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Parker Pathology Block 2 > Hemodynamics 1 > Flashcards

Hemodynamics 1 Flashcards

1
Q

What is edema?

A

swelling of tissue due to increased fluid in interstitial tissue spaces; can be localized or generalized

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2
Q

What is the most common cause of generalized edema?

A

heart failure

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3
Q

What is hydrothorax?

A

fluid in a pleural cavity (pleural effusion)

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4
Q

What is ascites?

A

fluid in the abdominal cavity (peritoneal effusion)

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5
Q

Anasarca is…?

A

generalized edema

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6
Q

Periorbital edema is..?

A

edema around the eyes

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7
Q

Periorbital edema is often the first sign noticed of what condition?

A

nephrotic syndrome

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8
Q

At what age range is nephrotic syndrome most common?

A

2-6 years old

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9
Q

Generalized edema due to renal failure may initially appear in what kind of tissues (general)?

A

loose connective tissue (i.e. around the eye)

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10
Q

If finger pressure on edematous subcutaneous tissue leaves an impression, it is called..?

A

pitting edema

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11
Q

99% of edema what kind of edema?

A

pitting edema

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12
Q

What are the 5 pathophysiologic categories of edema?

A

1) increased hydrostatic pressure
2) decreased plasma osmotic pressure
3) lymphatic obstruction
4) sodium retention
5) inflammation
(they are not mutually exclusive)

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13
Q

How does edema due to increased hydrostatic pressure occur in the leg?

A

It occurs in the leg due to deep venous thrombosis

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14
Q

How does edema due to increased hydrostatic pressure occur in the lungs?

A

left heart failure

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15
Q

How does edema due to increased hydrostatic pressure occur in the lower body?

A

right heart failure

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16
Q

What is the process of edema due to heart failure?

A

Increased hydrostatic pressure; decreased renal blood flow –> activation of renin-angiotensin-aldosterone system –> increased aldosterone –> sodium (and water) retention

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17
Q

Edema from decreased plasma osmotic pressure is a feature of nephrotic syndrome due to..?

A

protein loss through the kidneys

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18
Q

Edema from hepatic cirrhosis can be due to what 2 things?

A

1) increased hydrostatic pressure in portal venous system

2) decreased plasma osmotic pressure due to protein loss into ascites and deficient hepatic protein synthesis

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19
Q

What is the term for generalized edema?

A

anasarca

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20
Q

What is it called when a person has fluid in a pleural cavity?

A

hydrothorax (pleural effusion)`

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21
Q

What is the term for when a person has fluid in their abdominal cavity?

A

ascites (peritoneal effusion)

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22
Q

What is the major protein maintaining plasma oncotic pressure?

A

albumin

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23
Q

What protein accounts for nearly half of total plasma protein?

A

albumin

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24
Q

Hypoalbuminemia that is severe enough to cause generalized edema also causes what?

A

secondary hyperaldosteronism

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25
Q

Hyperaldosteronism causes edema due to what?

A

sodium retention

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26
Q

Hypoalbuminemia causes what 2 categories of edema?

A

1) edema due to decreased plasma osmotic pressure

2) edema due to sodium retention

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27
Q

What is the primary cause of lymphedema?

A

lymphatic obstruction

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28
Q

Is lymphedema usually localized or generalized?

A

localized

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29
Q

Lymphedema can be secondarily caused by (5):

A

tumor, inflammation, surgery, radiation, scar

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30
Q

What is “peau d’orange” referring to clinically?

A

lymphedema due to breast cancer, making the skin resemble an orange peel

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31
Q

Is pulmonary edema common?

A

yes…duh!!

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32
Q

Is pulmonary edema serious?

A

you betcha!

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33
Q

What is the most common cause of pulmonary edema?

A

left heart failure

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34
Q

What are the causes of pulmonary edema (5)?

A

1) left heart failure
2) acute respiratory distress (ARDS)
3) hypersensitivity reactions
4) pneumonia
5) renal failure

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35
Q

What is the gross manifestation of pulmonary edema?

A

clear frothy fluid (pink if blood is mixed in) in the alveoli and, in severe cases, the airways

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36
Q

What are alveoli?

A

airspaces

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37
Q

What is the major symptom of pulmonary edema?

A

dyspnea

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38
Q

What is the major sign of pulmonary edema?

A

pulmonary crackles

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39
Q

What are crackles?

A

an inspiratory crackling sound on listening to the lungs with a stethoscope
(aka “rales”)

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40
Q

Cerebral edema is what?

A

swelling of the brain

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41
Q

What are examples of localized cerebral edema?

A

around abscess or tumor

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42
Q

What is an example of generalized cerebral edema?

A

with encephalitis

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43
Q

What does generalized brain swelling do to sulci and gyri?

A

narrow sulci

swollen gyri

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44
Q

How is cerebral edema fatal?

A

herniation of cerebellar tonsils into foramen magnum compressing the brainstem respiratory center

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45
Q

What is herniation?

A

protrusion of something somewhere it doesn’t belong

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46
Q

What is hyperemia?

A

active increase in arterial blood flow

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47
Q

Why does hyperemia cause a reddish coloration?

A

presence of excess oxygenated blood in tissue

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48
Q

What is the most common cause of hyperemia?

A

inflammation

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49
Q

What is congestion?

A

passive decrease in venous outflow; causes cyanosis

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50
Q

What is cyanosis?

A

an abnormal bluish coloration due to the presence of excess deoxygenated blood in a tissue

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51
Q

What are some common causes of cyanosis?

A

1) congestion
2) pulmonary failure–failure of the lungs to load blood with oxygen
3) anatomic abnormality that causes blood to bypass the lungs and reenter the arterial circulation without getting any oxygen in the lungs

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52
Q

What are some causes “central” cyanosis?

A

1) pulmonary failure–failure of the lungs to load blood with oxygen
2) anatomic abnormality that causes blood to bypass the lungs and reenter the arterial circulation without getting any oxygen in the lungs

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53
Q

Cyanosis that is due to cardiovascular or pulmonary disease tends to first be visible where?

A

around the lips and nailbeds

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54
Q

What condition causes passive congestion of the liver due to the backup of blood inadequately pumped by the heart?

A

right heart failure

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55
Q

Right heart failure congestion is first and worst where?

A

centrilobular areas

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56
Q

What is “nutmeg liver”?

A

alternating red and tan tissue causing the cut surface of liver to resemble the cut surface of nutmeg;
grossly visible nutmeg liver usually shows hemorrhagic necrosis spanning multiple lobules alternating with steatotic areas

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57
Q

What condition is “nutmeg liver” associated with?

A

passive congestion

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58
Q

Chronic sublethal left heart failure causes hemophages to accumulate where?

A

pulmonary alveoli

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59
Q

Chronic sublethal left heart failure causes hemophages to accumulate in pulmonary alveoli. Why does this happen?

A

iron from the blood that has leaks into the alveoli due to capillaries bursting from the high pressure

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60
Q

Hyperemia and congestion have what main thing in common?

A

They both feature abnormal amounts of liquid blood in blood vessels

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61
Q

Are hyperemia and congestion serious conditions?

A

Nope (they are common but have never killed anybody)

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62
Q

What is a hemorrhage?

A

extravasation of blood due to blood vessel rupture

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63
Q

What is a hematoma?

A

when a hemorrhage is enclosed within a tissue

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64
Q

What are petechiae?

A

tiny (1-2 mm) hemorrhages due to platelet deficiency

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65
Q

What are purpura?

A

medium (3-10 mm) hemorrhages due to vasculitis, vessel fragility, etc.

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66
Q

What are ecchymoses?

A

larger (over 1 cm) subcutaneous hemorrhages that go from red-blue to blue-green to gold-brown as the hemoglobin breaks down

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67
Q

What is the common name for ecchymoses?

A

bruise

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68
Q

What are causes of ecchymoses?

A

trauma, vascular fragility

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69
Q

What is a hemothorax?

A

hemorrhage into a pleural cavity

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70
Q

Hemopericardium is…?

A

hemorrhage into the pericardial space

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71
Q

What is hemoperitoneum?

A

hemorrhage into the abdominal cavity

72
Q

What is hemorrhage into a pleural cavity called?

A

hemothorax

73
Q

What is hemorrhage into a pericardial space called?

A

hemopericardium

74
Q

What is hemorrhage into the abdominal cavity called?

A

hemoperitoneum

75
Q

Hemarthrosis is..?

A

hemorrhage into a joint

76
Q

Hemarthrosis is commonly associated with what condition?

A

hemophilia

77
Q

The mortality associated with hemorrhages depends on what 2 things?

A

1) location (leg is more trivial than brain)

2) timing (slow is more trivial than fast)

78
Q

Hemostasis is most often defined as what?

A

the formation of a blood clot (hemostatic plug) at the site of vascular injury

79
Q

What is the less commonly used definition for hemostasis?

A

the maintenance of blood in a free-flowing liquid state in normal blood vessels

80
Q

What 3 components regulate hemostasis?

A

1) vascular wall (endothelium)
2) platelets
3) coagulation cascade

81
Q

What are the contents of platelets (6)?

A

ADP, fibrinogen, clotting factors V and VIII, calcium, and epinephrine

82
Q

Do platelets have a nucleus?

A

NO

83
Q

What are the 4 stages of hemostasis at a site of vascular injury?

A

1) vasoconstriction
2) primary hemostasis
3) secondary hemostasis
4) thrombus and antithrombotic events

84
Q

What is endothelin?

A

a potent endothelium-derived vasoconstrictor

85
Q

What stage of hemostasis at a site of vascular injury involves brief arteriolar vasoconstriction?

A

stage 1 (vasoconstriction)

86
Q

What mediates stage 1 of hemostasis at a site of vascular injury?

A

reflex neurogenic mechanisms that are augmented by local secretion of vasconstrictors (endothelin, etc.)

87
Q

What stage of hemostasis at a site of vascular injury involves platelet adhesion to thrombogenic extracellular matrix, forming a primary hemostatic plug?

A

stage 2 (primary hemostasis)

88
Q

What mediates platelet adhesion to ECM?

A

von Willebrand factor binding to platelet GpIb receptors

89
Q

Von Willebrand factor binding to platelet GpIb receptors causes what change in the platelets?

A

changes shape from smooth disks to spheres with long spiky projections –> facilitates platelets aggregation

90
Q

In stage 2 of hemostasis at a site of vascular injury, platelets changing shape causes a conformational change in what receptor?

A

GpIIb/IIIa

91
Q

What does the conformational change induced by ADP in platelet GpIIb/IIIa make the receptor bind to that leads to platelet aggregation?

A

fibrinogen

92
Q

What 2 things are released from platelets in stage 2 of hemostasis at a site of vascular injury?

A

ADP and TXA2

93
Q

What stage of hemostasis at a site of vascular injury is associated with the coagulation cascade?

A

stage 3 (secondary hemastasis)

94
Q

What factors activate the coagulation cascade?

A

tissue factor and platelet factors

95
Q

What is tissue factor?

A

membrane-bound procoagulant made by endothelium); it is also called clotting factor III

96
Q

What is thromboplastin?

A

laboratory reagent containing phospholipids and tissue factor

97
Q

What does thrombin do (5 things)?

A

1) converts fibrinogen to fibrin
2) stimulates platelets to release TXA2
3) activates monocytes and lymphocytes
4) stimulates endothelial cells to adhere to neutrophils
5) stimulates endothelial cells to release NO, tissue plasminogen activator and prostacyclin

98
Q

What stage of hemostasis at a site of vascular injury is associated with the formation of a solid, semipermanent plug of aggregated platelets and polymerized fibrin?

A

stage 4 (thrombus and antithrombotic events)

99
Q

How is a hemostatic plug limited to the site of injury?

A

thrombomodulin is expressed on the surface of endothelial cells –> binds to thrombin to activate protein C

100
Q

How does the body break down clots?

A

fibrinolytic system

101
Q

What are the components of the fibrinolytic system?

A

t-PA, plasmin, tissue factor pathway inhibitor, antithrombin III, heparin-like molecules, protein S, urokinase

102
Q

Deficiency in what factor leads to a tendency to bleed excessively with surgery or menstruation?

A

von Willebrand factor

103
Q

What is the name of the disease that causes a tendency to bleed excessively with surgery or menstruation?

A

von Willebrand disease

104
Q

Overactivity of what factor leads to a tendency to clot in small blood vessels and then bleed from having used up too many platelets and clotting factors? What is the name of the disease?

A

von Willebrand factor; Thrombotic thrombocytopenic pupura

105
Q

Deficiency of platelet GpIb receptors for von Willebrand factor leads to a bleeding tendency in a disease called…?

A

Bernard-Soulier syndrome

106
Q

Deficiency of platelet GpIIa/IIIa receptors causes bleeding tendency due to deficient platelet aggregation in a disease called…?

A

Glanzmann thrombasthenia

107
Q

Some snake venoms can mimic Glanzmann thrombasthenia by binding to what?

A

GpIIb/IIIa receptors

108
Q

What is the drug that works by binding to GpIIb/IIIa receptors and is given to patients who are clotting off their coronary arteries?

A

Eptifibatide (Integrilin)

109
Q

What does clopidogrel (Plavix) do?

A

blocks platelet ADP receptors (taken by patients who have clotting of critical coronary or cerebral arteries)

110
Q

What is thrombosis?

A

inappropriate formation of blood clot in a blood vessel, usually occlusive

111
Q

What are the 3 predisposing factors for thrombosis?

A

1) endothelial injury
2) abnormal blood flow (turbulence or stasis)
3) hypercoagulability

112
Q

What is the most important factor predisposing thrombosis?

A

endothelial injury

113
Q

What different stresses/toxicities can cause increased endothelial precoag. factors or decrease anticoag. factors (causing thrombosis)?

A

hemodynamic stress of hypertension, toxicity of hypercholesterolemia, products absorbed from smoking

114
Q

Is thrombosis more common in veins or arteries?

A

veins

115
Q

Is thrombosis more serious in veins or arteries?

A

arteries

116
Q

Most people die of what 2 things? (according to Nichols)

A

thrombosis or hemorrhage

117
Q

What are the congenital (genetic) hypercoagulable states?

A
  • Factor V leiden mutation
  • prothrombin gene mutation
  • methyl-tetra-hydro-folate reductase gene mutation
  • anti-thrombin 3 deficiency
  • protein C deficiency
  • protein S deficiency
118
Q

What are the acquired hypercoagulable states?

A
  • surgery
  • cancer
  • trauma
  • bed-ridden state
  • disseminated intravascular coagulation
  • heparin-induced thrombocytopenia
  • antiphospholipid syndrome
119
Q

Hypercoagulable states dispose to what type of thrombus (venous or arterial)?

A

venous

120
Q

What is the most common inherited hypercoagulable state (5% of whites)?

A

Factor V Leiden mutation

121
Q

What are the risks for venous thrombosis for heterozygotes and homozygotes with Factor V Leiden?

A

Hetero - 5-fold higher

Homo- 50-fold higher

122
Q

What does the mutation in Factor V Leiden do to the patient?

A

the mutation in clotting factor V makes it resistant to activated protein C, resulting in loss of an important clot-limiting counter-regulatory mechanism

123
Q

What is the second most common inherited hypercoagulable state (2% of whites)?

A

Prothrombin G20210A mutation

124
Q

Prothrombin G20210A mutation causes __-fold risk of venous thrombosis.

A

3

125
Q

How does surgery lead to hypercoagulability?

A

Surgery cuts blood vessels, which activates platelets and clotting factors that are not used at the surgical site. Some of them get swept away into the general circulation and therefore lead to hypercoagulability.

126
Q

How does cancer lead to hypercoagulability?

A
  • inflammatory response of malignant tumors
  • necrosis of malignant tumors that have outgrown their blood supply (releasing thrombogenic necrotic debris into general circulation)
  • malignant tumors can compress veins or invade them, creating turbulent flow or statis of blood
127
Q

Why is antiphospholipid antibody syndrome life-threatening?

A

it causes arterial thrombosis

128
Q

What population of people is antiphospholipid antibody syndrome most common in?

A

young females (5% in pregnant women, 15% in women with recurrent miscarriages)

129
Q

Why is “lupus anticoagulant” a double misnomer?

A

most patients with them do not have lupus and all are hypercoagulable

130
Q

Patients presenting with recurrent miscarriages, DVTs in their legs, cerebral infarctions, migraine headaches, cardiac vegetations, ischemic hands or feet, thrombocytopenia, etc. most likely have ________?

A

antiphospholipid antibody syndrome (although 1-5% of patients are asymptomatic)

131
Q

Patients with antiphospholipid antibody syndrome have autoantibodies against what?

A

plasma protein antigens unveiled by binding to phospholipids

132
Q

What are the 3 types of thrombi?

A

1) arterial (“white thrombi”)
2) venous (“red thrombi”)
3) mural

133
Q

Which type of thrombus is rich in erythrocytes?

A

venous

134
Q

Which type of thrombus is rich in platelets?

A

arterial

135
Q

Which type of thrombus in located in the wall of the heart?

A

mural

136
Q

What type of thrombus is most commonly at sites of stasis and tend to grow on the side closer to the heart?

A

venous

137
Q

What part of a thrombus is most likely to be organized and densely adhered to blood vessel?

A

oldest parts

138
Q

What part of a thrombus is most likely to break off and be carried with the blood stream (embolization)?

A

newest parts

139
Q

What is a cause of false negatives in ultrasound testing for deep venous thrombosis of the leg?

A

obesity

140
Q

What are vegetations?

A

thrombi on heart valves

141
Q

Vegetations are mostly in the category of _______ before infection.

A

non-bacterial thrombotic endocarditis/marantic endocarditis

142
Q

Vegetations are mostly in the category of _______ after infection.

A

infective endocarditis

143
Q

Libman-Sacks endocarditis in systemic lupus erythematosus is a form of a ________ vegetation.

A

autoimmune

144
Q

The bigger the vegetation, the _______(more/less) likely it is infected.

A

more

145
Q

The four fates of thrombus are:

A

1) dissolution
2) propagation
3) embolization
4) organization (and recanalization)

146
Q

What is a PICC line? What is the major risk of using one?

A

peripherally inserted central catheters; DVT in arm of the patient

147
Q

Intravascular catheters and cardiac pacer wires always form _____, which causes a risk of embolization and infection.

A

clots

148
Q

What is organization?

A

ingrowth by fibroblasts, who convert thrombus to fibrous tissue, with ingrowth of new capillaries, which can coalesce to recanalize a thrombosed blood vessel

149
Q

What happens to a thin-walled vein when you pull out a long-dwelling catheter with an organized thrombus around it continuous with the lining of the vein?

A

thromboembolism

150
Q

What is an embolus?

A

detached intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin

151
Q

What are types of emboli?

A

thrombus (*most common), atheromatous debris, fat, air, amniotic fluid, fragment of tumor

152
Q

What is the main source of pulmonary thromboemboli? What are other sources?

A

Main source: DVT in the thighs

Others: PICC lines in arms, pelvic veins

153
Q

What percent of pulmonary thromboemboli are clinically silent?

A

~ 80%

154
Q

What are “saddle emboli”?

A

emboli in the pulmonary trunk

155
Q

What are paradoxical emboli?

A

emboli that pass through a patent foramen ovale or atrial septal defect to go to organs besides the lungs (rare)

156
Q

Small emboli can often cause ____?

A

pulmonary hypertension

157
Q

Systemic thromboemboli are most commonly from the ______ and most commonly travel to the ______ and ______.

A

heart (80%); legs (75%) and brain (10%)

158
Q

Where is fat embolism most commonly from?

A

long bone fractures

159
Q

What often causes a syndrome of sudden onset dyspnea, tachypnea, tachycardia, irritability, restlessness, anemia, and thrombocytopenia usually 1-3 days following trauma?

A

fat embolism

160
Q

Why can sickle cell disease causing bone infarcts be fatal?

A

fat embolism from the bone infarcts

161
Q

What are causes of air embolism?

A

1) getting air into an IV infusion
2) sudden change in atmospheric pressure
3) chest wall injury
4) back surgery in a prone position

162
Q

How may mL of air embolism are needed to have any clinical effect?

A

100 mL

163
Q

Can an air embolism be fatal?

A

YES

164
Q

What are causes of amniotic fluid embolism?

A

tears in the placental membranes during the course of labor and delivery, leading to squamous cells, lanugo hair, vernix caseosa fat and mucin in the pulmonary microcirculation

165
Q

What could a syndrome of sudden severe dyspnea, cyanosis and shock during labor or delivery be due to?

A

amniotic fluid embolism (rare)

166
Q

What is an infarct?

A

area of ischemic necrosis (death of organ or tissue)

167
Q

What is an area of ischemic necrosis leading to an infarct usually due to?

A

thrombotic or embolic occlusion of an artery

168
Q

What are other less common causes of an infarct (besides thrombi or emboli)?

A
  • vasospasm
  • atheroma expansion by intraplaque hemorrhage
  • tumor compressing an artery
  • twisting of blood vessels (torsion or volvulus)
  • trauma
  • incarcerated hernia
169
Q

What is the most common histologic form of infarct?

A

coagulative necrosis

170
Q

What are the characteristics of coagulative necrosis? (timing and response)

A
  • apparent after 12-18 hours

- usually elicits acute inflammatory response

171
Q

Where is ischemic necrosis liquefactive?

A

brain

172
Q

What are the 4 things that determine the likelihood of an infarction?

A

1) organ’s vulnerability to hypoxia
2) rate of development of vascular occlusion
3) nature of an organ’s blood supply (i.e. dual supply of liver)
4) oxygen content of the blood

173
Q

What are the 5 aspects to systematically describe lesions?

A

1) size
2) shape
3) color
4) consistency/texture
5) relationships

174
Q

What type of infarcts are typical of solid organs with end-arterial circulation?

A

white anemic

175
Q

What organs would have white anemic infarctions?

A

kidney, heart, spleen

176
Q

What organs would have red hemorrhagic infarctions?

A

ovary, lung, intestines

177
Q

What type of infarcts are typical with venous occlusion, dual or anastomosing blood supply, or with reperfusion?

A

red hemorrhagic

Parker Pathology Block 2 (2 decks)

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