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Robbins' Basic Pathology > Robbins Ch. 3: Hemodynamics, Thromboembolism, and Shock > Flashcards

Robbins Ch. 3: Hemodynamics, Thromboembolism, and Shock Flashcards

1
Q

What is the process of blood clotting that prevents excessive bleeding after blood vessel damage?

A

hemostasis

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2
Q

What can a massiven and rapid hemorrhage lead to?

A

hypotension
shock
death

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3
Q

What is inappropriate clotting?

A

thrombosis

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4
Q

T or F: thromboembolism can cause an Mis, strokes, and pulmonary embolisms.

A

T

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5
Q

T or F: There is an increase in blood volume within a tissue during hyperemia and a decrease of blood volume in a tissue during congestion.

A

F: they BOTH refer to an inc in blood volume within a tissue–hyperemia = inc inflow and congestion = dec outflow

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6
Q

Why are hyperemic tissues redder than normal?

A

they are engorged with oxygenated blood

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7
Q

____ is an active process while ______ is a passive process (blanks are either hyperemia or congestion)

A 
hyperemia = active
congestion = passive
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8
Q

T or F: congestion can be both localized or systemic.

A

true: systemic occurs w/ heart failure

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9
Q

What are some consequences of chronic congestion?

A
  1. inadequate perfusion/persistant hypoxia –> parenchymal cell death and secondary tissue fibrosis
  2. inc intravascular pressure –> edema and focal hemorrages (from ruptured capillaries)
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10
Q

What is the difference between acute pulmonary congestion and chronic pulmonary congestion?

A

acute: blood engorged alveolar capillaries, alveolar septal edema, intra-alveolar hemorrhage
chronic: thicked and fibrotic septa, hemosiderin filled macrophages in alveolar spaces

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11
Q

What is the difference between acute hepatic congestion and chronic passive congestion of the liver?

A

acute: central veins and sinusoids distended with bood, loss of central hepatocytes due to necrosis, reversible fatty change in periprtal hepatocytes
chronic: central region of hepatic lobules are red-brown and slightly depressed (due to cell loss) and are surrounded by uncongested tan/fatty liver = “nutmeg liver”; hemosiderin in macrophages, cirrosis

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12
Q

___% of lean body weight is water and ___% of it is intracellular

A

60%; 66%

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13
Q

___% of the body’s water is in the plasma

A

5%

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14
Q

T or F: edema is the accumulation of extracellular fluid within tissues.

A

T: specifically, interstitial fluid

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15
Q

Ascities is the accumulation of fluid within the ____ cavity

A

peritoneal

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16
Q

Liver cirrosis (ascities) can cause edema 2 ways:

A
  1. impaired venous return

2. reduced plasma osmotic pressure (hypoproteinemia)

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17
Q

What can cause a reduction in the plasma osmotic pressure (leading to edema)? (4)

A
  1. protein loss in due to a glomerulopathy
  2. liver cirrhosis
  3. malnutrition
  4. protein losing gastroenteropathy
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18
Q

What can impair venous return (leading to edema)?

A
  1. congestive heart failure
  2. constrictive pericarditis
  3. Ascites (liver cirrhosis)
  4. venous obstruction or compression (thrombosis, external pressure (mass), and lower extremity inactivity)
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19
Q

Describe how the fluid movement between vascular and interstitial spaces is maintained in physiological state (no disease).

A

The inc hydrostatic pressure at the arteriolar end causes fluid to move from the vasculature to the interstitial spaces. This is balanced out by the slightly elevated osmotic pressure at the venular end which causes fluid to move back into the vasculature.

Ultimately, there is a slight net outflow of fluid into the interstitium but this is drained/returned to the blood stream by the lymphatic system through the thoracic duct

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20
Q

_____ hydrostatic pressure or _______ plasma osmotic pressure leads to extravascular fluid accumulation.

A

increased; decreased

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21
Q

T or F: if the capacity of the lymphatic system is exceeded, edema will result

A

true

22
Q

When is edema caused by transudate and when is it caused by exudate:

A

transudate: when there is inc hydrostatic or dec osmotic pressure
exudate: when there is inc vascular permeability due to inflammation

23
Q

Describe how heart failure leads to edema

A
  1. inc in capillary hydrostatic pressure –> EDEMA
  2. dec cardiac output–> dec renal blood flow –> activation of renin-angiotensin-aldosterone system –> retention of Na and H2O –> inc blood volume –> EDEMA
24
Q

What is the role of secondary hyperaldosteronism in an individual with normal heart function? What is the role of 2ndary hyper aldosteronism in dec albumin levels?

A

normal heart: The Na and H2O retention signals the heart to inc output so restore blood flow to the kidneys

dec albumin: 2ndary hyperaldosteronism is triggerd and makes the generalized edema worse bc this process does not address the primary defect, low plasma albumin/protein

25
Q

How can edema due to inc hydrostatic pressure we remedied?

A
  1. restore cardiac output

2. restore Na and H2O retention by (A) dec Na in diet, (B) administer diuretics, or (C) admin aldosterone antagonist

26
Q

How does nephrotic syndrome lead to edema?

A

glomerular capillaries become leaky –> albumin and other plasma proteins are excreted in urine –> dec in osmotic pressure –> edema

27
Q

T or F: The synthesis of albumin decreases in the setting of liver cirrhosis.

A

True –> leads to dec in osmotic pressure –> edema

28
Q

Why does low albumin plasma levels lead to a vicious circle of edema?

A

low albumin causes edema –> edema reduces intravascular pressure –> renal hypoperfusion –> 2ndary hyperaldosteronism –> inc Na and H2O retention –> more edema –> cycle continues

29
Q

Lymphendema usually results from a _____ caused by a _____ or ______ condition.

A

localized obstruction

inflammatory or neoplastic condition

30
Q

Why does excessive retention of salt lead to edema?

A

water follows it into the bloodstream and causes an inc in hydrostatic pressure which in turn reduces plasma osmotic pressure

31
Q

Edema due to _________ often maniests first in loose connective tissues (i.e. eyelinds –>periorbital edema)

A

renal dysfunction or nephrotic syndrome

32
Q

T or F: brain edema can be localized or generalized

A

T: localized due to abscess or tumor and generalized

33
Q

Why can extensive hemorrhages result in jaundice?

A

massive breakdown or RBCs and hemoglobin

34
Q

Where are petechiae found?

A

skin, mucous membranes, and serosal surfaces

35
Q

What accounts for the color change in bruises?

A

enzymatic conversion of hemoglobin to bilirubin to hemosiderin (within a macrophage?)

36
Q

T or F: internal bleeding leads to an iron deficiency.

A

False: internally, iron is able to be efficiently recycled from phagocytosed RBCs

37
Q

T or F: Normal (resting) endothelium express anticoagulant factors.

A

true: once activated they express pro-coagulant factors

38
Q

What molecules does normal endothelium express to inhibits thrombosis and what does each one inhibit/activate? (5)

A
  1. secrete PGI2 (aka prostacyclin), NO, and ADPase: inhibit platelet aggregation and vasodilate
  2. secretes heparin like molecules that bind Antithrombin III: inactivate thrombin and factors IXa and Xa)
  3. Thromodulin: binds Thrombin and modulates thrombin’s activity so that it cleaves protein C to activate it (as opposed to cleaving fibrinogen into fibrin to form a clot)** protein C binds protein S (made by endothelium) and together they inactivate factor Va and VIIIa
  4. TFPI: inactivates tissue factor-VIIa complex and factor Xa
  5. t-PA: cleaves plasminogen to plasmin –> activates fibrinolysis to cleave fibrin

SEE pg 12-13 of Robbins

39
Q

T or F: von Williebrand factor functions as a platelet aggregation molecule

A

F: it binds platelets to subendothelial collagen–it does not directly cause platelet aggregation

40
Q

What does vWF bind on platelets to make them adhere to the endothelium?

A

GpIb (glycoprotien/platelet receptor

41
Q

Platelet aggregation is accomplished by ____ binding to platelet _____ receptors on diff platelets.

A

fibrinogen to GpIIb-IIIa receptors

42
Q

In response to _______ endothelial cells produce _____ and downregulate ______ to promote thrombosis.

A

TFN and IL-1 (or an endotoxin)
produce tissue factor
downregulate thrombomodulin

43
Q

Once activated, endothelial cells secrete _____ to limit fibrinolysis

A

PAIs (plasminogen activator inhibitors)

44
Q

When is vWF present?

A

after loss of endothelial integrity it becomes exposed and will bind platelets

45
Q

ADP is a … and made by…

A

potent activator of resting platelets

made by platelets and is released from their granules once the platelet is activated

46
Q

TXA2 is made by ___ and its role is …

A

made by ACTIVATED platelets and activates nearly platelets and is a potent vasoconstrictor

47
Q

What are the differences between a resting and an activated platelet?

A
  1. smooth to spiky –> inc SA for coag factors and agg
  2. activated platelets inc expression of neg charged phospholipids which are binding sites for calcium and coagulation factors
  3. conf change in GpIIb/IIIb that permits its binding to fibrinogen
48
Q

_____ leads to an irreverisble shape change and release of platelet granule contents

A

platelet adhesion (via cWF and GpIb)

49
Q

Deficiency of GpIIb/IIIb causes…

A

glanzmann thrombasthenia = platelets cannot aggregate

**target for antithrombotic agents

50
Q

Concurrent platelet Aggregation and activation of the coagulation cascade generates ____

A

thrombin

51
Q

PGI2 is made by ____ and acts as ____

A

made by normal endothelium

vasodilator, inhibits platelet aggregation

52
Q

How is asprin a potent anti-coagulant.

A

it permanently inhibits COX-2 which produces TXA2 production in platelets (a pro-coagulant factor) and PGI2 in endothelium (an anti-coag factor). The platelets are unable to synthesize new COX (no nucleus) however, endothelium is so PGI2 effects dominate = anti-coagution

Robbins' Basic Pathology (5 decks)

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