Exam 2 Flashcards
1
Q
What percentage of blood vol is normally within systemic veins?
A
65%
2
Q
congestion
A
passive accumulation of blood within vasculature
3
Q
what causes congestion
A
obstruction of venous system - heart failure, etc
4
Q
gross appearance of congestion in tissue
A
dark red or purple due to poor oxygenation
5
Q
hypostatic congestion
A
postmortem pooling of blood in the dependent portion of the body - due to gravity basically livor mortis for organs
6
Q
hyperemia
A
active increase of blood flow to a tissue
7
Q
physiologic hyperemia
A
increased demand for nutrients in tissues
8
Q
pathologic hyperemia
A
response to vasodilation in inflammation
9
Q
gross appearance of hyperemia
A
tissue becomes red and warm
10
Q
edema
A
excessive accumulation of fluid in intercullular spaces (in extracellular matrix and body cavities)
11
Q
3 forces that balance appropriate fluid in tissues and body cavities
A
hold in vessels: plasma oncotic pressure
push out of vessels: hydrostatic pressure, interstitial oncotic pressure
12
Q
plasma oncotic pressure
A
force that holds fluid in vessels - due to high protein enviro in plasma (usually created by Albumin)
13
Q
hydrostatic pressure
A
intravascular pressure creatde by amount of fluid and force of pumping (force that pushes fluid out of vessels)
14
Q
interstitial oncotic pressure
A
low protein enviro that draws fluid out of vessels
15
Q
A
A. Plasma oncotic pressure
B. interstitial oncotic pressure
C. hydrostatic pressure
16
Q
4 mechanisms of edema
A
- increased intravascular hydrostatic pressure
- increased microvasular permeability
- decreased plasma oncotic pressure
- decreased lymphatic drainage
17
Q
causes of increased intravascular hydrostatic pressure
A
hypertension
congestion
fluid overload
18
Q
causes of increased microvascular permeability
A
inflamm. with contraction of endothelial cells
direct endothelial cell damage
19
Q
causes of decreased plasma oncotic pressure
A
decreased albumin production (liver failure)
increased albumin loss
20
Q
causes of decreased lymphatic drainage
A
local obstruction
lymphangitis
21
Q
generalized edema
A
due to increased hydrostatic pressure or hypoalbumenemia
22
Q
localized edema
A
due to increase hydrostatic pressure from impaired venous return, lymphatic drainage, or local inflammation
23
Q
3 types of edema
A
- transudate
- modified transudate
- exudate
24
Q
transudate
A
low protein fluid
normal integrity od endothelium is maintained
25
modified transudate
variable protein content, moderate cellularity, least specific
26
exudate
high protein fluid, often turbid due to high cellularity.
due to increased permeability of vessels
27
consolidation of lung presents as:
lung is rubbery and heavy due to water replacing alveolar air space. floats poorly or sinks in water.
due to edema into lungs
28
atelectasis
collapse of the lungs due to outside pressure on the lungs or blockage of airways
29
hydrothorax
edema into thorax
30
hydroperitoneum
edema into abdomen
31
hydropericardium
edema into pericardial sac
32
anascara
edema into entire body
33
pitting edema
most common, fluid dispaced by digital pressure
fluid displaced from the tissue into the lymphatics and returned
34
non-pitting edema
lymphedema
lymphatic return is obstructed
35
chylous effusion
(chyle)
leakage of lymph from the thoracic duct into the thoracic cavity
most common in cats, most often idiopathic
36
chyle gross appearance
milky, transleucent white fluid. +/- glistening lipid droplets
37
pyothorax gross appearance
opaque white fluid due to presence of neutrophils and fibrin in fluid
(sometimes can present as opaque pink/red due to hemorrhage)
38
hemmorhage
loss of all components of blood due to damage to the cardiovascular system
39
causes of hemorrhage
trauma, bacterial toxins, vasculotropic viruses, etc
40
3 kinds of hemorrhage
petechia, ecchymosis, hematoma
41
petechia
pinpoint hemorrhages. often seen w/ septicemia, clotting factor defecits, and thrombocytopenia
42
ecchymosis
"bruise" - larger hemorrhages due to loss of large amts of blood into tissue
43
hematoma
pooling of blood in tissue or an organ. typically in connective tissue where large amounts of blood can accumulate locally
44
hemothorax
hemorrhage into thorax
45
hemoperitoneum
hemorrhage into abdomen
46
hemopericardium
hemorrhage into pericardial sac
47
hematochezia
frank blood in the stool (red color)
48
melena
digested blood in the stool (black, dark, tar like)
49
hematemesis
vomiting blood
50
hematuria
urinating blood
51
epistaxis
blood from the nares
52
hyphema
hemorrhage into anterior chamber of the eye
53
anemia
a decrease in hematocrit or hemoglobin concentration or whole blood
54
hematocrit
ratio of vol of RBCs to total blood vol
55
3 mechanisms of anemia
hemorrhage, hemolysis, decreased production
56
clinical signs of anemia
* pallor (pale mucous membranes)
* weakness/exercise intolerance
* tachycardia
* syncope
* heart murmur
* weak pulse
57
exsanguination
death due to loss of blood
58
hypovolemia
loss of blood
59
hypovolemic shock
loss of 1/3 or more of the blood vol. may result in death
60
in domestic animals, blood is what % of total body weight?
7-9%
(can estimate 10% for easy calculation)
61
shock
insufficient vascular perfusion of vital organs
62
3 types of shock
1. hypovolemic
2. cardiogenic
3. vasogenic
63
3 types of vasogenic shock
1. septic
2. neurogenic
3. anaphylactic
64
cardiogenic shock
due to heart failure. decrease in SV and CO
65
causes of cardiogenic shock
myocardial infarction, arrhythmias, cardiomyopathy, cardiac tamponade
66
what is cardiac tamponade
R side of the heart is compressed to blood doesnt fill the R ventricle suffieciently to puch blood forward
67
vasogenic shock
decrease in peripheral vascular tone leading to blood pooling in vessels
68
septic shock
most common
vasodilation caused by components of bacteria or fungi that induce the release of excessive inflamm. mediators
69
anaphylactic shock
generalized type I hypersensitivty - widespread degranulation of mast cells with the release of histamine causing vasodilation
70
neurogenic shock
due to trauma to CNS (typically cranial to T6) or electrocution resulting in loss of sympathetic stimualtion to vasculature (w/o symp stimulation, vasculature dilates)
71
typical clinical presentation of shock
* hypotension
* weak pulse
* tachycardia (neurogenic will have brachycardia due to unopposed sympathetics)
* hyperventilation
* reduced urine output (overall GFR is increased)
72
hemostasis
stopping bleeding
73
primary components in hemostasis
endothelium, platelets, coagulation factors
74
normal endothelium job (no injury)
allows smooth bloodflow and prevents adhesion of platelets
75
endothelium when injured
1. arteriole vasoconstriction from neurogenic stimuli and mediators
2. platelets attach due to exposed subendothelial collagen
3. platelet adhesion strengthened with von Willebrand's factor
4. tissue factor is now exposed to the blood and activates the coagulation cascade
76
where is tissue factor found
tuncia media and tunica adventitia
77
primary hemostasis
platelets
78
end product of the coagulation cascade
fibrin
79
secondary hemostasis
fibrin links together platelets to form a thrombus
80
major stimulus for the coagulation cascade
tissue factor
81
intrinsic pathway of the coagulation cascade
initiated by the effects of abnormal surfaces on components normally present in the blood - i.e. glass in a red-top tube activates hageman factor and causes blood to clot
82
extrinsic pathway of the coagulation cascade
initiated when blood contacts tissue factor
83
common pathway of coagulation cascade
Ca++ important!!!
No Ca++ = no clotting
prothrombin --> thrombin --> polymerizes fibrinogen to fibrin strands
84
fibrinolysis
plasmin breaks down fibrin
85
thrombolysis
dissolves the fibrin-platelet thrombus after vessel healing
86
prevent further hemostatis with ?
inhibition of thrombin
87
What is DIC?
disseminated intravascular coagulation - uncontrolled coagulation throughout the body, causing widespread tissue damage
88
2 potential outcomes of thrombi
1. dissolution - the thrombis is broken down
2. persistance
89
thrombosis
persistent thrombi - pathologic formation of one or more intravascular thrombi that partially or fully occlude a vessel
90
major determinants of thrombosis
1. endothelial injury (most important)
2. abnormal blood flow (turbulent flow, blood stasis)
3. hypercoagulability (inflamm., loss of antithrombin III, increased platelet activation)
91
main complications of thrombosis
1. obstruction of blood flow (partial or complete)
2. ischemia and infarction of local tissues
3. increassed intravascular pressure
4. embolization
92
thromboemboli
whole or part of thrombus breaks loose and gets lodged in a vessel downstream
93
embolism
a detatched intravascular solid, liquid, or gasseous mass that is carried by the blood to a site distant from its origin
94
ischemia
reduced blood flow to an area
95
example of a synthesized chemical mediator
arachidonic acid metabolites (PGE2)
96
example of exogenous microbial products
lipopolysaccharide, peptidoglycan..
97
preformed chemical mediators
histamine, serotonin, kinins
98
pus
exudate composed largely of neutrophils
99
purulent/suppurative
composed of pus
100
abscess
a pocket of pus
101
chemoattractants of eosinophils
parasites, mast cells (histamine, eotaxin)
102
eosinophils degranulate to release ..?
major basic protein
103
granulomatous
largely macrophages surrounding, enclosing, and phagocytizing with granuloma formation
104
granulomatous inflammation - lesions grow quickly or slowly?
slowly - can take weeks to months
105
When do lymphocytes arrive to the inflamm site?
24-48 hrs
(last to arrive)
106
lymphoplasmacytic inflammation
largely lymphocytes and plasma cells responding to chronic antigenic stimulation
107
fibrinous inflammation
fibrin comprises large part of visible inflammation
108
catarrhal inflammation
excessive mucus production
109
proliferative inflammation
seems to be forming more tissue
110
4 phases of healing after tissue injury
1. hemostasis
2. acute inflammation
3. proliferation
4. remodeling
111
2 main mechanisms of tissue repair (proliferation)
regeneration - same cells
replacement - replaced cells
112
what cell produces collagen
fibroblasts
113
presence of fibrin means the inflamm is **acute/chronic**?
acute
114
presence of collagen means inflamm is **acute/chronic**?
chronic
115
fibrosis - acute or chronic?
chronic
116
permanent cell
cells are terminally differentialted and have little to no ability to divide and regenerate
117
examples of permanent cells
neurons, cardiomyocytes
118
stable cells
cells normally exhibit low turnover, but will readily divide and regenerate if stimulated
119
examples of stable cells
hepatocytes, renal tubular epithelial cells, osteoblasts, fibroblasts
120
labile cells
cells normally exhibit high turnover with constant division and regeneration
121
examples of labile cells
keratinocytes, gastrointestinal epithelial cells, hematopoietic cells
122
histologic evidence of regeneration
* cells in mitosis
* hypertrophy
* hyperplasia
* karyomegaly
* bi- or multinucleated cells
* cytoplasmic basophilia
* attenuation
