, lead to hypotension, shock, and death.

A

hemorrhage

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4
Q

Inappropriate clotting

A

thrombosis

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5
Q

migration of clots in the vasculature

A

Embolism

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6
Q

blood vessel obstruction and ischemic cell death

A

infarction

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7
Q

What underlies

  1. myocardial infarction
  2. pulmonary embolism
  3. cerebrovascular accident (stroke).
A

thromboembolism

Clotting and migration of clot

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8
Q

is an active process resulting from arteriolar dilation and increased blood inflow; it occurs at sites of inflammation and in exercising skeletal muscle.

A

Hyperemia

Red tissues, lots of O2 blood

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9
Q

Passive process resulting from impaired outflow of venous blood from a tissue

occurs systemically in *cardiac failure *and locally as a consequence of venous obstruction.

A

Congestion

Tissues are blue-red color (cyanosis) Acc. of deoxygenated hemoglobin

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10
Q

What kind of Congestion?

Microscopicall marked by** blood-engorged alveolar** capillaries and variable alveolar septal edema and intraalveolar hemorrhage.

A

acute pulmonary congestion

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11
Q

What kind of Congestion?

the septa become thickened and fibrotic and the alveolar spaces contain *numerous macrophages *laden with hemosiderin (“heart failure cells) derived from phagocytosed red cells.

A

chronic pulmonary congestion

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12
Q

the central vein and sinusoids are** distended with blood** and centrally located hepatocytes may undergo necrosis.

** Periportal hepatocytes, which experience less severe hypoxia because of their proximity to hepatic arterioles, may develop fatty change**

A

Acute hepatic congestion

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13
Q

What kind of Congestion?

the central regions of the hepatic lobules are congested, red-brown, and **slightly depressed **(owing to necrosis and cell loss)

are accentuated by surrounding zones of *tan, sometimes Fatty, periportal hepatocytes (nutmeg liver)

A

chronic passive liver congestion

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14
Q

Extravascular fluid can collecting in body cavities

A

effusion

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15
Q

Examples of?

1.pleural cavity (hydrothorax)
2.pericardial cavity (hydropericardium)
3.peritoneal cavity (hydroperitoneum, or ascites)

A

Effusion

Extravascular fluid can collecting in body cavities

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16
Q

severe, generalized edema marked by profound swelling of subcutaneous tissues and accumulation of fluid in body cavities.

A

Anasarca

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17
Q

In inflammation, edema is due to what?

A

Increased vascular permability

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18
Q

GOverns movment of fluid in and out of aterioles
Controled by Na+ and K levels

A

Hydrostaic Pressure

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19
Q

2

Under normal circumstances what is the **balance **of hydrostatic pressure and osmotic pressure?

A

outflow of fluid produced by hydrostatic pressure at the arteriolar end of the microcirculation is nearly balanced by inflow at the venular end owing to osmotic pressure.

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20
Q

GOverns movment of fluid in and out of venules
Controled by protein concentration

A

Osmotic Presure

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21
Q

What 2 trends in hydrostatic pressure and osmotic pressure cause :

increased movement of water into the interstitium and if the drainage capacity of the lymphatics is exceeded, edema results.

A
  1. Increased hydrostatic pressure
  2. diminished colloid osmotic pressure
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22
Q

Edema fluid that accumulates due to high Hydrostatic pressue or low osmotic pressure is:

A

protein-poor transudate

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23
Q

increased vascular permeability, inflammatory edema fluid is

A

Protein rich exudate

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24
Q

are mainly caused by disorders that impair venous return

A

Increases in hydrostatic pressure

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25
Q

Impaired venous return Causes What?

the lower extremity may cause edema restricted to the distal portion of the affected leg,

deep venous thrombosis

A

Increase in Hydrostatic Pressure

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26
Q

Impaired venous return Causes What?

leads to a systemic increase in venous pressure and, often, widespread edema.

Congestive Heart faliue

A

Increase in hydrostatic pressure

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27
Q

ALL DO WHAT?

  • Congestive heart failure
  • Constrictive pericarditis
  • Liver cirrhosis
  • Venous obstruction or compression
  • Thrombosis
  • External pressure (e.g.,mass)
  • Lower extremity inactivity with prolonged dependency
A

All things that cause Stagnation in venous portion of vascular because arterial end is empty no pressure pushing= whole system to backup = high hydrostatic pressure= water pushed out.

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28
Q

Reduced cardiac output leads to pooling of blood in the _____ and** increased capillary hydrostatic pressure**

A

venous circulation

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29
Q

The Reduction in cardiac output also results inhypoperfusion of the kidneys, triggering the renin-angiotensin-aldosterone axis and inducing ______ (secondary hyperaldosteronism).

A

Sodium and water retention

secondary hyperaldosteronism

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30
Q

Reduced plasma albumin is a common feature of disorders in which edema is caused by ____

A

Decreases in colloid osmotic pressure

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31
Q

Protien. Accounts for almost half of the total plasma protein and is the biggest contributor to colloid osmotic pressure.

A

Albumin

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32
Q

All result in?

  • Nephrotic syndrome
  • Reduced albumin synthesis is seen in the setting of severe liver disease (e.g.,cirrhosis)
  • protien malnutriotion
A

Decrease of Osmotic pressure (protien out)

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33
Q

Excessive retention of ____ (and associated water) can lead to edema by increasing hydrostatic pressure (owing to expansion of the intravascular volume) and **reducing plasma osmotic pressure **

A

Retention of Salt; Na+ and K

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34
Q

defined as the extravasation of blood from vessels, results from damage to blood vessels and may be exacerbated by defects in blood clotting.

A

Hemorrhage

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35
Q
  • Trauma
  • atherosclerosis
  • inflammatory or neoplastic erosion of a vessel wall also may lead to::
A

Hemmorage

36
Q

What kind of hemorrhage?

Hemorrhage may take the form of external bleeding or may accumulate within a tissue

no iron deficiency

A

Hematoma

Bruises or massive retroperitoneal hematoma rupure in aorta, hemothorax

37
Q

What kind of hemorrhage?

minute (1 to 2mm in diameter) hemorrhages into skin, mucous membranes, or serosal surfaces

Low platlet count, or defective platlet function

A

Petechiae

38
Q

What kind of hemorrhage?

lightly larger (3 to 5mm) hemorrhages

Caused by trauma, vascular inflammation (vasculitis), and increased vascular fragility

A

Purpura

39
Q

What kind of hemorrhage?

larger (1 to 2cm) subcutaneous hematomas (colloquially called “bruises”).

Extravasated red cells are phagocytosed and degraded by macrophages; the characteristic color changes of a bruise result from the enzymatic conversion of** hemoglobin** (red-blue color) to** bilirubin** (blue-green color) and eventually hemosiderin (golden-brown

A

Ecchymoses

40
Q

relatively trivial in the subcutaneous tissues may cause death if located in the ___

A

Brain bleed

41
Q

chronic or recurrent external blood loss can lead to a what defiinceny?

Peptic ulcer or menstration

A

Anemia; iron deficiency

42
Q

precisely orchestrated process **involving platelets, clotting factors, and endothelium **that occurs at the site of vascular injury and leads to the formation of a blood clot, which serves to prevent or limit the extent of bleeding.

A

Homeostatis

43
Q

1st. markedly reduces blood flow to the injured area
* local seretion of endothelin vasoconstrictor

Transient effect, bleeding will resume

A

Arteriolar vasoconstriction

44
Q

2nd Step
* Basment membrane exposed* (collagen)*
* Bind Von Willebrand factor (VWF); Promotes platelet adherence and activation
* Platlet undergo shape change (small round flat to **spickey) **
* Release secratory granules (ADP, TXA2 vasoconstrictor)
* Bring more plugs in
* Plug formed

A

Primary hemostasis: the formation of the platelet plug.

45
Q

3rd step
* Injury exposes tissue factor
* Tissue factor binds & activates Factor VII (7)
* Cascade reaction activated
* Thrombi generated
* Thrombin cleaves circulating fibrogenn into insoluble Fibrin
* More paltlet agregation
* More plug

A

Secondary hemostasis: deposition of fibrin. Vascular injury exposes tissue factor

46
Q

4th Step
* Polymerized fibrin is crosslinked covalently by factor XIII (13)
* Platlet agregate contracts
* Formation of solid permanent plug = no more beleediing
* Size of clot resticted by anticoagulatory mechaims

A

Clot stabalization

47
Q

potent endothelium-derived vasoconstrictor.

A

endothelin

48
Q

molecule that promotes platelet adherence and activation
produced by enothelial cells

A

von Willebrand factor (VWF)

49
Q

What are 2 secretory granuales released by activated platlets?

A

ADP & TXA2 (vasoconstrictor)

50
Q

a membrane-bound procoagulant glycoproteinthat is normally expressed by subendothelial cells in the vessel wall, such as smooth muscle cells and fibroblasts.

A

tissue factor

51
Q

Tissue factor binds and activates factor ?

A

Factor VII (7)

Sets action of cascade that makes Thrombin

52
Q

cleaves circulating fibrinogen into insoluble fibrin, creating a fibrin meshwork, and is a potent activator of platelets, leading to additional platelet aggregation at the site of injury.

A

Thrombonin

53
Q

Insoluble fibrin mesh does what? Green.

A

Prevent blood loss, forms plug to stop bleeding.

54
Q

Acute phase protiens Il-1, Il-6 and TNF is released from kidney along with what?

A

Fibrogen proteins

55
Q

participate in a series of amplifying enzymatic reactions that lead to the deposition of an insoluble fibrin clot

Roman numerals; circulate as** inacitve enzymes** (zymgogens)

A

Coagulation Factors

56
Q

when coagulation factors activate, many become protien cleaves enzymes that contains serine .

A

Serine proteases

57
Q
  1. Sequential activation of clotting factor zymogens (normal is low level activation
  2. Amplication with endothelial damage
  3. Results in fibrin generation

*Sequential= mutlple steps for feedback inhibition.

A

Coagulation Casacade

58
Q

Assesses the function of the proteins in the extrinsic pathway (factors X, VII, V, II [prothrombin], and fibrinogen).

A

prothrombin time (PT)

Lab test

59
Q

assesses the function of the proteins in the intrinsic pathway (factors XII, XI, X, IX, VIII, V, II, and fibrinogen).

A

partial thromboplastin time (PTT)

Lab test

60
Q

what pathway?

Deficiencies of factors V, VII, VIII, IX, and X are associated with ____ and prothrombin deficiency is incompatible with life.

A

moderate to severe bleeding

61
Q

Deficiency in XI causes

A

only causes a mild bleeding disorder

62
Q

Deficiency in XII causes

A

No bleeding disorder

63
Q

What is most important control amongst coagulation factors, controls diverse aspct of hemostasis and linsks clotting to inflmation and repair

A

Thrombin

64
Q

In coagulation Cascade

X to Xa is what?

A

most central point to both pathways. Activation makes fibrin.

Drugs= block both arms.

65
Q

Needed to produce all coagulation factors, vitamin K deficency results is less coagulation

A

Vitamin K

66
Q

Xa converts what to what?

A

Prothrombin(II) to Thrombin (IIa)

67
Q

Thrombin IIa catalyzes what conversion?

A

Fibrogen to FIbrin

68
Q

Xa inhibitors, Rivaroxaban, Apixanbam all do what?

A

Decrease Thrombin
Block Xa no conversion of prothombrin to thrombin

69
Q

Direct thrombin ibhibitors, hirudin, aragtorban, dabiagatran (PO) all do what?

A

**All decrease Fibrin **
Block conversion of fibrogen to fibrin.

70
Q
  • Glycoprotien
  • Expressed in sub-endothelial cells
  • Major activator of coagulation system
  • Basis for Prothrombin time PT = time for blood clot
  • No contact with circulating bloood
A

Tissue Factor Thromboplastin (extrinsic)

71
Q

Primary event is exposure of tissue factor in sub endothelial cells

Factor VII and VIIa

tissue factor activates X to Xa

A

Extrinsic coagulation cascase

72
Q

Thrombin IIa makes what?

A

MORE THROMBIN

73
Q

Factor VIII and Factor IX are deficient in people with ____, extrinsic tissue factor pathway shut off.

A

Hemophillia

74
Q
  • Produced by endothelial cells (not liver)
  • Circulates bound to vWF
  • Released only at site of damage
  • Platlet agregation & adhesion to each other
A

Factor VIII

75
Q

A VERY important for coagulationNEEDED as cofactor for activation of multiple component complexworking downstream to activate downdstream components

A

Calcium

76
Q

How many complexes come together to changes X to Xa

A

2 complexes

77
Q
  • Phospholipid TF-Bearing
  • Tissue Factor
  • Substrate: Factor X
A

Extrinsic Xase

78
Q
  • Phosopholid: Platelet
  • Enzyme: Factor IXa
  • Co-factor Factor VIII (VIIa) substrate; Factor X
A

Intrinsic Xase

79
Q

Reslts in clot formation, activataton if this enzyme activates platlets and they release calcium.

A

Factor IV (4)

80
Q

EDTA in blood collection tube binds calcium which does what?

A

Prevents clotting

81
Q

Crosslink fibrin make hemostatic plug*
* stabalizes fibrin plug
* absence= inadequate plug formation
* requires calcium as co-factor
* Activated by thrombin

A

Factor 13 (XIII)

82
Q
  • can actiavte factor XI -> XIa
  • Importance in testing of coagulation system
  • activated by contact of (-) charged substances (ex. silica)
  • Basis and inital factor in Parital Thromboplastin time PTT
    *
A

Factor XII Hangeman Factor

83
Q

Add plasma to what to start forming clot in intrinsic pathway? PTT

A

Negatively charged substance, ex.silica

84
Q

Add plasma to what to start forming clot in extrinsic pathway? PT

A

Tissue factor

85
Q

Edma may result in this, compromises resorption of fluid from interstitial spaces.

Ex. parasitic infection filariasis, elephantitis!

A

Lymphatic Obstruction

IHP 1001 (18 decks)

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