Hemodynamics-1 Lecture and Word Doc Flashcards
1
Q
What is edema?
A
Swelling of tissue due to increased fluid in interstitial tissue spaces
2
Q
What is ascities?
A
Fluid in the abdominal cavity
3
Q
What is anasarca?
A
Generalized edema
4
Q
What is hyperemia?
A
An active increase in arterial blood flow
5
Q
What is congestion?
A
Passive decrease in venous flow
6
Q
What is a hemorrhage?
A
Extravasation of blood due to blood vessel rupture
7
Q
What is petechia?
A
Tiny (1-2 mm) hemorrhage due to platelet deficiency
8
Q
What is hematoma?
A
A hemorrhage enclosed within a tissue
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
10
Q
What is a hemostatic plug?
A
Another term for blood clot
11
Q
What are platelets?
A
Anucleate cellular components of blood
12
Q
What are platelets important in?
A
Initiation and propagation of clotting
13
Q
T or F: Platelets have granules.
A
True
14
Q
What is thrombosis?
A
Inappropriate formation of blood clot in a blood vessel
15
Q
T or F: Blood clots formed during thrombosis are not usually occlusive.
A
False
16
Q
What is hypercoagulability?
A
Abnormal tendency to form clots
17
Q
What is coagulopathy?
A
Abnormal tendency to bleed
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
19
Q
What is an infarction?
A
Area of ischemic necrosis
20
Q
What are the 2 types of edema?
A
Localized and generalized
21
Q
Where does generalized edema initially appear?
A
Tissues with a loose connective tissue matrix (i.e. around the eyes = periorbital edema)
22
Q
What is pitting edema?
A
Transient pit in the skin at the site of finger pressure
23
Q
Important concept 1: What are four most common causes of edema?
A
Increased hydrostatic pressure
Decreased plasma oncotic pressure
Sodium retention
Inflammation
24
Q
What can cause edema in the lungs due to increased hydrostatic pressure?
A
Left heart failure
25
What can cause edema in the lower body due to increased hydrostatic pressure?
Right heart failure
26
What can cause edema in the leg body due to increased hydrostatic pressure?
Venous thrombosis
27
What is dependent edema?
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
28
T or F: dependent edema is specific to increased hydrostatic pressure as the etiology
false
29
What can nephrotic syndrome (protein loss) cause?
Edema due to decreased plasma osmotic pressure
30
Why can hepatic cirrhosis lead to edema?
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
31
What usually causes edema due to sodium retention?
Heart or renal failure
32
Edema due to sodium retention is always ___(type of edema) _____ and seen with ______. (this is testing you ability to read minds too)
Generalized; increased hydrostatic pressure
| (and, to a lesser extent, dilutional decrease in plasma osmotic pressure
33
Where does localized edema due to inflammation present?
At the site of infection
34
Generalized edema due to inflammation is seen with _______
SIRS or sepsis
35
What type of edema is associated with edema due to lymphatic obstruction (lymphedema)?
Usually localized
36
What causes edema due to lymphatic obstruction (lymphedema)?
```
Tumor
Inflammation
Surgery
Radiation
Scar
```
37
What is peau d’ orange?
Lymphedema due to breast cancer (causes skin over tumor to resemble the skin of an orange)
38
What is the most common cause of pulmonary edema?
Left heart failure
39
Describe the fluid that can be aspirated from pulmonary edema.
Frothy fluid (pink if blood in it)
40
What symptom is associated with pulmonary edema? Sign?
```
Dyspnea (symptom)
Pulmonary crackles (sign)
```
41
Important Concept 2: Pulmonary edema is common and (serious or not serious)
serious
42
Cerebral edema can be localized as a(n) ____ or _____
Abscess or tumor
43
Describe the (gross?) morphology of generalized cerebral edema.
Swollen gyri and narrowed sulci all over brain
44
Important concept 3: Brain edema can be fatal and due to ____
Herniation of cerebellar tonsils into foramen magnum which compresses the brainstem (respiratory center)
45
Erythema is _____
Hyperemia
46
Cyanosis is _____
Congestion
47
When heart failure causes cyanosis/congestion, the patient often will also have ______ and ______
“Nutmeg liver”: alternating red centrilobular and tan peripherilobular tissue (whatever the fuck that is)
AND
hemophages in pulmonary alveoli
48
Important concept 4: Hyperemia and congestion are common and (serious or not serious)
Not serious
49
What is purpura?
Medium (3-10 mm) bleed due to vasculitis, vessel fragility, etc.
50
What is ecchymosis?
Larger (over 1 cm) subcutaneous hemorrhage that goes from red-blue → blue green → gold-brown as the hemoglobin breaks down
51
What is a hemothorax?
Hemorrhage into pleural cavity
52
What is the size of a pupra?
3-10 mm
53
What is the size of an ecchymosis?
Over 1 cm
54
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
serious
55
What are the 4 stages of hemostasis at the site of vascular injury?
1. vasoconstriction
2. primary hemostasis
3. secondary hemostasis
4. thrombus and antithrombic events
56
Describe stage 1 of hemostasis at the site of vascular injury. What mediates it and augments it.
Brief arteriolar vasoconstriction mediated by reflex neurogenic mechanism and augmented by local secretion of vasoconstrictors (i.e. endothelium, a potent endothelium-derived vasoconstrictor)
57
What is endothelin?
a potent endothelium-derived vasoconstrictor; mediates the first stage (vasoconstriction) of hemostasis at the site of vascular injury
58
Describe stage 2 of hemostasis at the site of vascular injury.
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
59
What is GpIIb/IIIa?
A receptor that is expressed on the surface of platelets after they become activated. This receptor binds fibrinogen and mediates aggregation.
60
What is released during primary homeostasis? Who releases this?
ADP and TXA2
61
Describe stage 3 of hemostasis at the site of vascular injury.
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
62
What is (/describe) the tissue factor that initiates the activation of the coag cascade during secondary hemostasis?
Clotting factor III
| -Membrane bound pro-coagulant made by endothelium
63
Describe stage 4 of hemostasis at the site of vascular injury.
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
64
What are 3 factors that predispose the formation of a thrombosis?
Endothelial injury
Abnormal blood flow
Hypercoagulability
65
Important concept 6: Thrombosis is common and (serious or not serious).
Serious
66
Thrombosis is more common in ________
Veins
67
Thrombosis is more serious in ________
Arteries
68
What is the most important factor prompting thrombosis?
Endothelial injury
69
What are 3 conditions that cause endothelial injury → thrombosis?
1. hemodynamic stress of hypertension
2. toxicity if hypercholesterolemia
3. products absorbed from smoking → inc pro-coag factors or decreases anti-coag factors
70
What types of blood flow promote thrombosis?
1. Turbulent blood flow over ulcerated antherosclerotic plaques → ARTERIAL thrombosis
2. Stasis in arterial aneurysms
71
What type of hypercoagulability is congenital or genetic?
Primary
72
What mutations or deficiencies lead to primary hypercoagulability?
```
Factor V Leiden mutation
Prothrombin G20210A mutation
Methylenetetrahydrofolate reductase homozygous C677T mutation
Anti-thrombin-3 deficiency
Protein C deficiency
Protein S deficiency
```
73
What type of hypercoagulability is acquired?
Secondary
74
What can cause secondary hypercoagulability?
```
Surgery
Cancer
Trauma
Bed-ridden state
Disseminated intravascular coagulation
Heparin-induced thrombocytopenia
Antiphospholipid antibody syndrome
```
75
What is the catch-22 surrounding surgery and hypercogulability?
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
Important concept 7: Surgery to treat ______ causes ______
Surgery to treat morbidity causes morbidity (including hypercoagulability and adhesions)
77
What is a white thrombi? Where do these tend to form?
Rich in platelets and is often arterial
78
What is a red thrombi? Where to these tend to form?
Rich in RBCs and is often venous
79
What is a mural thrombi?
Thrombus on the wall of the heart
80
What are thrombi on heart valves called?
Vegetations
- nonbacterial thrombotic endocarditis
- infective endocarditis
- autoimmune (i.e. Libman-Sacks endocarditis in SLE)
81
What are the 4 fates of thrombus?
Dissolution
Propagation
Embolism
Organization (and recanalization)
82
T or F: Orgnaization as a fate is exclusive to thrmobi.
False. Can occur in pneumonias, exudates, injuries
83
What is orgnaization?
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
Important concept 8: Clots forms around every ____ you put in, bringing eith it the ever present dangers of ___ and ______
Catheter
| Embolism and infection of the clot
85
What are the types of emboli? WHat is the most common?
```
Thrombus (most common)
Antheromatous debris
Fat
Air
Amniotic fluid
Fragments of tumor
```
86
What are most pulomoary thromboemboli from?
Deep thrombosis in legs
87
Medium sized pulmonary thromboemboli can cause ______
Hemorrhagic infarction (if broncial part of dual lung blood supply is impaired)
88
Larged sized pulmonary thromboemboli can cause ______
Acute cor pulmonale (RT heart failure) and SUDDEN DEATH
89
What are “saddle emboli”?
Pulmonary thromboemboli in pulmonary trunk
90
What are paradoxical emboli?
Emboli that pass thru patent foramen ovale or atrial septal defect to go to organs besides the lungs
91
Numerous small emboli can cause ________
Pulmonary hypertension
92
Important concept 9: pulmoary thromboemboli are common and (serious, not serious)
Serious (and becoming even more common with obesity epidemic)
93
Sytemic thromboemboli are most commonly from _______ and go to _____
From heart to legs (or brain)
94
Where do fat emboli most commonly originate?
Long bone fractures
95
WHat signs or sympoms are assc with fat emboli?
Most are silent
But can cause a sudden onset of dyspnea, tachypnea, tachycardia, irritability, restlessness, anemia, and thrombocytopenia
96
When do fat emboli commonly arise?
1-3 days following trauma
97
What can cause air embolism?
```
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
What causes amniotic fluid embolism?
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
What signs and sympoms are assc with amniotic fluid embolysim?
Sudden severe…
- dyspenea
- cyanoisis
- shock during delivery
100
What usually causes an infarct?
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
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 ______
How to diagnose ischemia
102
White anemic infarcts are typical of ____(type of organ)____
Typical of solid organs with end-arterial circulaion (heart, spleen, kidney)
103
Red hemorrhagic infarcts are typical with _____(characteristic of organs)______
```
Venous occulsion (ex: ovarian torsion)
Dual or anastomosing blood supply (ex: lung, intestine)
Reperfusion
```
104
What is the most common histiologic form of infarct?
Coagulative necrosis
105
What determines the likelihood of an infarction?
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
What are the 5 aspects to the systemic descritopn of a lesion?
1. size
2. shape
3. color
4. consistency
5. relationships
107
What is the most common cause of generalized edema?
Heart failure
108
What is hydrothorax?
Fluid in a pleural cavity (pleural effusion)
109
What is peritoneal effusion?
Fluid in the abdominal cavity or Ascites
110
Periorbital edema is frequently the first sign of ____
Nephrotic syndrome and is noticed by mothers of 2 to 6 year old children (= age when nephrotic syndrome is most common among children
111
In 99% of edema, you will see ______
Pitting
112
How does heart failure cause edema?
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
What protein is responsible for maintaining plasma onconic pressure?
Albumin (it accounts for nearly half of total plasma proteins)
114
Hypoalbumininemia sufficiently severe enough causes __________
Generalized edema
AND
Secondary hyperaldosteronism
115
What is the effect of hyperaldosteronism on edema?
Increases sodium, retention which further decreases plasma onconic pressure and causes more edema
116
What is the most common cause of hyperemia?
Inflammation
117
Why does hyperemia cause an abnormal reddish coloration?
Due to the presence of oxygenated blood in a tissue
118
Failure of the lungs to load the blood with oxygen cause _______
cyanosis
119
T or F: Cyanosis can occur without congestion
True
120
Cyanosis due to CV or pulmonary disease tens to first be visible _______
Around the lips or the nail beds
121
Why does right heart failure cause cyanosis?
Back up of blood that is inadequately pumped by the heart
122
Where is congestion first occur first and is the area of worst congestion?
Centrilobular areas
123
What liver findings is passive congestion associated with?
"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
Describe the gross appearance of nutmeg liver
hemorrhagic necrosis spanning multiple lobules alternating with steatotic areas
125
Chronic sub-lethal left heart failure causes _____ to accumulate in pulmonary alveoli?
hemophages (contains iron from blood that as leaked into the alveoli due to capillary burst from high BP)
126
T or F: Hyperemia and congestion both increases the amount blood in vessels.
true
127
T or F: Both hyperemia and congestion are fatal.
False they have never killed anyone
128
What are the size of the visible hemorrhages that are seen with Petechia?
1-2 mm
129
Another name for bruises
ecchymoses
130
What is a hemorrage into the pericardial space?
hemopericardium
131
What is a hemorrhage into the abdominal cavity?
hemoperitoneum
132
What is a hemorrhage into a joint? What is this commonly associated with?
hemathrosis; assc with hemophillia
133
Hemostasis is regulated by 3 components:
1. endothelium (vascular wall)
2. platelets
3. coagulation cascade
134
What molecule mediates platelet adhesion to ECM? How does it do this?
von Willebrand factor which binds to GpIb receptors to cause a change in shape of the platelets (smooth --> spiky)
135
What causes the change platelet shape from smooth to spiky?
conformational change in GpIIb/IIIa receptors allows them to bind to fibrinogen. and fibrinogen can bind other platelets
136
Describe the process of platelet aggregation
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
At does ADP and TXA2 do when they are released from the granules of activated platelets?
recruit platelets and cause aggregation = formation of primary hemostatic plug
138
On what stage of hemostatsis is the coagulation cascade activated?
3/secondary hemostasis
139
What activates the coagulation cascade?
tissue factor = Clotting factor III (membrane bound procoagulant made by endothelium)
140
What is thromboplastin?
a laboratory reagent that contains phosphilipids and tissue factor
141
What is the role of thrombin (produced during coag cascade)?
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
What is thrombomodulin and what is its role?
expressed on the surface of endothelial cells and binds thrombin so that together they can activate C reactive protein --> anticoagulation effect
143
What molecules are players in the fibrolytic system?
```
tissue plasminogen activator
plasmin
tissue factor pathway inhibitor
antithrombin III
heparin-like molecules
protein S
urokinase
```
144
What does deficiency in von Willibrand factor lead to?
excessive bleeding with surgery or menstruation
145
What does overactivity of von Willibrand factor lead to?
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
What is thrombotic thrombocytopenic purpura?
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
What does deficiency in GpIb receptors cause?
excessive bleeding (Bernard-Soulier syndrome, rare)
148
Deficiency of platelet GpIIb/IIIa receptors causes...
a bleeding tendency due to deficient platelet aggregation (Glanzmann thrombasthenia, rare)
149
Some snake venoms contain substances that bind to _______, mimicking Glanzmann thrombasthenia syndome.
platelet GpIIb/IIIa receptors
150
What is the MOA of clopidogrel (Plavix)?
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
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.
true
152
What is the most common inherited hyper-coagulable state?
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
Factor V Leiden mutations: Heterozygotes have a ___-fold higher risk of venous thrombosis and homozygotes have a ___-fold increased risk
5; 50
154
What is the 2nd most common inherited hyper-coagulable state?
Prothrombin G20210A mutation (2% of whites affected)
155
Prothrombin G20210A mutation confers a __-fold increased risk of venous thrombosis.
3
156
Why does surgery lead to a hyper-coagulable state?
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
Why can cancer place a patient in a hyper-coagulable state?
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 --> ??
3. tumors commonly compress veins or invade them --> obstructing blood flow --> turbulence or stasis --> predisposition to thrombosis
158
Why is antiphospholipid Ab syndrome life threatening?
it causes arterial thrombosis due to autoantibodies against phospholipids
159
What is the epidemiology of Antiphospholipid antibody syndrome?
common in young females
160
T or F: Most patients with a “lupus anticoagulant” do not have lupus and all are hypercoagulable
true
161
WHat is the presentation of pt with a lupus anticoagulant
```
recurrent miscarriages
deep vein thromboses in their legs
cerebral infarctions
migraine headaches
cardiac vegetations
ischemic hands or feet
thrombocytopenia
```
162
Antiphospholipid antibodies are present in___% of asymptomatic individuals
1-5%
163
Arterial thrombi are usually at
sites of endothelial injury
164
Venous thrombi are most commonly at
sites of stasis.
165
Venous thrombi tend to grow on the side ______ to the heart
closer
166
The (oldest or newest) parts of thrombi are the most likely to be organized and densely adherent to the blood vessel
oldest
167
The (oldest or newest) parts of thrombi are the most likely to break off and be carried with the bloodstream (the process of embolization)
newest
168
_______ has been the most standard modality for diagnosing deep vein thrombosis in the legs
Ultrasound examination
*but obesity can give false negative
169
T or F: The bigger the vegetation, the more likely it is infected.
True: the growth of the infecting organisms is added to the growing clot
170
Where can organization occur?
pneumonias
exudates
injuries
thrombi
171
Up to __ % of pulmonary thrombi are silent
80%
172
__ % of systemic thromboemboli are from the heart. __ % go to the legs and ___ % go to the brain.
heart: 80%
legs: 75%
brain: 10%
173
How long after infarction is coagulative necrosis apparent/elicits an acute inflammatory response?
12-18 hrs
174
T or F: Ain't nobody got time for this.
TRUE DAT
