Hemodynamic disorders Flashcards
1
Q
What are two types of edema?
A
Exudate and Transudate
2
Q
What is exudate made of?
A
It is rich in protein and blood cells and are typical of inflammation
3
Q
What is transudate made of?
A
- Contains less protein and fewer cells
- an ultra-filtrate of plasma fluid
4
Q
What is a typical cause of transudate?
A
Typical of hydrostatic or osmotic pressure pathology
5
Q
What is the specific gravity of transudate?
A
Specific gravity is usually less than 1.012 and a protein content of less than 2gm/100mL
6
Q
What are some factors towards the pathogenesis of Edema?
A
1) increase in hydrostatic pressure
2) Increase in wall permeability
3) Decrease oncotic pressure (decrease albumin concentration)
4) Lymphatic obstruction
7
Q
Is transudate hypocellular or cellular?
A
Hypocellular
8
Q
Is transudate protein rich or poor?
A
Protein poor
9
Q
What is the specific gravity of transudate?
A
Specific gravity <1.012
10
Q
What is transudate due to?
A
Increased hydrostatic pressure
Decreased Oncotic pressure
Na+ retention
11
Q
Is exudate hypocellular or cellular?
A
Cellular
12
Q
Is exudate protein rich or poor?
A
Protein rich
13
Q
What is the specific gravity of exudate?
A
Specific gravity >1.020
14
Q
What is exudate due to?
A
Lymphatic obstruction
Inflammation
15
Q
What Is the different types of pathogenesis causes of Edema?
A
1) Inflammatory
2) Hydrostatic
3) Oncotic
4) Obstructive
5) Hypervolemic
16
Q
Why does inflammatory lead to the pathogenesis of edema?
A
Increases permeability & hyperemia
17
Q
How does hydrostatic lead to the pathogenesis of edema?
A
Increased arterial pressure (hypertension)
Increased venous back pressure (heart failure)
18
Q
How does the oncotic pressure lead to the pathogenesis of edema?
A
Hypoalbuminemia due to:
- loss/proteinuria
- decreased protein synthesis
19
Q
How does the obstruction lead to the pathogenesis of edema?
A
- Most often b tumor or chronic inflammation
- Filaria (worm) -> elephantiasis
20
Q
How does hypovolemia lead to the pathogenesis of edema?
A
Usually d/t sodium and water retention:
- kidney function, renin, angiotensinogen, & aldosterone
- Kidney disease -> increased renin release -> angiotensinogen -> increased aldosterone -> increased Na retention -> increased water retention
21
Q
What are some clinical forms of edema?
A
1) Cerebral edema
2) Pulmonary edema (d/t left-sided heart failure, post-surgery)
3) Pitting edema of the lower extremities
4) Periorbital (facial) edema
5) Hydrothroax
6) Hydropericardium
7) Hydroperitoneum (ascites)
8) Anasarca (Extremegeneralized edema)
22
Q
What are some clinical correlations of edema in regards to the heart?
A
- edema of lower extremities
- edema of back if pt is supine
- left ventricular failure - pulmonary effects
23
Q
What are some clinical correlations of edema in regards to the kidneys?
A
- typically diffuse
- renal failure or nephrotic syndrome
24
Q
What are some clinical correlations of edema in regards to the liver?
A
- ascites d/t low albumin & portal hypertension
25
What is active hyperemia?
Dilatation of arterioles leading to blushing, exercise, inflammation
26
What is passive hyperemia?
Venous back pressure; often associated with hydrostatic edema, cyanosis
- heart failure - pulmonary edema and heart failure cells
27
What does a chronic passive congestion of lungs lead to?
Leads to edema and RBC extravasation into alveoli
28
What is a chronic passive congestion of lungs accompanied by?
Accompanied by anoxia & often results in pulmonary fibrosis
29
In a chronic passive congestion of the lungs, what does an alveolar macrophage do?
Alveolar macrophages take up RBC & degrade hemoglobin = hemosiderin accumulation
30
Cardiac hemorrhage is often what? And what is it caused by?
- often fatal
| - MI, Gun Shot Wound, stabbing wound
31
What is an aortic hemorrhage caused by?
- MVA (organs kee moving at a high speed and rips off part of aorta via ligamentum arteriosum
- weakness due to copper deficiency -> aneurysm
32
What will an arterial hemorrhage look like? What causes it?
- penetrating wound, fractured bones
| - presents as a bright red, pulsating/squirting
33
What will cause a capillary hemorrage? What does it do to venous pressure?
- Trauma, weakness due to vitamin C (scurvy) -increase in venous pressure
34
With the venous, how does it present as a hemorrhage?
Dark/bluish color, oozing
35
In a hemorrage what are some signs and symptoms?
- Intracerebral hemorrhage
- Hematemesis or hemoptysis
- Cardiac hemorrhage
- Venous hemorrhage
- Aortic hemorrhage
- Capillary hemorrhage
- hematochezia or melena (from anus)
- Hematuria
36
What are some clinically important forms of hemorrhage?
- skin/surface hemorrhage
- large accumulation of blood in body cavities/space
- hemoptysis
- epistaxis
37
What are some different types of skin/surface hemorrhage?
- petechia
- purpura
- ecchymosis
38
What is a petechia?
<1 mm and speckles of blood vessels
39
What is purpura?
Between 1 mm- 1cm and larger blotches
40
What is ecchymosis?
Large/blotchy bruises
41
What are some large accumulation of blood in body cavities/spaces?
Hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis
42
What is a hemoptysis?
Respiratory tract/expectoration of blood
43
What is a epistaxis?
Nose bleed
44
What is hematemesis?
Vomiting blood
45
What is hematochezia
anorectal bleeding
46
what is melena
passage of black blood in stool
47
what is hematuria
blood in urine
48
What is metrorrhagia?
bleeding not related to normal monthly menses
49
what is menorrhagia?
Profound menstrual bleeding
50
What happens in a massive hemorrhage?
Blood loss, hypovolemic shock, exsanguination, death
51
If <500 ml of blood is lost what happens?
homeostatic compensation but it is reversible
52
If 1000-1500 ml of blood is lost what happens?
Circulatory shock
53
If >1500 ml of blood is lost what happens?
Lethal
54
What are some of the types of hemorrhage?
- Massive hemmorhage
- Hematoma
- Intracerebral hemorrhage
- Chronic hemorrhage
55
What can an intracerebral hemorrhage lead to?
Stroke, death
56
What can a chronic hemorrhage lead to?
Slow blood loss, iron deficiency anemia (70 ml for normal menstruation)
57
Which hemorrhage has a better outcome, Subdural or epidural hemorrhage?
A subdural hemorrhage because the lower pressure veins bleed more slowly than arteries
58
What is a thrombosis?
clotting due to a transformation of the fluid blood into a solid aggregate encompassing RBCs and fibrin
59
Women smokers who use oral contraceptives have a serious risk for what?
Consequences including increased risk of developing cardiovascular diseases such as blood clots, heart attacks and strokes
60
What are three principal components of intravascular coagulation?
1) Coagulation factors
2) Platelets
3) Endothelial cells
61
What are coagulation factors?
Endogenous (intrinsic) and/or exogenous (extrinsic) pathways
62
What are platelets?
- Neutralize heparin & other anticoagulant factors
| - secrete thromboxane - stimulate coagulation process
63
What properties do endothelial cells have and what normally activates them?
Normally endothelial cells have antithrombotic properties that are activated by IL-1 & TNF which causes them to lose their negative charge and antithrombotic
64
Name the 3 body fluid compartments?
intracellular, interstitial, intravascular.
65
How much fluid is taken in a day?
2.5 liters.
66
How much fluiid is let out in a day and how?
2.5 liters. 0.1 in stool, 0.9 in respiration/sweat, 1.5 in urine.
67
Elephantiasis is caused by what?
Lymph blockage from a parasite.
68
Skin hemorrhages are what?
Bruises
69
What is the first step in forming a thrombi?
Defect is covered with fibrin and platlets.
70
What is the second step in forming a thrombi?
Fibrin meshwork anchors RBCs into nascent thrombus.
71
What is the third step in forming a thrombi?
Fully formed thrombi consists of layers of fibrin and RBCs
72
Intramural thrombi of the heart causes what?
overlying Myocardial infarct.
73
Valvular thrombi of the heart causes what?
mimic endocarditis.
74
arterial thrombi cause what?
atherosclerosis when attached to the walls. Can be found with aortic aneurysms
75
When is a venous thrombi found?
in dialated veins. (varicose veins)
76
Where are microvascular thrombi found at?
Arterioles, capillaries, and venules.
77
Deep venous thrombosis is predisposed by Virchow's triad which is what 3 things?
1. Stasis.
2. Hypercoagulability.
3. endothelial damage.
78
Who is at risk for deep venous thrombosis?
Elderly people on transcontinental flights and birth control pills and smoking
79
What are lines of zahn?
Distinct layering of cellular elements and fibrin that occur in atrial and venous thrombi.
80
Occlusion of the lumen from a thrombi is called what?
Infarct.
81
Lysis of the thrombus is called?
reperfusion.
82
Recanalization of a thrombus leads to what?
reestablished blood flow.
83
What is embolization of a thrombi?
Breaking off of a clot.
84
What are the five different fates for thrombi?
1) Occlusion of the lumen
2) Lysis of the thrombus
3) Organization of the thrombus (find another route)
4) Recanalization
5) Embolization
85
What is an embolus?
Undissolved materials like thrombus in blood.
86
Name 4 types of embolisms?
1) thromboemboli
2) liquid emboli
3) gaseous emboli
4) solid particle emboli.
87
Amniotic fluid emboli can lead to what?
DIC (disseminated intravascular coagulation), especially postpartum.
88
What can cause liquid emboli?
Fat (long bone fracture), oil, amniotic fluid
89
What can cause gaseous emboli?
Aire injection, caisson disease (decompression sickness from N2)
90
What can cause solid particle emboli?
Cholesterol crystals (atheromatous plaques), bone marrow (fractures), tumor emboli (most common solid particle emboli)
91
Pulmonary embolus clinically present with what?
Chest pain, tachypnea, dyspnea.
92
95% of pulmonary emboli arise from what?
Deep leg veins.
93
What are the origins of venous thromboemboli?
Anywhere (but on diagram it is saddle, lung, venous thrombi.)
94
What are the origins of arterial thromboemboli?
Cerebral infarcts
Left ventricle
(on diagram it is: brain, kidney, spleen, Intestinal, ventricular and extremity infarct.)
95
A white infarct is typical of what?
`Arterial occlusion in solid organs with single blood supply. (ie: heart, kidney, spleen)
96
Red infarct is typical of what?
Venous obstruction like intestines and testes twisting.
97
The fate of infarcts depends on what?
Their anatomical site, type of cells forming the tissue, circulatory status , extent of necrosis.
98
What areas do white infarcts occur on organs?
Rimmed areas
99
What is a volvulus?
Twisting
100
What type of infarct is seen with volvulus?
Red infarct
101
What are 3 possible causes of shock?
1. Pump failure of the heart.
2. Loss of fluid from circulation.
3. Loss of peripheral vascular tone.
102
Pump failure leads to what type of shock?
Cardiogenic shock.
103
Loss of fluid from circulation lead to what type of shock?
Hypovolemic shock.
104
Loss of peripheral vascular tone leads to what type of shock?
Hypotensive shock.
105
Loss of blood, myocardial or valvular disease, or vasodilation leads to what?
Heart failure
106
heart failure leads to what?
Decreased cardiac output.
107
Decreased cardiac output leads to what?
Decreased blood to tissues.
108
Decreased blood to tissues leads to what?
Cell anoxia.
109
Cell anoxia leads to what?
Shock and edema
110
Shock leads to what?
Coma, renal failure, lung failure, death, gi bleeding.
111
What are the 3 clinical stages of shock?
1. early or compensated shock.
2. Decompensated but reversible shock.
3. Irreversible shock.
112
What happens with the heart during compensated shock?
Tachycardia (beats faster). (D/t CO = SV X HR, low SV means higher HR to compensate)
113
Besides heart compensation, what else happens with compensated shock?
Vasoconstriction of arterioles and reduced urine production.
114
What happens with decompensated reversible shock?
hypotension, tachypnea and shortness of breath, oliuria, acidosis.
115
What happens with irreversible shock?
1. Circulatory collapse.
2. marked hypoperfusion of vital organs.
3. Loss of vital functions.
