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CMD Block 2 > Hemodynamics-1 Lecture and Word Doc > Flashcards

Hemodynamics-1 Lecture and Word Doc Flashcards

1
Q

What is edema?

A

Swelling of tissue due to increased fluid in interstitial tissue spaces

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2
Q

What is ascities?

A

Fluid in the abdominal cavity

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3
Q

What is anasarca?

A

Generalized edema

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4
Q

What is hyperemia?

A

An active increase in arterial blood flow

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5
Q

What is congestion?

A

Passive decrease in venous flow

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6
Q

What is a hemorrhage?

A

Extravasation of blood due to blood vessel rupture

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7
Q

What is petechia?

A

Tiny (1-2 mm) hemorrhage due to platelet deficiency

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8
Q

What is hematoma?

A

A hemorrhage enclosed within a tissue

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9
Q

What is hemostasis?

A

(1) the maintenance of blood in a free-flowing liquid state in normal blood vessels and (2) the formation of a blood clot at a sit of vascular injury

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10
Q

What is a hemostatic plug?

A

Another term for blood clot

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11
Q

What are platelets?

A

Anucleate cellular components of blood

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12
Q

What are platelets important in?

A

Initiation and propagation of clotting

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13
Q

T or F: Platelets have granules.

A

True

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14
Q

What is thrombosis?

A

Inappropriate formation of blood clot in a blood vessel

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15
Q

T or F: Blood clots formed during thrombosis are not usually occlusive.

A

False

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16
Q

What is hypercoagulability?

A

Abnormal tendency to form clots

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17
Q

What is coagulopathy?

A

Abnormal tendency to bleed

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18
Q

What is an embolus?

A

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

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19
Q

What is an infarction?

A

Area of ischemic necrosis

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20
Q

What are the 2 types of edema?

A

Localized and generalized

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21
Q

Where does generalized edema initially appear?

A

Tissues with a loose connective tissue matrix (i.e. around the eyes = periorbital edema)

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22
Q

What is pitting edema?

A

Transient pit in the skin at the site of finger pressure

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23
Q

Important concept 1: What are four most common causes of edema?

A

Increased hydrostatic pressure
Decreased plasma oncotic pressure
Sodium retention
Inflammation

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24
Q

What can cause edema in the lungs due to increased hydrostatic pressure?

A

Left heart failure

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25
Q

What can cause edema in the lower body due to increased hydrostatic pressure?

A

Right heart failure

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26
Q

What can cause edema in the leg body due to increased hydrostatic pressure?

A

Venous thrombosis

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27
Q

What is dependent edema?

A

Edema that worsens due to gravity

**when in lying down, dependent edema is worse in the sacrum and when standing, it is worse in the legs

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28
Q

T or F: dependent edema is specific to increased hydrostatic pressure as the etiology

A

false

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29
Q

What can nephrotic syndrome (protein loss) cause?

A

Edema due to decreased plasma osmotic pressure

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30
Q

Why can hepatic cirrhosis lead to edema?

A

It causes…

  1. an increase in the hydrostatic pressure in the portal venous system
  2. a decrease in the plasma osmotic pressure due to protein loss from (a) proteins going into ischities and (b) deficient hepatic protein synthesis
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31
Q

What usually causes edema due to sodium retention?

A

Heart or renal failure

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32
Q

Edema due to sodium retention is always ___(type of edema) _____ and seen with ______. (this is testing you ability to read minds too)

A

Generalized; increased hydrostatic pressure

(and, to a lesser extent, dilutional decrease in plasma osmotic pressure

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33
Q

Where does localized edema due to inflammation present?

A

At the site of infection

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34
Q

Generalized edema due to inflammation is seen with _______

A

SIRS or sepsis

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35
Q

What type of edema is associated with edema due to lymphatic obstruction (lymphedema)?

A

Usually localized

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36
Q

What causes edema due to lymphatic obstruction (lymphedema)?

A 
Tumor
Inflammation
Surgery
Radiation
Scar
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37
Q

What is peau d’ orange?

A

Lymphedema due to breast cancer (causes skin over tumor to resemble the skin of an orange)

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38
Q

What is the most common cause of pulmonary edema?

A

Left heart failure

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39
Q

Describe the fluid that can be aspirated from pulmonary edema.

A

Frothy fluid (pink if blood in it)

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40
Q

What symptom is associated with pulmonary edema? Sign?

A 
Dyspnea (symptom)
Pulmonary crackles (sign)
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41
Q

Important Concept 2: Pulmonary edema is common and (serious or not serious)

A

serious

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42
Q

Cerebral edema can be localized as a(n) ____ or _____

A

Abscess or tumor

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43
Q

Describe the (gross?) morphology of generalized cerebral edema.

A

Swollen gyri and narrowed sulci all over brain

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44
Q

Important concept 3: Brain edema can be fatal and due to ____

A

Herniation of cerebellar tonsils into foramen magnum which compresses the brainstem (respiratory center)

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45
Q

Erythema is _____

A

Hyperemia

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46
Q

Cyanosis is _____

A

Congestion

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47
Q

When heart failure causes cyanosis/congestion, the patient often will also have ______ and ______

A

“Nutmeg liver”: alternating red centrilobular and tan peripherilobular tissue (whatever the fuck that is)

AND

hemophages in pulmonary alveoli

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48
Q

Important concept 4: Hyperemia and congestion are common and (serious or not serious)

A

Not serious

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49
Q

What is purpura?

A

Medium (3-10 mm) bleed due to vasculitis, vessel fragility, etc.

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50
Q

What is ecchymosis?

A

Larger (over 1 cm) subcutaneous hemorrhage that goes from red-blue → blue green → gold-brown as the hemoglobin breaks down

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51
Q

What is a hemothorax?

A

Hemorrhage into pleural cavity

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52
Q

What is the size of a pupra?

A

3-10 mm

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53
Q

What is the size of an ecchymosis?

A

Over 1 cm

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54
Q

Important concept 5: hemorrhages are common and (serious or not serious) and described with a large number of precise terms that are commonly used imprecisely

A

serious

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55
Q

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

A
  1. vasoconstriction
  2. primary hemostasis
  3. secondary hemostasis
  4. thrombus and antithrombic events
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56
Q

Describe stage 1 of hemostasis at the site of vascular injury. What mediates it and augments it.

A

Brief arteriolar vasoconstriction mediated by reflex neurogenic mechanism and augmented by local secretion of vasoconstrictors (i.e. endothelium, a potent endothelium-derived vasoconstrictor)

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57
Q

What is endothelin?

A

a potent endothelium-derived vasoconstrictor; mediates the first stage (vasoconstriction) of hemostasis at the site of vascular injury

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58
Q

Describe stage 2 of hemostasis at the site of vascular injury.

A

Primary homeostasis:

  1. platelet adhesion to thrombogenic ECM
  2. Activation and shape change
  3. GpIIb/IIIa receptor expressed (binds fibrinogen and mediates aggregation)
  4. Release of ADP and TXA2
  5. Platelet recruitment and aggregation
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59
Q

What is GpIIb/IIIa?

A

A receptor that is expressed on the surface of platelets after they become activated. This receptor binds fibrinogen and mediates aggregation.

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60
Q

What is released during primary homeostasis? Who releases this?

A

ADP and TXA2

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61
Q

Describe stage 3 of hemostasis at the site of vascular injury.

A

Secondary Hemostasis

  1. activation of the coag cascade by tissue factor and platelet factors
  2. culminates in conversion of fibrinogen to fibrin by activated thrombin
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62
Q

What is (/describe) the tissue factor that initiates the activation of the coag cascade during secondary hemostasis?

A

Clotting factor III

-Membrane bound pro-coagulant made by endothelium

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63
Q

Describe stage 4 of hemostasis at the site of vascular injury.

A

Thrombus maturation and antithrombotic events:

  1. Formation of a solid, permanent plug of aggregated platelets and polymerized fibrin
  2. Counterreglatory mechanisms to limit the hemostatic plug at the site of injury
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64
Q

What are 3 factors that predispose the formation of a thrombosis?

A

Endothelial injury
Abnormal blood flow
Hypercoagulability

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65
Q

Important concept 6: Thrombosis is common and (serious or not serious).

A

Serious

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66
Q

Thrombosis is more common in ________

A

Veins

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67
Q

Thrombosis is more serious in ________

A

Arteries

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68
Q

What is the most important factor prompting thrombosis?

A

Endothelial injury

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69
Q

What are 3 conditions that cause endothelial injury → thrombosis?

A
  1. hemodynamic stress of hypertension
  2. toxicity if hypercholesterolemia
  3. products absorbed from smoking → inc pro-coag factors or decreases anti-coag factors
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70
Q

What types of blood flow promote thrombosis?

A
  1. Turbulent blood flow over ulcerated antherosclerotic plaques → ARTERIAL thrombosis
  2. Stasis in arterial aneurysms
71
Q

What type of hypercoagulability is congenital or genetic?

A

Primary

72
Q

What mutations or deficiencies lead to primary hypercoagulability?

A 
Factor V Leiden mutation
Prothrombin G20210A mutation
Methylenetetrahydrofolate reductase homozygous C677T mutation
Anti-thrombin-3 deficiency
Protein C deficiency
Protein S deficiency
73
Q

What type of hypercoagulability is acquired?

A

Secondary

74
Q

What can cause secondary hypercoagulability?

A 
Surgery
 Cancer
 Trauma
 Bed-ridden state
 Disseminated intravascular coagulation
 Heparin-induced thrombocytopenia
 Antiphospholipid antibody syndrome
75
Q

What is the catch-22 surrounding surgery and hypercogulability?

A

Surgery inevitably creates a hypercoagulable state in the patient (the bigger the surgery the more coagulable the patient) but anticoagulation therapy risks bleeding in the surgical site

76
Q

Important concept 7: Surgery to treat ______ causes ______

A

Surgery to treat morbidity causes morbidity (including hypercoagulability and adhesions)

77
Q

What is a white thrombi? Where do these tend to form?

A

Rich in platelets and is often arterial

78
Q

What is a red thrombi? Where to these tend to form?

A

Rich in RBCs and is often venous

79
Q

What is a mural thrombi?

A

Thrombus on the wall of the heart

80
Q

What are thrombi on heart valves called?

A

Vegetations

  • nonbacterial thrombotic endocarditis
  • infective endocarditis
  • autoimmune (i.e. Libman-Sacks endocarditis in SLE)
81
Q

What are the 4 fates of thrombus?

A

Dissolution
Propagation
Embolism
Organization (and recanalization)

82
Q

T or F: Orgnaization as a fate is exclusive to thrmobi.

A

False. Can occur in pneumonias, exudates, injuries

83
Q

What is orgnaization?

A

Ingrowth of FIBROBLASTS who convert it to fibrous tissue with an inngrowth of new capillaries who can coalesce to recanalize a thrombosed blood vessel

84
Q

Important concept 8: Clots forms around every ____ you put in, bringing eith it the ever present dangers of ___ and ______

A

Catheter

Embolism and infection of the clot

85
Q

What are the types of emboli? WHat is the most common?

A 
Thrombus (most common)
Antheromatous debris
Fat
Air
Amniotic fluid
Fragments of tumor
86
Q

What are most pulomoary thromboemboli from?

A

Deep thrombosis in legs

87
Q

Medium sized pulmonary thromboemboli can cause ______

A

Hemorrhagic infarction (if broncial part of dual lung blood supply is impaired)

88
Q

Larged sized pulmonary thromboemboli can cause ______

A

Acute cor pulmonale (RT heart failure) and SUDDEN DEATH

89
Q

What are “saddle emboli”?

A

Pulmonary thromboemboli in pulmonary trunk

90
Q

What are paradoxical emboli?

A

Emboli that pass thru patent foramen ovale or atrial septal defect to go to organs besides the lungs

91
Q

Numerous small emboli can cause ________

A

Pulmonary hypertension

92
Q

Important concept 9: pulmoary thromboemboli are common and (serious, not serious)

A

Serious (and becoming even more common with obesity epidemic)

93
Q

Sytemic thromboemboli are most commonly from _______ and go to _____

A

From heart to legs (or brain)

94
Q

Where do fat emboli most commonly originate?

A

Long bone fractures

95
Q

WHat signs or sympoms are assc with fat emboli?

A

Most are silent
But can cause a sudden onset of dyspnea, tachypnea, tachycardia, irritability, restlessness, anemia, and thrombocytopenia

96
Q

When do fat emboli commonly arise?

A

1-3 days following trauma

97
Q

What can cause air embolism?

A 
Getting air into IV infusion
sudden change in atmospheric pressue’
chest wall injury
back surgery in prone posiiton 
**Generally. More than 100 mL needed to have clinical effect, but it can be fatal
98
Q

What causes amniotic fluid embolism?

A

Tear in placental membrane
→ get fetal squamous cells, lanugo hair, vernix caseousa fat and mucin in pulmonary micocirculstion
→ causes diffuse alveolar damage and DIC

99
Q

What signs and sympoms are assc with amniotic fluid embolysim?

A

Sudden severe…

  • dyspenea
  • cyanoisis
  • shock during delivery
100
Q

What usually causes an infarct?

A

Thrombotic or embolic occulsion of an artery (most commonly)

Less commonly…
Vasospasm
Atheroma expansion by intraplaque hemorrhage
Tumor compressing artery
Twisting of blood vessels (torsion or volvulus)
Trauma
Incarcerated hernia

101
Q

Important concept 10: Infarction is death of an organ or tissue when ischemia as not been fixed before it is too late; it is common and seriosu, but you want to concentrate on ______

A

How to diagnose ischemia

102
Q

White anemic infarcts are typical of ____(type of organ)____

A

Typical of solid organs with end-arterial circulaion (heart, spleen, kidney)

103
Q

Red hemorrhagic infarcts are typical with _____(characteristic of organs)______

A 
Venous occulsion (ex: ovarian torsion) 
Dual or anastomosing blood supply (ex: lung, intestine)
Reperfusion
104
Q

What is the most common histiologic form of infarct?

A

Coagulative necrosis

105
Q

What determines the likelihood of an infarction?

A
  1. vulnerabilit to hypoxis (neurons dead after 3 mins, heart after 20 mins)
  2. rate of development of occulsion (slow allows collaterals to develop)
  3. nature of blood supply (ex: dual is protective, as in liver)
  4. oxygen content of blood
106
Q

What are the 5 aspects to the systemic descritopn of a lesion?

A
  1. size
  2. shape
  3. color
  4. consistency
  5. relationships
107
Q

What is the most common cause of generalized edema?

A

Heart failure

108
Q

What is hydrothorax?

A

Fluid in a pleural cavity (pleural effusion)

109
Q

What is peritoneal effusion?

A

Fluid in the abdominal cavity or Ascites

110
Q

Periorbital edema is frequently the first sign of ____

A

Nephrotic syndrome and is noticed by mothers of 2 to 6 year old children (= age when nephrotic syndrome is most common among children

111
Q

In 99% of edema, you will see ______

A

Pitting

112
Q

How does heart failure cause edema?

A

Heart failure causes decreased renal blood flow, which activates the renin-angiotensin-aldosterone system.
Increased aldosterone causes retention of sodium (and water), which then causes edema due to sodium retention, creating edema of two different types at the same time

113
Q

What protein is responsible for maintaining plasma onconic pressure?

A

Albumin (it accounts for nearly half of total plasma proteins)

114
Q

Hypoalbumininemia sufficiently severe enough causes __________

A

Generalized edema
AND
Secondary hyperaldosteronism

115
Q

What is the effect of hyperaldosteronism on edema?

A

Increases sodium, retention which further decreases plasma onconic pressure and causes more edema

116
Q

What is the most common cause of hyperemia?

A

Inflammation

117
Q

Why does hyperemia cause an abnormal reddish coloration?

A

Due to the presence of oxygenated blood in a tissue

118
Q

Failure of the lungs to load the blood with oxygen cause _______

A

cyanosis

119
Q

T or F: Cyanosis can occur without congestion

A

True

120
Q

Cyanosis due to CV or pulmonary disease tens to first be visible _______

A

Around the lips or the nail beds

121
Q

Why does right heart failure cause cyanosis?

A

Back up of blood that is inadequately pumped by the heart

122
Q

Where is congestion first occur first and is the area of worst congestion?

A

Centrilobular areas

123
Q

What liver findings is passive congestion associated with?

A

“nutmeg liver” consisting of alternating red and tan tissue causing the cut surface of the liver to resemble the cut surface of a nutmeg

124
Q

Describe the gross appearance of nutmeg liver

A

hemorrhagic necrosis spanning multiple lobules alternating with steatotic areas

125
Q

Chronic sub-lethal left heart failure causes _____ to accumulate in pulmonary alveoli?

A

hemophages (contains iron from blood that as leaked into the alveoli due to capillary burst from high BP)

126
Q

T or F: Hyperemia and congestion both increases the amount blood in vessels.

A

true

127
Q

T or F: Both hyperemia and congestion are fatal.

A

False they have never killed anyone

128
Q

What are the size of the visible hemorrhages that are seen with Petechia?

A

1-2 mm

129
Q

Another name for bruises

A

ecchymoses

130
Q

What is a hemorrage into the pericardial space?

A

hemopericardium

131
Q

What is a hemorrhage into the abdominal cavity?

A

hemoperitoneum

132
Q

What is a hemorrhage into a joint? What is this commonly associated with?

A

hemathrosis; assc with hemophillia

133
Q

Hemostasis is regulated by 3 components:

A
  1. endothelium (vascular wall)
  2. platelets
  3. coagulation cascade
134
Q

What molecule mediates platelet adhesion to ECM? How does it do this?

A

von Willebrand factor which binds to GpIb receptors to cause a change in shape of the platelets (smooth –> spiky)

135
Q

What causes the change platelet shape from smooth to spiky?

A

conformational change in GpIIb/IIIa receptors allows them to bind to fibrinogen. and fibrinogen can bind other platelets

136
Q

Describe the process of platelet aggregation

A

von Willebrand factor binds to GpIIb which causes a conf change in the platelet and receptors to allow the recpetors to bind fibrinogen. Many platelets can bind many fibrinogen molecules–> linking them all together

137
Q

At does ADP and TXA2 do when they are released from the granules of activated platelets?

A

recruit platelets and cause aggregation = formation of primary hemostatic plug

138
Q

On what stage of hemostatsis is the coagulation cascade activated?

A

3/secondary hemostasis

139
Q

What activates the coagulation cascade?

A

tissue factor = Clotting factor III (membrane bound procoagulant made by endothelium)

140
Q

What is thromboplastin?

A

a laboratory reagent that contains phosphilipids and tissue factor

141
Q

What is the role of thrombin (produced during coag cascade)?

A
  1. cleaves fibrinogen into fibrin
  2. stimulates platelets to release TXA2
  3. activates monocytes and lymphocytes
  4. activates endothelium for neutrophil adherence and
  5. stimulates endothelium to release NO, tissue plasminogen factor, and prostacyclin
142
Q

What is thrombomodulin and what is its role?

A

expressed on the surface of endothelial cells and binds thrombin so that together they can activate C reactive protein –> anticoagulation effect

143
Q

What molecules are players in the fibrolytic system?

A 
tissue plasminogen activator
plasmin 
tissue factor pathway inhibitor
antithrombin III
heparin-like molecules 
protein S
urokinase
144
Q

What does deficiency in von Willibrand factor lead to?

A

excessive bleeding with surgery or menstruation

145
Q

What does overactivity of von Willibrand factor lead to?

A

abnormally large multimers of it leads to a tendency to clot in small blood vessels and then excessive bleeding from having used up too many platelets and clotting factors

146
Q

What is thrombotic thrombocytopenic purpura?

A

overactivation of von Willie brand factor = tendency to clot in small blood vessels and then excessive bleeding from having used up too many platelets and clotting factors

147
Q

What does deficiency in GpIb receptors cause?

A

excessive bleeding (Bernard-Soulier syndrome, rare)

148
Q

Deficiency of platelet GpIIb/IIIa receptors causes…

A

a bleeding tendency due to deficient platelet aggregation (Glanzmann thrombasthenia, rare)

149
Q

Some snake venoms contain substances that bind to _______, mimicking Glanzmann thrombasthenia syndome.

A

platelet GpIIb/IIIa receptors

150
Q

What is the MOA of clopidogrel (Plavix)?

A

blocks platelet ADP receptors and is taken orally by patients who have suffered clotting of their critical coronary

  • ADP induces the conformational change that mediates the binding of platelet GpIIb/IIIa receptors to fibrinogen and other platelets –> aggregation
151
Q

T or F: In sickle cell disease, when polymerization of the abnormal hemoglobin deforms the erythrocytes, they get stuck in small blood vessels and this occlusion leads to stasis predisposing to thrombosis.

A

true

152
Q

What is the most common inherited hyper-coagulable state?

A

Factor V Leiden mutation (5% of whites affected)

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

153
Q

Factor V Leiden mutations: Heterozygotes have a ___-fold higher risk of venous thrombosis and homozygotes have a ___-fold increased risk

A

5; 50

154
Q

What is the 2nd most common inherited hyper-coagulable state?

A

Prothrombin G20210A mutation (2% of whites affected)

155
Q

Prothrombin G20210A mutation confers a __-fold increased risk of venous thrombosis.

A

3

156
Q

Why does surgery lead to a hyper-coagulable state?

A

Surgery cuts blood vessels, which activates platelets and clotting factors, which are not all used at the surgical site. Some of these activated platelets and clotting factors inevitably get swept into the general circulation, rendering operative and postoperative patients hypercoagulable

157
Q

Why can cancer place a patient in a hyper-coagulable state?

A
  1. there is an inflammatory response to malignant tumors
    2, malignant tumors outgrow their blood supply and have some necrosis, which releases highly thrombogenic necrotic debris into the general circulation –> ??
  2. tumors commonly compress veins or invade them –> obstructing blood flow –> turbulence or stasis –> predisposition to thrombosis
158
Q

Why is antiphospholipid Ab syndrome life threatening?

A

it causes arterial thrombosis due to autoantibodies against phospholipids

159
Q

What is the epidemiology of Antiphospholipid antibody syndrome?

A

common in young females

160
Q

T or F: Most patients with a “lupus anticoagulant” do not have lupus and all are hypercoagulable

A

true

161
Q

WHat is the presentation of pt with a lupus anticoagulant

A 
recurrent miscarriages
deep vein thromboses in their legs
cerebral infarctions
migraine headaches
cardiac vegetations
ischemic hands or feet
thrombocytopenia
162
Q

Antiphospholipid antibodies are present in___% of asymptomatic individuals

A

1-5%

163
Q

Arterial thrombi are usually at

A

sites of endothelial injury

164
Q

Venous thrombi are most commonly at

A

sites of stasis.

165
Q

Venous thrombi tend to grow on the side ______ to the heart

A

closer

166
Q

The (oldest or newest) parts of thrombi are the most likely to be organized and densely adherent to the blood vessel

A

oldest

167
Q

The (oldest or newest) parts of thrombi are the most likely to break off and be carried with the bloodstream (the process of embolization)

A

newest

168
Q

_______ has been the most standard modality for diagnosing deep vein thrombosis in the legs

A

Ultrasound examination

*but obesity can give false negative

169
Q

T or F: The bigger the vegetation, the more likely it is infected.

A

True: the growth of the infecting organisms is added to the growing clot

170
Q

Where can organization occur?

A

pneumonias
exudates
injuries
thrombi

171
Q

Up to __ % of pulmonary thrombi are silent

A

80%

172
Q

__ % of systemic thromboemboli are from the heart. __ % go to the legs and ___ % go to the brain.

A

heart: 80%
legs: 75%
brain: 10%

173
Q

How long after infarction is coagulative necrosis apparent/elicits an acute inflammatory response?

A

12-18 hrs

174
Q

T or F: Ain’t nobody got time for this.

A

TRUE DAT

CMD Block 2 (38 decks)

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