Circulatory Dysregulation Flashcards
(102 cards)
1
Q
What is edema?
A
excess accumulation of fluid
2
Q
What does edema result from?
A
altered vascular homeostasis
3
Q
What does edema result in?
A
change in net movement of water across vascular wall
4
Q
What are some edemas in the body cavities?
A
- Hydrothorax
- hydropericardium
- Hydroperitoneum (ascites)
5
Q
What is an edema in the interstitial tissue spaces called?
A
anasarca- generalized edema
6
Q
What are the MAJOR causes of edema?
A
- increased hydrostatic pressure in vessels = heart failure
- Decreased plasma oncotic pressure= hypoproteinemia
- Vascular permeability is altered= allergic response-histamine
7
Q
what are other causes of adema?
A
- increased sodium retention
5. lymphatic obstruction or damage
8
Q
What two types of edema are due to congestive heart failre?
A
- pulmonary edema
2. peripheral (subcutaneous edema)
9
Q
What causes LEFT sided heart failure?
A
- accumulation of fluid in alveoli of lung
2. increased hydrostatic pressure in pulmonary vascular bed= resulting from failure of the left side of the heart
10
Q
What causes RIGHT side heart failure?
A
- accumulation of fluid in subcutaneous tissues
- caused by increased hydrostatic pressure in the systemic venous system= resulting from failure of the right side of the heart
11
Q
What causes decreased plasma oncotic pressure?
A
hypoproteinemia (insufficient albumin)
12
Q
What is nephrotic syndrome?
A
loss of protein in kidney
13
Q
What does hypoproteinemia lead to?
A
- nephrotic syndrome
2. decreased albumin production by cirrhotic lier
14
Q
What causes altered vascular permeability?
A
- allergic responses liberating histamine
- acute inflammation
- burn injury
15
Q
What is primary increased sodium retention associated with?
A
renal disorders
16
Q
What is secondary increased sodium retention associated with?
A
congestive heart failure
-decreased cardiac output–> decreased renal blood flow–> activation of renin-angiotensin system–> aldosterone activated–> retention of sodium and water
17
Q
What causes lymphatic obstruction?
A
tumor or damage to lymphatics
18
Q
What does lymphatic obstruction lead to ?
A
lymphedema
19
Q
What is transudate?
A
non-inflammatory edema fluid that results from altered intravascular hydrostatic pressure or osmotic pressure= low protein content and specific gravity
20
Q
What are the transudate values?
A
low protein content and specific gravity
21
Q
What is exudate?
A
Edema fluid from increased vascular permeability as a result of inflammation
22
Q
What are the exudate values?
A
- high protein contenet and specificity> 1.020
- contains large numbers of inflammatory leukocytes which consume glucose and thus results in fluid with greatly reduced glucose content
23
Q
What are 4 types of edema?
A
- Anasarca
- Hydrothorax
- Hydropericardium
- Hydroperitoneum (Ascites)
24
Q
What is anasarca?
A
generalized edema
25
What is hydrothorax?
Accumulation of fluid in the pleural cavity
26
Hydropericardium
Abnormal accumulation of fluid in the pericardial cavity- may result in cardiac tamponade
27
What is hydroperitoneum (ascites)?
abnormal accumulation of fluid int he peritoneal cavity
28
What is hyperemia?
It is localized increased in the volume of blood in capillaries and small vessels
29
Where does chronic passive congestion occur
lung, liver, and lower extremities
30
What causes a hemorrhage?
rupture of blood vessels
31
In a hemorrhage, escape of blood from the vasculature goes into?
1. surrounding tissues
2. hollow organ
3. body cavity
4. to the outside
32
What is a thrombus?
A structured solid mass composed of elements derived from the coagulation cascade
33
What is considered as a dynamic biologically active structure, rather than a passive plug?
a thrombus!
34
What is in a thrombus/coagulation cascade?
platelets, insoluble fibrin, embedded RBCs
35
What are the 3 main pro-thrombotic factors?
1. endothelial dysfunction
2. changes in the flow patter of blood
3. changes in the potential blood coagulability
36
What causes endothelial dysfunction?
Direct Injury
- trauma and inflammation
- atheroma
37
What is a result of the activation of the normal blood coagulation system?
thrombosis
38
What are there types of thrombi?
thrombi in diff parts of the circulation have different causative factors and different appearances
39
What are the 4 types of thrombi?
1. arterial thrombus
2. venous thrombus
3. occlusive thrombus
4. mural thrombus
40
What kind of thrombus occurs in areas of fast moving blood flow?
Arterial Thrombus
41
What is an arterial thrombus made of?
layers of platelets interspersed with layers of fibrin containing entrapped RBC's= lines of Zahn
42
What are lines of Zahn
layers of fibrin with trapped RBCs
43
What kind of thrombus does not contain lines of Zahn?
```
Venous Thrombus (Phlebothrombosis)
- dark red, soft, & gelitanous with greater proportion of entrapped RBCs relative to amount of platelets/fibrin
```
44
What kind of thrombus occurs in areas of slow moving blood flow most often in veins of lower extremities and periprostatic or other pelvic veins?
venous thrombus (phlebothrombosis)
45
What is fibrinolysis?
As a vessel wall is repaired, a small platelet/fibrin thrombus is normally removed via fibrinolysis
46
What is a multi-enzyme process that destroys fibrin filament meshwork allowing dissolution of the thrombus?
fibrinolysis
47
How does fibrinolysis occur?
the enzyme plasmin cleaves fibrin
| -formed from plasminiogen
48
Where is plasminogen derived from?
endothelial cells
- usually inhibited by plasminogen activator inhibitor
- activated protein C prevents inhibition thereby facilitating fibrinolysis
49
What are the 4 main outcomes of occlusive thrombi?
1. lysis by the fibrinolytic system
2. propagation (pathologic thrombus)
3. Organization and recanalization
4. Thromboembolism
50
What is Thromboembolism?
Fragments break off thrombus and carried by the circulation to impact other vessels
51
What is an embolism?
occlusion of a vessel by a mass of material that is transported in the blood stream (an embolus)
52
What causes the most common type of embolus?
Fragments of circulating thrombus (thromboembolus)
53
How does Thromboembolus occur?
Fragment breaks off site of thrombosis and blood circulation carries it to a point where it meets a blood vessel with a lumen too small to permit further passage
54
What is the most common preventable cause of sudden death in a hospital patient?
Pulmonary thromboembolism
55
What usually causes pulmonary thromboemblism?
thrombosis of deep leg vein
| -calf, popliteal, femoral, iliac veins
56
What are other rare sources of pulmonary thromboembolism?
- periprostatic venous plexus in males
| - small pelvic veins in women
57
What are the consequences of pulmonary thromboembolism?
- increase in pulmonary arterial pressure
| - ischemia of the lung
58
What are clinical predisposers of pulmonarythromboembolism
immobility and bed rest (postoperative period, pregnancy and post partum), nephrotic syndrome, severe burns, trauma, cardiac failure, disseminated malignancy
59
What are the 4 types of pulmonary thromboembolism?
1. massive pulmonary embolism (5%)
2. major pulmonary embolism (10%)
3. minor pulmonary embolism (85%)
4. recurrent minor pulmonary embolism
60
What is massive pulmonary embolism (5%)?
If 60% of pulmonary vasculature if suddenly blocked, then the heart cannot pump blood through the lungs--> cardiovascular collapse--> beat with no output--> rapid death
61
What is major pulmonary embolism (10%)?
- blockage of middle-sized pulmonary arteries
| - breathlessness; infarction of lungs (10%); hemoptysis; pleuritic chest pain; can lead to massive type if untreated
62
Where does a saddle embolus travel?
pulmonary artery bifurcation
63
What does the saddle embolus do?
- travels to the pulmonary artery bifurcation
| - straddles the bifurcation and blocks pulmonary circulation
64
What does a saddle embolus result in?
hemorrhagic pulmonary infarct
65
What is a minor pulmonary embolism (85%)?
- blockage of small peripheral vessels by small emboli
| - asymptomatic or breathlessness, pleuritic chest pain; can lead to massive type if untreated
66
What is recurrent minor pulmonary embolism?
- very rare
| - blockage of many small vessels over many months--> pulmonary hypertension
67
What are the key facts to know about pulmonary thromboembolism?
- usually follows thrombosis in leg veins, often deep calf veins
- small pulmonary emboli impact peripheral branches of the pulmonary artery and cause pulmonary infarcts
- a small pulmonary embolus (PREMONITORY EMBOLUS) may be followed by a much larger fatal embolus
- large pulmonary emboli may impact in and obstruct a major pulmonary artery to cause sudden death
68
What is the best way to prevent pulmonary embolus?
prevention of leg vein thrombosis
69
What are the sites of origin for arterial emboli?
- mural thrombus (adherent to wall of a heart chamber or major artery)
- at junction of internal and external carotid artery
- left ventricle
- left atrium (atrial thrombosis)
70
What are mural thrombuses of the left atrium (artrial thrombosis) associated with?
mitral stenosis or atrial fibrillation
71
What causes a mural thrombus of the left ventricle?
MI
72
What is an infarct?
tissue of necrosis due to interference with blood flow
73
What results from ischemia?
infarction
- failure of adequate blood supply to a tissue causes a cell damage and coagulative tissue necrosis
- major cause of morbidity and mortality
74
What are major causes of morbidity and mortality?
myocardial infarction, cerebral infarction, pulmonary infarction, gangrene of lower limb, bowel infarction
75
What are most infarctions caused by?
obstruction of arterial supply to a tissue; some due to blockage of venous drainage
76
What shapes the infarct according to the territory of supply of the blocked vessel?
artery blockage
| -occlusion of small vessels results in wedge-shaped infarct with the occluded vessel at the apex
77
What are the two types of infarctions?
1. red (hemorrhagic) infarcts
| 2. white (ischemic) infarcts
78
Describe white infarcts
arterial insufficiency AND not reperfused AND single blood supply
79
Describe red infarcts
Venous insufficiency OR reperfused OR dual blood spply
80
Red (Hemorrhagic) infarcts
"Red because RBCs ooze into necrotic tissue
-loose, well vascularized tissue with redundant arterial blood supplies (hemorrahge into the infarct occurs from the nonobstructed portion of the vasculature
81
Where do red infarcts occur?
lung, GI tract, liver testes, brain (venous sinus occlusion by thrombosis)
82
What does slow occlusion of a vessel result in?
- development of a collateral circulation- not in areas supplied by a single artery OR
- tissue undergoes ischemic atrophy(not infarction)
83
What happens to tissues that undergo ischemic atrophy?
- specialized cells shrink
| - support tissue becomes amorphous pink staining and hyalinized
84
**What is an infarction?
death of tissue due to anoxia following abrupt interference with the blood supply
85
**What is an arterial infarction?
Sudden obstruction to the arterial supply to a tissue or organ
86
**What is a venous infarction?
sudden and persistent obstruction to venous drainage of an organ or tissue
87
What is shock?
- clinical state associated with generalized (systemic) failure of tissue perfusion due to reduction in tissue blood flow and manifested by hypotension
- circulatory collapse with decreased oxygenation of tissues
88
What are the diff types of schock?
cardiogenic, hyovolemic, septic, anaphylactic
89
What is cardiogenic shock?
circulatory collapse from pump failure of the left ventricle most often caused by massive myocardial infarction
90
What is hypovolemic shock?
- acute reduction in circulating blood volume caused by severe hemorrhage or massive loss of fluid from the skin from extensive burns or free severe trauma OR
- loss of fluid from GI tract through severe vomiting or diarrhea
91
What is septic shock most often associated with?
gram neg infections--> gram neg endotoxemia
92
What is the result of septic shock?
initial vasodilation--> increased blood flow--> significant peripheral pooling--> relative hypovolemia and impaired perfusion
93
What is the result of a septic gram neg endotoxemia?
lippolysaccharide endotoxin--> cytokines--> direct toxic injury to vessels--> coagulation pathway and DIC or
superantigens in toxic shock syndrome (staphylococcus aureus)
94
What is anaphylactic shock most associated with?
Type 1 hypersensitivity reaction
95
What is neurogenic shock?
sudden loss of the Autonomic Nervous System signals to the Smooth muscle in vessel walls (results from severe CNS damage)
or
sudden loss of background sympathetic stimulation (vessels suddenly relax resulting in a sudden decrease in peripheral vascular resistance (vasodilation ) and decreased blood pressure
96
Is acute tubular necrosis of kidney reversible?
Yes, w/ appropriate medical management
97
What are morphologic manifestations of shock?
acute tubular necrosis of kidney, (most important)
- areas of brain necrosis
- centrilobular necrosis of the liver
- fatty changes of heart or liver
- patchy mucosal hemorrages in the colon
- depletion of lipid in the adrenal cortex
- pulmonary edema
98
What is a sign of shock in the kidneys?
necrosis of tubular epithelium
99
What are the 3 pathways of the coagulation cascade?
common pathway
extrinsic pathway
intrinsic pathway
100
What is the common pathway of the coagulation cascade?
- results in cross linked fibrin
- thrombin is the key protease **
- has feedback to activate co-factors, other proteases and thus amplifies the cascade
101
What is the extrinsic pathway of the coagulation cascade?
coagulation initiated by Tissue Factor (generated by damaged tissue) interacting with factor VII
102
What is the intrinsic pathway of the coagulation cascade?
coagulation initiated by contact with surface agents (collagen, kallikrein) acting through factor XII
- currently thought to have minor role for in vivo coagulation
- activation of factor XI and coagulation stimulation is seen mainly after severe injury (e.g. trauma)
