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
# Impaired venous return Causes What? the lower extremity may cause edema restricted to the distal portion of the affected leg, | deep venous thrombosis
Increase in Hydrostatic Pressure
26
# Impaired venous return Causes What? leads to a systemic increase in venous pressure and, often, widespread edema. | Congestive Heart faliue
Increase in hydrostatic pressure
27
# 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
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.
28
Reduced cardiac output leads to pooling of blood in the _____ and** increased capillary hydrostatic pressure**
venous circulation
29
The **Reduction in cardiac output a**lso results in hypoperfusion of the kidneys, triggering the renin-angiotensin-aldosterone axis and inducing ______ (secondary hyperaldosteronism).
Sodium and water retention | secondary hyperaldosteronism
30
Reduced plasma albumin is a common feature of disorders in which edema is caused by ____
Decreases in colloid osmotic pressure
31
**Protien.** Accounts for almost half of the total plasma protein and is the **biggest contributor to colloid osmotic pressure.**
Albumin
32
# All result in? * Nephrotic syndrome * Reduced albumin synthesis is seen in the setting of severe liver disease (e.g., cirrhosis) * protien malnutriotion
Decrease of Osmotic pressure (protien out)
33
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 **
Retention of Salt; Na+ and K
34
defined as the **extravasation of blood from vessels**, results from damage to blood vessels and may be exacerbated by defects in blood clotting.
Hemorrhage
35
* Trauma * atherosclerosis * inflammatory or neoplastic erosion of a vessel wall also may lead to::
Hemmorage
36
# What kind of hemorrhage? Hemorrhage may take the form of external bleeding or may accumulate within a tissue **no iron deficiency**
Hematoma | Bruises or massive retroperitoneal hematoma rupure in aorta, hemothorax
37
# What kind of hemorrhage? minute (1 to 2 mm in diameter) hemorrhages into skin, mucous membranes, or serosal surfaces Low platlet count, or defective platlet function
Petechiae
38
# What kind of hemorrhage? lightly larger (3 to 5 mm) hemorrhages Caused by trauma, vascular inflammation (vasculitis), and increased vascular fragility
Purpura
39
# What kind of hemorrhage? larger (1 to 2 cm) 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
Ecchymoses
40
relatively trivial in the subcutaneous tissues may cause death if located in the ___
Brain bleed
41
chronic or recurrent external blood loss can lead to a what defiinceny? | Peptic ulcer or menstration
Anemia; iron deficiency
42
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.
Homeostatis
43
1st. markedly reduces blood flow to the injured area * local seretion of endothelin **vasoconstrictor** | Transient effect, bleeding will resume
Arteriolar vasoconstriction
44
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**
Primary hemostasis: the formation of the platelet plug.
45
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
Secondary hemostasis: deposition of fibrin. Vascular injury exposes tissue factor
46
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
Clot stabalization
47
potent endothelium-derived vasoconstrictor.
endothelin
48
molecule that promotes platelet adherence and activation produced by enothelial cells
von Willebrand factor (VWF)
49
What are 2 secretory granuales released by activated platlets?
ADP & TXA2 (vasoconstrictor)
50
a **membrane-bound procoagulant glycoprotein**that is normally expressed by subendothelial cells in the vessel wall, such as smooth muscle cells and fibroblasts.
tissue factor
51
Tissue factor binds and activates factor ?
Factor VII (7) | Sets action of cascade that makes Thrombin
52
**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.
Thrombonin
53
Insoluble fibrin mesh does what? Green.
Prevent blood loss, forms plug to stop bleeding.
54
Acute phase protiens Il-1, Il-6 and TNF is released from kidney along with what?
Fibrogen proteins
55
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)
Coagulation Factors
56
when coagulation factors activate, many become protien cleaves enzymes that contains serine .
Serine proteases
57
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.
Coagulation Casacade
58
Assesses the function of the proteins in the **extrinsic pathway** (factors X, VII, V, II [prothrombin], and fibrinogen).
prothrombin time (PT) | Lab test
59
assesses the function of the proteins in the **intrinsic pathway** (factors XII, XI, X, IX, VIII, V, II, and fibrinogen).
partial thromboplastin time (PTT) | Lab test
60
# what pathway? Deficiencies of factors V, VII, VIII, IX, and X are associated with ____ and prothrombin deficiency is incompatible with life.
moderate to severe bleeding
61
Deficiency in XI causes
only causes a mild bleeding disorder
62
Deficiency in XII causes
No bleeding disorder
63
What is **most important control** amongst coagulation factors, controls diverse aspct of hemostasis and linsks clotting to inflmation and repair
Thrombin
64
# In coagulation Cascade X to Xa is what?
most central point to both pathways. Activation makes fibrin. | Drugs= block both arms.
65
Needed to produce all coagulation factors, vitamin K deficency results is less coagulation
Vitamin K
66
Xa converts what to what?
Prothrombin(II) to Thrombin (IIa)
67
Thrombin IIa catalyzes what conversion?
Fibrogen to FIbrin
68
Xa inhibitors, Rivaroxaban, Apixanbam all do what?
**Decrease Thrombin** Block Xa no conversion of prothombrin to thrombin
69
Direct thrombin ibhibitors, hirudin, aragtorban, dabiagatran (PO) all do what?
**All decrease Fibrin ** Block conversion of fibrogen to fibrin.
70
* 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
Tissue Factor Thromboplastin (extrinsic)
71
Primary event is exposure of tissue factor in sub endothelial cells Factor VII and VIIa tissue factor activates X to Xa
Extrinsic coagulation cascase
72
Thrombin IIa makes what?
MORE THROMBIN
73
Factor VIII and Factor IX are deficient in people with ____, extrinsic tissue factor pathway shut off.
Hemophillia
74
* Produced by endothelial cells (not liver) * Circulates bound to vWF * Released only at site of damage * Platlet agregation & adhesion to each other
Factor VIII
75
A VERY important for coagulation**NEEDED as cofactor for activation of multiple component complex**working downstream to activate downdstream components
Calcium
76
How many complexes come together to changes X to Xa
2 complexes
77
* Phospholipid TF-Bearing * Tissue Factor * Substrate: Factor X
Extrinsic Xase
78
* Phosopholid: Platelet * Enzyme: Factor IXa * Co-factor Factor VIII (VIIa) substrate; Factor X
Intrinsic Xase
79
Reslts in clot formation, activataton if this enzyme activates platlets and they release calcium.
Factor IV (4)
80
EDTA in blood collection tube binds calcium which does what?
Prevents clotting
81
**Crosslink fibrin make hemostatic plug*** * stabalizes fibrin plug * absence= inadequate plug formation * requires calcium as co-factor * Activated by thrombin
Factor 13 (XIII)
82
* 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 *
Factor XII Hangeman Factor
83
Add plasma to what to start forming clot in intrinsic pathway? PTT
Negatively charged substance, ex.silica
84
Add plasma to what to start forming clot in extrinsic pathway? PT
Tissue factor
85
Edma may result in this, compromises resorption of fluid from interstitial spaces. Ex. parasitic infection filariasis, elephantitis!
Lymphatic Obstruction