Hemodynamics 1 Flashcards
(177 cards)
1
Q
What is edema?
A
swelling of tissue due to increased fluid in interstitial tissue spaces; can be localized or generalized
2
Q
What is the most common cause of generalized edema?
A
heart failure
3
Q
What is hydrothorax?
A
fluid in a pleural cavity (pleural effusion)
4
Q
What is ascites?
A
fluid in the abdominal cavity (peritoneal effusion)
5
Q
Anasarca is…?
A
generalized edema
6
Q
Periorbital edema is..?
A
edema around the eyes
7
Q
Periorbital edema is often the first sign noticed of what condition?
A
nephrotic syndrome
8
Q
At what age range is nephrotic syndrome most common?
A
2-6 years old
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)
10
Q
If finger pressure on edematous subcutaneous tissue leaves an impression, it is called..?
A
pitting edema
11
Q
99% of edema what kind of edema?
A
pitting edema
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)
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
14
Q
How does edema due to increased hydrostatic pressure occur in the lungs?
A
left heart failure
15
Q
How does edema due to increased hydrostatic pressure occur in the lower body?
A
right heart failure
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
17
Q
Edema from decreased plasma osmotic pressure is a feature of nephrotic syndrome due to..?
A
protein loss through the kidneys
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
19
Q
What is the term for generalized edema?
A
anasarca
20
Q
What is it called when a person has fluid in a pleural cavity?
A
hydrothorax (pleural effusion)`
21
Q
What is the term for when a person has fluid in their abdominal cavity?
A
ascites (peritoneal effusion)
22
Q
What is the major protein maintaining plasma oncotic pressure?
A
albumin
23
Q
What protein accounts for nearly half of total plasma protein?
A
albumin
24
Q
Hypoalbuminemia that is severe enough to cause generalized edema also causes what?
A
secondary hyperaldosteronism
25
Hyperaldosteronism causes edema due to what?
sodium retention
26
Hypoalbuminemia causes what 2 categories of edema?
1) edema due to decreased plasma osmotic pressure
| 2) edema due to sodium retention
27
What is the primary cause of lymphedema?
lymphatic obstruction
28
Is lymphedema usually localized or generalized?
localized
29
Lymphedema can be secondarily caused by (5):
tumor, inflammation, surgery, radiation, scar
30
What is "peau d'orange" referring to clinically?
lymphedema due to breast cancer, making the skin resemble an orange peel
31
Is pulmonary edema common?
yes...duh!!
32
Is pulmonary edema serious?
you betcha!
33
What is the most common cause of pulmonary edema?
left heart failure
34
What are the causes of pulmonary edema (5)?
1) left heart failure
2) acute respiratory distress (ARDS)
3) hypersensitivity reactions
4) pneumonia
5) renal failure
35
What is the gross manifestation of pulmonary edema?
clear frothy fluid (pink if blood is mixed in) in the alveoli and, in severe cases, the airways
36
What are alveoli?
airspaces
37
What is the major symptom of pulmonary edema?
dyspnea
38
What is the major sign of pulmonary edema?
pulmonary crackles
39
What are crackles?
an inspiratory crackling sound on listening to the lungs with a stethoscope
(aka "rales")
40
Cerebral edema is what?
swelling of the brain
41
What are examples of localized cerebral edema?
around abscess or tumor
42
What is an example of generalized cerebral edema?
with encephalitis
43
What does generalized brain swelling do to sulci and gyri?
narrow sulci
| swollen gyri
44
How is cerebral edema fatal?
herniation of cerebellar tonsils into foramen magnum compressing the brainstem respiratory center
45
What is herniation?
protrusion of something somewhere it doesn't belong
46
What is hyperemia?
active increase in arterial blood flow
47
Why does hyperemia cause a reddish coloration?
presence of excess oxygenated blood in tissue
48
What is the most common cause of hyperemia?
inflammation
49
What is congestion?
passive decrease in venous outflow; causes cyanosis
50
What is cyanosis?
an abnormal bluish coloration due to the presence of excess deoxygenated blood in a tissue
51
What are some common causes of cyanosis?
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
52
What are some causes "central" cyanosis?
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
53
Cyanosis that is due to cardiovascular or pulmonary disease tends to first be visible where?
around the lips and nailbeds
54
What condition causes passive congestion of the liver due to the backup of blood inadequately pumped by the heart?
right heart failure
55
Right heart failure congestion is first and worst where?
centrilobular areas
56
What is "nutmeg liver"?
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
57
What condition is "nutmeg liver" associated with?
passive congestion
58
Chronic sublethal left heart failure causes hemophages to accumulate where?
pulmonary alveoli
59
Chronic sublethal left heart failure causes hemophages to accumulate in pulmonary alveoli. Why does this happen?
iron from the blood that has leaks into the alveoli due to capillaries bursting from the high pressure
60
Hyperemia and congestion have what main thing in common?
They both feature abnormal amounts of liquid blood in blood vessels
61
Are hyperemia and congestion serious conditions?
Nope (they are common but have never killed anybody)
62
What is a hemorrhage?
extravasation of blood due to blood vessel rupture
63
What is a hematoma?
when a hemorrhage is enclosed within a tissue
64
What are petechiae?
tiny (1-2 mm) hemorrhages due to platelet deficiency
65
What are purpura?
medium (3-10 mm) hemorrhages due to vasculitis, vessel fragility, etc.
66
What are ecchymoses?
larger (over 1 cm) subcutaneous hemorrhages that go from red-blue to blue-green to gold-brown as the hemoglobin breaks down
67
What is the common name for ecchymoses?
bruise
68
What are causes of ecchymoses?
trauma, vascular fragility
69
What is a hemothorax?
hemorrhage into a pleural cavity
70
Hemopericardium is...?
hemorrhage into the pericardial space
71
What is hemoperitoneum?
hemorrhage into the abdominal cavity
72
What is hemorrhage into a pleural cavity called?
hemothorax
73
What is hemorrhage into a pericardial space called?
hemopericardium
74
What is hemorrhage into the abdominal cavity called?
hemoperitoneum
75
Hemarthrosis is..?
hemorrhage into a joint
76
Hemarthrosis is commonly associated with what condition?
hemophilia
77
The mortality associated with hemorrhages depends on what 2 things?
1) location (leg is more trivial than brain)
| 2) timing (slow is more trivial than fast)
78
Hemostasis is most often defined as what?
the formation of a blood clot (hemostatic plug) at the site of vascular injury
79
What is the less commonly used definition for hemostasis?
the maintenance of blood in a free-flowing liquid state in normal blood vessels
80
What 3 components regulate hemostasis?
1) vascular wall (endothelium)
2) platelets
3) coagulation cascade
81
What are the contents of platelets (6)?
ADP, fibrinogen, clotting factors V and VIII, calcium, and epinephrine
82
Do platelets have a nucleus?
NO
83
What are the 4 stages of hemostasis at a site of vascular injury?
1) vasoconstriction
2) primary hemostasis
3) secondary hemostasis
4) thrombus and antithrombotic events
84
What is endothelin?
a potent endothelium-derived vasoconstrictor
85
What stage of hemostasis at a site of vascular injury involves brief arteriolar vasoconstriction?
stage 1 (vasoconstriction)
86
What mediates stage 1 of hemostasis at a site of vascular injury?
reflex neurogenic mechanisms that are augmented by local secretion of vasconstrictors (endothelin, etc.)
87
What stage of hemostasis at a site of vascular injury involves platelet adhesion to thrombogenic extracellular matrix, forming a primary hemostatic plug?
stage 2 (primary hemostasis)
88
What mediates platelet adhesion to ECM?
von Willebrand factor binding to platelet GpIb receptors
89
Von Willebrand factor binding to platelet GpIb receptors causes what change in the platelets?
changes shape from smooth disks to spheres with long spiky projections --> facilitates platelets aggregation
90
In stage 2 of hemostasis at a site of vascular injury, platelets changing shape causes a conformational change in what receptor?
GpIIb/IIIa
91
What does the conformational change induced by ADP in platelet GpIIb/IIIa make the receptor bind to that leads to platelet aggregation?
fibrinogen
92
What 2 things are released from platelets in stage 2 of hemostasis at a site of vascular injury?
ADP and TXA2
93
What stage of hemostasis at a site of vascular injury is associated with the coagulation cascade?
stage 3 (secondary hemastasis)
94
What factors activate the coagulation cascade?
tissue factor and platelet factors
95
What is tissue factor?
membrane-bound procoagulant made by endothelium); it is also called clotting factor III
96
What is thromboplastin?
laboratory reagent containing phospholipids and tissue factor
97
What does thrombin do (5 things)?
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
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?
stage 4 (thrombus and antithrombotic events)
99
How is a hemostatic plug limited to the site of injury?
thrombomodulin is expressed on the surface of endothelial cells --> binds to thrombin to activate protein C
100
How does the body break down clots?
fibrinolytic system
101
What are the components of the fibrinolytic system?
t-PA, plasmin, tissue factor pathway inhibitor, antithrombin III, heparin-like molecules, protein S, urokinase
102
Deficiency in what factor leads to a tendency to bleed excessively with surgery or menstruation?
von Willebrand factor
103
What is the name of the disease that causes a tendency to bleed excessively with surgery or menstruation?
von Willebrand disease
104
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?
von Willebrand factor; Thrombotic thrombocytopenic pupura
105
Deficiency of platelet GpIb receptors for von Willebrand factor leads to a bleeding tendency in a disease called...?
Bernard-Soulier syndrome
106
Deficiency of platelet GpIIa/IIIa receptors causes bleeding tendency due to deficient platelet aggregation in a disease called...?
Glanzmann thrombasthenia
107
Some snake venoms can mimic Glanzmann thrombasthenia by binding to what?
GpIIb/IIIa receptors
108
What is the drug that works by binding to GpIIb/IIIa receptors and is given to patients who are clotting off their coronary arteries?
Eptifibatide (Integrilin)
109
What does clopidogrel (Plavix) do?
blocks platelet ADP receptors (taken by patients who have clotting of critical coronary or cerebral arteries)
110
What is thrombosis?
inappropriate formation of blood clot in a blood vessel, usually occlusive
111
What are the 3 predisposing factors for thrombosis?
1) endothelial injury
2) abnormal blood flow (turbulence or stasis)
3) hypercoagulability
112
What is the most important factor predisposing thrombosis?
endothelial injury
113
What different stresses/toxicities can cause increased endothelial precoag. factors or decrease anticoag. factors (causing thrombosis)?
hemodynamic stress of hypertension, toxicity of hypercholesterolemia, products absorbed from smoking
114
Is thrombosis more common in veins or arteries?
veins
115
Is thrombosis more serious in veins or arteries?
arteries
116
Most people die of what 2 things? (according to Nichols)
thrombosis or hemorrhage
117
What are the congenital (genetic) hypercoagulable states?
- 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
What are the acquired hypercoagulable states?
- surgery
- cancer
- trauma
- bed-ridden state
- disseminated intravascular coagulation
- heparin-induced thrombocytopenia
- antiphospholipid syndrome
119
Hypercoagulable states dispose to what type of thrombus (venous or arterial)?
venous
120
What is the most common inherited hypercoagulable state (5% of whites)?
Factor V Leiden mutation
121
What are the risks for venous thrombosis for heterozygotes and homozygotes with Factor V Leiden?
Hetero - 5-fold higher
| Homo- 50-fold higher
122
What does the mutation in Factor V Leiden do to the patient?
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
What is the second most common inherited hypercoagulable state (2% of whites)?
Prothrombin G20210A mutation
124
Prothrombin G20210A mutation causes __-fold risk of venous thrombosis.
3
125
How does surgery lead to hypercoagulability?
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
How does cancer lead to hypercoagulability?
- 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
Why is antiphospholipid antibody syndrome life-threatening?
it causes arterial thrombosis
128
What population of people is antiphospholipid antibody syndrome most common in?
young females (5% in pregnant women, 15% in women with recurrent miscarriages)
129
Why is "lupus anticoagulant" a double misnomer?
most patients with them do not have lupus and all are hypercoagulable
130
Patients presenting with recurrent miscarriages, DVTs in their legs, cerebral infarctions, migraine headaches, cardiac vegetations, ischemic hands or feet, thrombocytopenia, etc. most likely have ________?
antiphospholipid antibody syndrome (although 1-5% of patients are asymptomatic)
131
Patients with antiphospholipid antibody syndrome have autoantibodies against what?
plasma protein antigens unveiled by binding to phospholipids
132
What are the 3 types of thrombi?
1) arterial ("white thrombi")
2) venous ("red thrombi")
3) mural
133
Which type of thrombus is rich in erythrocytes?
venous
134
Which type of thrombus is rich in platelets?
arterial
135
Which type of thrombus in located in the wall of the heart?
mural
136
What type of thrombus is most commonly at sites of stasis and tend to grow on the side closer to the heart?
venous
137
What part of a thrombus is most likely to be organized and densely adhered to blood vessel?
oldest parts
138
What part of a thrombus is most likely to break off and be carried with the blood stream (embolization)?
newest parts
139
What is a cause of false negatives in ultrasound testing for deep venous thrombosis of the leg?
obesity
140
What are vegetations?
thrombi on heart valves
141
Vegetations are mostly in the category of _______ before infection.
non-bacterial thrombotic endocarditis/marantic endocarditis
142
Vegetations are mostly in the category of _______ after infection.
infective endocarditis
143
Libman-Sacks endocarditis in systemic lupus erythematosus is a form of a ________ vegetation.
autoimmune
144
The bigger the vegetation, the _______(more/less) likely it is infected.
more
145
The four fates of thrombus are:
1) dissolution
2) propagation
3) embolization
4) organization (and recanalization)
146
What is a PICC line? What is the major risk of using one?
peripherally inserted central catheters; DVT in arm of the patient
147
Intravascular catheters and cardiac pacer wires always form _____, which causes a risk of embolization and infection.
clots
148
What is organization?
ingrowth by fibroblasts, who convert thrombus to fibrous tissue, with ingrowth of new capillaries, which can coalesce to recanalize a thrombosed blood vessel
149
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?
thromboembolism
150
What is an embolus?
detached intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin
151
What are types of emboli?
thrombus (*most common), atheromatous debris, fat, air, amniotic fluid, fragment of tumor
152
What is the main source of pulmonary thromboemboli? What are other sources?
Main source: DVT in the thighs
| Others: PICC lines in arms, pelvic veins
153
What percent of pulmonary thromboemboli are clinically silent?
~ 80%
154
What are "saddle emboli"?
emboli in the pulmonary trunk
155
What are paradoxical emboli?
emboli that pass through a patent foramen ovale or atrial septal defect to go to organs besides the lungs (rare)
156
Small emboli can often cause ____?
pulmonary hypertension
157
Systemic thromboemboli are most commonly from the ______ and most commonly travel to the ______ and ______.
heart (80%); legs (75%) and brain (10%)
158
Where is fat embolism most commonly from?
long bone fractures
159
What often causes a syndrome of sudden onset dyspnea, tachypnea, tachycardia, irritability, restlessness, anemia, and thrombocytopenia usually 1-3 days following trauma?
fat embolism
160
Why can sickle cell disease causing bone infarcts be fatal?
fat embolism from the bone infarcts
161
What are causes of air embolism?
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
How may mL of air embolism are needed to have any clinical effect?
100 mL
163
Can an air embolism be fatal?
YES
164
What are causes of amniotic fluid embolism?
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
What could a syndrome of sudden severe dyspnea, cyanosis and shock during labor or delivery be due to?
amniotic fluid embolism (rare)
166
What is an infarct?
area of ischemic necrosis (death of organ or tissue)
167
What is an area of ischemic necrosis leading to an infarct usually due to?
thrombotic or embolic occlusion of an artery
168
What are other less common causes of an infarct (besides thrombi or emboli)?
- vasospasm
- atheroma expansion by intraplaque hemorrhage
- tumor compressing an artery
- twisting of blood vessels (torsion or volvulus)
- trauma
- incarcerated hernia
169
What is the most common histologic form of infarct?
coagulative necrosis
170
What are the characteristics of coagulative necrosis? (timing and response)
- apparent after 12-18 hours
| - usually elicits acute inflammatory response
171
Where is ischemic necrosis liquefactive?
brain
172
What are the 4 things that determine the likelihood of an infarction?
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
What are the 5 aspects to systematically describe lesions?
1) size
2) shape
3) color
4) consistency/texture
5) relationships
174
What type of infarcts are typical of solid organs with end-arterial circulation?
white anemic
175
What organs would have white anemic infarctions?
kidney, heart, spleen
176
What organs would have red hemorrhagic infarctions?
ovary, lung, intestines
177
What type of infarcts are typical with venous occlusion, dual or anastomosing blood supply, or with reperfusion?
red hemorrhagic
