Hemodynamics Flashcards
(185 cards)
1
Q
Edema
A
Swelling of tissue due to increased fluid in interstitial tissue spaces
2
Q
What is the most common cause of generalized edema?
A
Heart failure
3
Q
Hydrothorax
A
Fluid in a pleural cavity
4
Q
Ascites
A
Fluid in the abdominal cavity
5
Q
Anasarca
A
Generalized edema
6
Q
If finger pressure on subcutaneous tissue leaves a temporary impression, it is called ______.
A
Pitting edema
7
Q
What are the 5 categories of edema?
A
- Increased hydrostatic pressure
- Decreased plasma oncotic pressure
- Lymphatic obstruction
- Sodium retention
- Inflammation
8
Q
Where is edema due to increased hydrostatic pressure commonly worse?
A
In the legs when standing and in the sacrum when recumbent
9
Q
Increased ________ causes retention of sodium, which then causes edema.
A
Aldosterone
10
Q
Heart failure causes decreased renal blood flow, which activates ________.
A
The renin-angiotensin-aldosterone system
11
Q
Edema from _________ is a feature of the nephrotic syndrome due to protein loss through the kidneys.
A
Decreased plasma osmotic pressure
12
Q
What is the major protein maintaining plasma oncotic pressure?
A
Albumin
13
Q
Hypoalbuminemia sufficiently severe enough to cause generalized edema causes __________.
A
Secondary hyperaldosteronism
14
Q
T or F: Edema due to sodium retention is always generalized.
A
T
15
Q
Edema due to sodium retention is usually caused by _________.
A
Heart failure
16
Q
T or F: Edema due to inflammation is always localized.
A
F: can be generalized or localized
17
Q
Lymphedema is usually localized and caused by __________.
A
Tumor, inflammation, surgery, radiation, or scar
18
Q
________ can make the skin resemble an orange peel.
A
Lymphedema due to breast cancer
19
Q
What is the most common cause of pulmonary edema?
A
Left heart failure
20
Q
What are the causes of pulmonary edema?
A
Left heart failure, ARDS (acute respiratory distress syndrome), hypersensitivity reactions, pneumonia, and renal failure
21
Q
What is the major symptom of pulmonary edema?
A
Dyspnea
22
Q
What is the major sign of pulmonary edema?
A
Pulmonary crackles
23
Q
T or F: Cerebral edema can be localized or generalized.
A
T
24
Q
When can cerebral edema be fatal?
A
When herniation of the cerebellar tonsils into the foramen magnum compresses the brainstem
25
Hyperemia (erythema)
Active increase in arterial blood flow
26
Hyperemia causes an abnormal reddish coloration due to ____________.
The presence of excess oxygenated blood in a tissue
27
What is the most common cause of hyperemia?
Inflammation
28
Congestion
A passive decrease in venous outflow
29
What is cyanosis and what causes it?
Abnormal bluish coloration due to the presence of excess deoxygenated blood; congestion is a common cause of cyanosis
30
Where is cyanosis due to cardiovascular or pulmonary disease tend to be first visible?
Around the lips (second is nail beds)
31
_________ causes passive congestion of the liver due to the backup of blood inadequately pumped by the heart.
Right heart failure
32
Passive congestion is associated with what pathological finding?
Nutmeg liver (alternating red and tan tissue)
33
Chronic sublethal left heart failure causes __________.
Hemophages to accumulate in pulmonary alveoli
34
T or F: Hyperemia and congestion are common and serious.
F: Common but not serious
35
Hemorrhage
Extravasation of blood due to blood vessel rupture
36
Hematoma
Hemorrhage enclosed within tissue
37
Petechiae
Tiny hemorrhages due to platelet deficiency (1-2 mm)
38
Purpura
Medium hemorrhages due to vasculitis, vessel fragility, etc. (3-10 mm)
39
Ecchymoses
Larger subcutaneous hemorrhages that go from red-blue to blue-green to gold-brown as the hemoglobin breaks down (over 1 cm)
40
Ecchymoses are frequently called _____.
Bruises
41
Hemopericardium
Hemorrhage into the pericardial space
42
Hemoperitoneum
Hemorrhage into the abdominal cavity
43
Hemarthrosis
Hemorrhage into a joint
44
Hemostasis (2)
1. Maintenance of blood in a free-flowing liquid state in normal blood vessels
2. Formation of a blood clot at a site of vascular injury
45
What is hemostasis regulated by (3)?
Vascular wall (endothelium), platelets, and the coagulation cascade
46
What do platelets contain (6)?
1. ADP
2. Fibrinogen
3. Clotting factor V
4. Clotting factor VIII
5. Calcium
6. Epinephrine
47
What are the four stages of hemostasis at site of vascular injury?
1. Vasoconstriction
2. Primary hemostasis
3. Secondary hemostasis
4. Thrombus and antithrombotic events
48
What regulates vasoconstriction at a site of vascular injury?
Reflex neurogenic mechanisms augmented by vasoconstrictors such as endothelin
49
What mediates platelet adhesion to thrombogenic extracellular matrix?
von Willebrand factor, which binds to their GpIb receptors
50
How does platelet aggregation occur?
1. Platelets adhere to the extracellular matrix (mediated by von Willebrand factor), which binds to their GpIb receptors
2. Platelet changes shape from smooth surfaced discs to spheres with long spiky projections (facilitates aggregation)
3. Change in the shape of the platelets allows a conformational change in their GpIIb/IIIa receptors, making them bind fibrinogen
4. Fibrinogen binds to the altered receptors on adjacent platelets, linking them in an aggregate
5. Release of ADP and thromboxane A2 causes additional platelet recruitment and aggregation, resulting in a primary hemostatic plug
51
Coagulation cascade is activated by ____________.
Tissue factor and platelet factors
52
The coagulation cascade culminates in ________.
The conversion of fibrinogen to fibrin by thrombin
53
What all does thrombin do? (4)
1. Converts fibrinogen to fibrin
2. Stimulates platelets to release thromboxane A2
3. Activates monocytes and lymphocytes
4. Stimulates endothelial cells to adhere to neutrophils and to release NO, tissue plasminogen activator, and prostacyclin
54
In what stage of hemostasis is a semi-permanent plug of aggregated platelets and polymerized fibrin formed?
Stage 4
55
What counter-regulatory mechanism limits the hemostatic plug to the site of injury?
Expression of thrombomodulin on the surface of endothelial cells
56
Thrombomodulin binds thrombin and together they activate ________.
Protein C
57
What is von Willebrand disease?
Deficiency of von Willebrand factor that leads to excess bleeding with surgery or menstruation
58
What is thrombotic thrombocytopenic purport?
Overactive von Willebrand factor causes a tendency to clot in small blood vessels then bleed from having used up too many platelets and clotting factors
59
What is Bernard-Soulier syndrome?
Deficiency platelet GpIb receptors for von Willebrand factor, which causes a bleeding tendency
60
What is Glanzmann thrombasthenia?
Deficiency of platelet GpIIb/IIIa receptors that causes a bleeding tendency due to deficient platelet aggregation
61
What does clopidogrel do?
Blocks platelet ADP receptors and is taken orally by patients who have suffered clotting of their critical coronary or cerebral arteries
62
Thrombosis
Inappropriate formation of a blood clot in a blood vessel
63
What are the three predisposing factors to thrombosis?
1. Endothelial injury
2. Abnormal blood flow
3. Hypercoagulability
64
What is the most important factor predisposing to thrombosis?
Endothelial injury
65
T or F: Thrombosis is more common in veins and more serious in arteries
T
66
What is the most common inherited hyper coagulable state?
Factor V Leiden mutation -- makes clotting factor V resistant to activated protein C, resulting in the loss of an important clot-limiting counter regulatory mechanism
67
What is the second most common inherited hyper coagulable state?
Prothrombin G20210A mutation
68
What is antiphospholipid antibody syndrome and how does it present?
A rare but life-threatening acquired hypercoagulable state -- it causes arterial thrombosis and is most common in young females
Presentation: recurrent miscarriages, deep vein thromboses, cerebral infarctions, migraine headaches, cardiac vegetations, ischemic hands or feet, and thrombocytopenia
69
T or F: Most patients with a lupus anticoagulant do not have lupus and all patients with the anticoagulant are hypercoagulable.
T
70
What are the three types of thrombi?
Arterial, venous, and mural
71
Arterial thrombi tend to be rich in _______ and venous thrombi tend to be rich in ______.
Arterial: Platelets (white thrombi)
Venous: Erythrocytes (red thrombi)
72
Where are mural thrombi located?
On the wall of the heart
73
Arterial thrombi are usually where?
At sites of endothelial injury
74
Venous thrombi are usually where?
At sites of stasis
75
How is deep vein thrombosis typically diagnosed in the legs?
By ultrasound examination
76
Vegetations
Thrombi on heart valves
77
What are the four fates of thrombus?
1. Dissolution
2. Propagation
3. Embolization
4. Organization (and recanalization)
78
Organization
Ingrowth by fibroblasts, who convert thrombus to fibrous tissue, with ingrowth of new capillaries, which can coalesce to reanalyze a thromboses blood vessel
79
Embolus
Detached intravascular solid, liquid, or gaseous mass carried by the blood to a site distant from its point of origin
80
Fat embolism is most commonly from ______.
Long bone fractures
81
Air embolism can be caused by ________.
Getting air into an intravenous infusion, a sudden change in atmospheric pressure, chest wall injury, or back surgery in a prone position
82
Amniotic fluid embolism can be caused by ________.
Tears in the placental membranes during the course of labor and delivery
83
An infarct is usually due to ___________.
Thrombotic or embolic occlusion of an artery
84
White anemic infarcts are typical of organs with __________.
End-arterial circulation
85
Red hemorrhagic infarcts are typical with _______.
Venous occlusion, dual or anastomosing blood supply, or reperfusion
86
What determines the likelihood of an infarction? (4)
1. An organs vulnerability to hypoxia
2. The rate of development of vascular occlusion
3. The nature of an organs blood supply
4. Oxygen content of the blood
87
What 5 aspects should you use to describe an infarct?
1. Size
2. Shape
3. Color
4. Consistency
5. Its relationships
88
Shock
State of systemic (total body) hypo perfusion, cardiovascular collapse
89
Shock is mainly caused by _________ (3).
1. Decreased circulating blood volume
2. Decreased cardiac output
3. Sepsis
90
Less common causes of shock include ________.
Anaphylaxis, SIRS, and neurogenic causes
91
__________ shock can be due to bleeding or fluid loss from vomiting, diarrhea, or extensive burns.
Hypovolemic
92
________ shock can be due to myocardial infarction, cardiac arrhythmia, or pulmonary embolism.
Cardiogenic
93
What types of shock make up the distributive shock group?
Septic shock, anaphylaxis, and other less common types of shock
94
What is the main feature associated with distributive shock?
Widespread vasodilation
95
T or F: Shock is defined by blood pressure below 100/60.
F: Shock is not defined by blood pressure below any particular level
96
One of the earliest symptoms of shock is _______.
Agitation
97
Patients in _________ shock have cool, clammy skin.
Hypovolemic or Cardiogenic
98
Patients in _______ shock have warm flushed skin.
Septic
99
You want to quickly start antibiotic therapy for _______ shock.
Septic
100
T or F: Young people in shock typically have deceptively normal vital signs until they reach the limits of their ability to compensate.
T
101
Why is accurate categorization of shock important?
Because the treatments are different
102
Hemorrhagic shock needs treatment with __________.
Blood transfusion
103
Cardiogenic shock needs what treatment?
Treatment that assists the heart
104
What is cardiac tamponade?
Bleeding into the pericardial sac prevents the heart from filling, which results in shock, distant heart sounds, and jugular venous distention.
105
Some would put shock from pulmonary embolism or cardiac tamponade into a category of shock known as ________.
Obstructive shock
106
What is neurogenic shock?
A form of vasogenic shock with vasodilation due to spinal cord injury or spinal anesthesia causing acute loss of SNS maintenance of a normal level of vasoconstriction
107
Trauma patients can have shock that is partly hemorrhagic and partly septic due to increased production of _______________.
Proinflammatory cytokines like TNF, IL-1, and IL-6
108
What is the most common form of shock?
Hypovolemic
109
The loss of about ______% of a person's blood volume is the threshold for shock.
25-30%
110
The loss of ____% of one's blood volume is commonly regarded as the dividing line between lethal and non-lethal hemorrhage.
50%
111
What is sepsis?
The patient-as-a-whole syndrome of response to infection
112
SIRS requires meeting two or more of what criteria?
1. Fever or hypothermia
2. Elevated heart rate (>90/min)
3. Tachypnea (>20/min)
4. WBC count high or low
113
What are the two subsets of sepsis and what differentiates them?
1. Severe sepsis (sepsis with acute organ dysfunction)
| 2. Septic shock (sepsis with refractory arterial hypotension)
114
T or F: The majority of patients with sepsis have positive blood cultures.
NO WAY
115
What does sepsis have to do with phospholipase A2?
Sepsis causes phospholipase A2 in the cell membranes of platelets, endothelial cells, neutrophils, monocytes, and other cells to generate platelet activating factor (PAF)
116
T or F: PAF is 100-1000 times more potent than histamine in inducing vasodilation and increased vascular permeability.
T
117
What are PAF's functions?
It induces vasodilation and vascular permeability, activates platelets(obvi), promotes leukocyte adhesion to endothelial cells, chemotaxis, degranulation, and oxidative burst
118
What is TGN1412?
A superagonist anti-CD28 monoclonal antibody that produced a systemic inflammatory response when administered to humans
119
Which cytokines cause mast cells to release histamine?
IL-1 and IL-8
120
Which prostaglandins cause vasodilation?
PGD2, PGE1, PGE2
121
Which prostaglandins cause vascular permeability?
PGD2 and PGE2
122
Extracellular release of small amounts of reactive nitrogen species and reactive oxygen species can increase the expression of _________.
IL-8 and other cytokines, and endothelial cell leukocyte adhesion molecules
123
Greatly decreased blood volume combined with vasodilation increasing vascular capacitance causes __________.
Septic shock
124
Within the clotting system _______ causes increased vascular permeability and leukocyte emigration from blood vessels.
Activated factor X
125
What cleaves complement C5 to release C5a, linking clotting and the complement cascade?
Thrombin
126
T or F: Sepsis causes increased tissue factor, which promotes clotting.
T
127
Sepsis causes increased ________, which indirectly promotes clotting by inhibiting fibrinolysis.
Plasminogen activator inhibitor-1
128
Sepsis results in decreased __________ (3), and all of these indirectly promote clotting by decreasing fibrinolysis.
Tissue factor pathway inhibitor, thrombomodulin, and protein C
129
Sepsis is complicated by _______ in up to half of septic patients. (sorry this one's vague.)
DIC -- disseminated intravascular coagulation
130
__________ inhibit neutrophil adhesion to endothelial cells and chemotaxis.
Lipoxins (generated from arachidonic acid)
131
What components of the complement system counter-regulate the pro-inflammatory effects of complement activation.
C1INH, Factor H, DAF
132
What is the major function of IL-10? What kind of cell secretes it?
To down regulate the responses of activated macrophages; secreted by macrophages (so they calm themselves down)
133
What does soluble tumor necrosis factor receptor (sTNFR) do?
It blocks TNF
134
Counter-regulatory mechanisms for sepsis and shock cause _______.
Immunosuppression
135
What are the 4 main risk factors for gallstones?
Fat, Female, Fertile, Forty
136
The anti-inflammatory counter-regulatory mechanism for sepsis and shock is known as __________.
Compensatory anti-inflammatory response syndrome (CARS)
137
What is a mixed antagonistic response syndrome (MARS)?
When patients swing back and forth between a pro-inflammatory response syndrome and a compensatory anti-inflammatory response syndrome.
138
Which therapies block TNF-alpha?
Infliximab, etanercept, and adalimumab
139
What therapy blocks IL-6 receptors?
Tocilizumab
140
T or F: Trauma/burns, acute pancreatitis, and extensive multi-organ ischemic necrosis can also cause SIRS.
T
141
Extensive necrosis induces a _______ inflammatory response.
Systemic
142
What are super antigens?
Molecules that promote T lymphocyte mitosis in a nonspecific way, bypassing antigen receptor specificity
143
What is significant about toxic shock syndrome toxin-1 (TSST-1)?
It can bind to any T-cell receptor with a V-beta 2 segment, activating a lot of T cell clones which produce enough cytokines for a cytokine storm.
144
When TSST-1 causes a cytokine storm leading to SIRS, the result is _________.
Toxic shock syndrome
145
Toxic shock syndrome is due to ________.
A nonspecific immunologic over-reaction to a secreted bacterial product
146
T or F: Genetics plays a role in determining which patients exposed to an antigen will get a cytokine storm due to their immune systems over-reacting.
T
147
What defines severe sepsis or SIRS?
Sepsis or SIRS with acute organ dysfunction
148
Patients with severe sepsis may have skeletal muscle dysfunction due to _______.
Buildup of lactic acid due to anaerobic metabolism
149
What are the three stages of shock?
1. Nonprogressive
2. Progressive
3. Irreversible
150
What's going on in the non progressive stage of shock?
Reflex compensatory mechanisms are still maintaining perfusion of vital organs
151
What's going on in the progressive stage of shock?
Manifestations of decompensating organ function
152
What's going on in the irreversible stage of shock?
Death is inevitable
153
The compensatory mechanisms for shock include _________.
Sympathetic nervous system responses, fluid shifts within the body, and neuroendocrine stress responses
154
The sympathetic nervous system and neuroendocrine response (increase/decrease) the heart rate.
Increase
155
What are the molecular mediators of the neuroendocrine response to shock?
Epi, norepi, vasopressin, renin
156
What stage of shock do you get lactic acidosis? Why?
Progressive; you get lactic acidosis because cells deprived of adequate oxygen resort to anaerobic metabolism, generating lactic acid
157
_______ provides a measure of the degree of tissue hypoxia?
Level of lactate in the blood
158
What biomarkers can tell you when you've reached the irreversible stage of shock?
Blood levels of TNF-alpha, IL-1, and IL-6
159
What are red neurons?
Dead neurons that develop condensed cytoplasm that is hypereosinophilic because of the closely packed cytoplasmic proteins
160
What is anoxic encephalopathy?
Patient has return of all organ functions except those of the brain
161
The body's compensatory mechanism of shutting off perfusion of the bowel can convert ______ shock into ________ shock.
Hypovolemic into septic
162
What is the only way to cure septic shock from ischemic bowel?
Surgically remove it
163
What does ischemic bowel look like?
Serosal surface has a dusky/dark red appearance
164
What is the gross pathology of acute kidney injury (AKI)?
Swollen kidney with pale cortex and congested medulla
165
What part of the kidney does AKI affect most?
The tubules
166
What are the steps of AKI?
1. Attenuation and loss of proximal tubule epithelial brush borders
2. Epithelial cell swelling and vacuolization
3. Epithelial cell necrosis and sloughing into the tubular lumen
167
What may obstruct the tubules in AKI?
1. Tamm-Horsfall protein, a urinary glycoprotein normally secreted by particular portions of the tubules
2. Myoglobin casts if shock has resulted in rhabdomyolysis
168
What is Waterhouse-Friderichsen syndrome?
Septic shock leads to massive adrenal hemorrhage and necrosis, obliterating the important adrenal collection to counteract shock
169
What do normal resting adrenal cortical cells look like?
They have clear cytoplasm on H&E stain because they're cleared of cholesterol, the precursor for cortisol, aldosterone, and other steroid adrenal hormones
170
What does shock liver look like grossly?
Nutmeg liver -- pattern of alternating red and brown tissue; alternating hemorrhagic necrosis and steatotic areas
171
The vulnerability of hepatocytes to ischemia is directly proportional to _________.
Their proximity to the hepatic lobular central veins
172
What is the most characteristic histological manifestation of shock lung?
Alveolar hyaline membranes
173
What does shock lung look like grossly?
It's typically enlarged and transformed from an air-filled pink-grey sponge into a firm, solidified, edematous, beefy red organ
174
What is the earliest finding of ALI?
Increased numbers of neutrophils in the capilarries in the walls between alveoli
175
What does IL-8 do?
Its a strong neutrophil chemotactic and activating agent
176
In shock lung, release of ________ activates endothelial cells and leads to sequestration of neutrophils in small pulmonary blood vessels.
IL-8, TNF, and IL-1
177
What is the result of alveolar edema and hyaline membranes in the alveolar spaces?
Hypoxemia -- decreased oxygen loading of the blood passing through the lungs
178
________ is the severe end of a spectrum with ALI.
Acute respiratory distress syndrome (ARDS)
179
What is ARDS?
An acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia without evidence for cardiogenic pulmonary edema
180
What are the features of contraction band necrosis of the heart?
Transverse bands of dense eosinophilic hyper contracted sarcomeres spa rated by relatively cleared spaces of cytoplasm
181
In shock, the hyper contraction of sarcomeres is thought to be due to ________.
The influx of calcium brought in by reperfusion
182
If a patient's urine output falls, what should you do before you order a diuretic?
Examine the patient for evidence of bleeding
183
T or F: The bigger the clot, the less likely dissolution becomes.
T
184
What is the relationship of vein and catheter size with clot size?
The bigger the vein and the length of the catheter in it, the bigger the clot that inevitably forms around it.
185
T or F: The longer a foreign body catheter remains in a vein, the less likely the clot will dissolve without a trace.
T
