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Gen Path > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What percentage of blood vol is normally within systemic veins?

A

65%

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2
Q

congestion

A

passive accumulation of blood within vasculature

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3
Q

what causes congestion

A

obstruction of venous system - heart failure, etc

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4
Q

gross appearance of congestion in tissue

A

dark red or purple due to poor oxygenation

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5
Q

hypostatic congestion

A

postmortem pooling of blood in the dependent portion of the body - due to gravity basically livor mortis for organs

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6
Q

hyperemia

A

active increase of blood flow to a tissue

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7
Q

physiologic hyperemia

A

increased demand for nutrients in tissues

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8
Q

pathologic hyperemia

A

response to vasodilation in inflammation

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9
Q

gross appearance of hyperemia

A

tissue becomes red and warm

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10
Q

edema

A

excessive accumulation of fluid in intercullular spaces (in extracellular matrix and body cavities)

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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

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12
Q

plasma oncotic pressure

A

force that holds fluid in vessels - due to high protein enviro in plasma (usually created by Albumin)

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13
Q

hydrostatic pressure

A

intravascular pressure creatde by amount of fluid and force of pumping (force that pushes fluid out of vessels)

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14
Q

interstitial oncotic pressure

A

low protein enviro that draws fluid out of vessels

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15
Q
A

A. Plasma oncotic pressure
B. interstitial oncotic pressure
C. hydrostatic pressure

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16
Q

4 mechanisms of edema

A
  1. increased intravascular hydrostatic pressure
  2. increased microvasular permeability
  3. decreased plasma oncotic pressure
  4. decreased lymphatic drainage
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17
Q

causes of increased intravascular hydrostatic pressure

A

hypertension
congestion
fluid overload

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18
Q

causes of increased microvascular permeability

A

inflamm. with contraction of endothelial cells

direct endothelial cell damage

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19
Q

causes of decreased plasma oncotic pressure

A

decreased albumin production (liver failure)

increased albumin loss

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20
Q

causes of decreased lymphatic drainage

A

local obstruction
lymphangitis

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21
Q

generalized edema

A

due to increased hydrostatic pressure or hypoalbumenemia

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22
Q

localized edema

A

due to increase hydrostatic pressure from impaired venous return, lymphatic drainage, or local inflammation

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23
Q

3 types of edema

A
  1. transudate
  2. modified transudate
  3. exudate
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24
Q

transudate

A

low protein fluid

normal integrity od endothelium is maintained

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25
Q

modified transudate

A

variable protein content, moderate cellularity, least specific

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26
Q

exudate

A

high protein fluid, often turbid due to high cellularity.

due to increased permeability of vessels

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27
Q

consolidation of lung presents as:

A

lung is rubbery and heavy due to water replacing alveolar air space. floats poorly or sinks in water.

due to edema into lungs

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28
Q

atelectasis

A

collapse of the lungs due to outside pressure on the lungs or blockage of airways

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29
Q

hydrothorax

A

edema into thorax

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30
Q

hydroperitoneum

A

edema into abdomen

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31
Q

hydropericardium

A

edema into pericardial sac

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32
Q

anascara

A

edema into entire body

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33
Q

pitting edema

A

most common, fluid dispaced by digital pressure

fluid displaced from the tissue into the lymphatics and returned

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34
Q

non-pitting edema

A

lymphedema

lymphatic return is obstructed

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35
Q

chylous effusion
(chyle)

A

leakage of lymph from the thoracic duct into the thoracic cavity

most common in cats, most often idiopathic

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36
Q

chyle gross appearance

A

milky, transleucent white fluid. +/- glistening lipid droplets

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37
Q

pyothorax gross appearance

A

opaque white fluid due to presence of neutrophils and fibrin in fluid

(sometimes can present as opaque pink/red due to hemorrhage)

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38
Q

hemmorhage

A

loss of all components of blood due to damage to the cardiovascular system

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39
Q

causes of hemorrhage

A

trauma, bacterial toxins, vasculotropic viruses, etc

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40
Q

3 kinds of hemorrhage

A

petechia, ecchymosis, hematoma

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41
Q

petechia

A

pinpoint hemorrhages. often seen w/ septicemia, clotting factor defecits, and thrombocytopenia

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42
Q

ecchymosis

A

“bruise” - larger hemorrhages due to loss of large amts of blood into tissue

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43
Q

hematoma

A

pooling of blood in tissue or an organ. typically in connective tissue where large amounts of blood can accumulate locally

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44
Q

hemothorax

A

hemorrhage into thorax

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45
Q

hemoperitoneum

A

hemorrhage into abdomen

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46
Q

hemopericardium

A

hemorrhage into pericardial sac

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47
Q

hematochezia

A

frank blood in the stool (red color)

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48
Q

melena

A

digested blood in the stool (black, dark, tar like)

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49
Q

hematemesis

A

vomiting blood

50
Q

hematuria

A

urinating blood

51
Q

epistaxis

A

blood from the nares

52
Q

hyphema

A

hemorrhage into anterior chamber of the eye

53
Q

anemia

A

a decrease in hematocrit or hemoglobin concentration or whole blood

54
Q

hematocrit

A

ratio of vol of RBCs to total blood vol

55
Q

3 mechanisms of anemia

A

hemorrhage, hemolysis, decreased production

56
Q

clinical signs of anemia

A
  • pallor (pale mucous membranes)
  • weakness/exercise intolerance
  • tachycardia
  • syncope
  • heart murmur
  • weak pulse
57
Q

exsanguination

A

death due to loss of blood

58
Q

hypovolemia

A

loss of blood

59
Q

hypovolemic shock

A

loss of 1/3 or more of the blood vol. may result in death

60
Q

in domestic animals, blood is what % of total body weight?

A

7-9%
(can estimate 10% for easy calculation)

61
Q

shock

A

insufficient vascular perfusion of vital organs

62
Q

3 types of shock

A
  1. hypovolemic
  2. cardiogenic
  3. vasogenic
63
Q

3 types of vasogenic shock

A
  1. septic
  2. neurogenic
  3. anaphylactic
64
Q

cardiogenic shock

A

due to heart failure. decrease in SV and CO

65
Q

causes of cardiogenic shock

A

myocardial infarction, arrhythmias, cardiomyopathy, cardiac tamponade

66
Q

what is cardiac tamponade

A

R side of the heart is compressed to blood doesnt fill the R ventricle suffieciently to puch blood forward

67
Q

vasogenic shock

A

decrease in peripheral vascular tone leading to blood pooling in vessels

68
Q

septic shock

A

most common
vasodilation caused by components of bacteria or fungi that induce the release of excessive inflamm. mediators

69
Q

anaphylactic shock

A

generalized type I hypersensitivty - widespread degranulation of mast cells with the release of histamine causing vasodilation

70
Q

neurogenic shock

A

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
Q

typical clinical presentation of shock

A
  • hypotension
  • weak pulse
  • tachycardia (neurogenic will have brachycardia due to unopposed sympathetics)
  • hyperventilation
  • reduced urine output (overall GFR is increased)
72
Q

hemostasis

A

stopping bleeding

73
Q

primary components in hemostasis

A

endothelium, platelets, coagulation factors

74
Q

normal endothelium job (no injury)

A

allows smooth bloodflow and prevents adhesion of platelets

75
Q

endothelium when injured

A
  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
Q

where is tissue factor found

A

tuncia media and tunica adventitia

77
Q

primary hemostasis

A

platelets

78
Q

end product of the coagulation cascade

A

fibrin

79
Q

secondary hemostasis

A

fibrin links together platelets to form a thrombus

80
Q

major stimulus for the coagulation cascade

A

tissue factor

81
Q

intrinsic pathway of the coagulation cascade

A

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
Q

extrinsic pathway of the coagulation cascade

A

initiated when blood contacts tissue factor

83
Q

common pathway of coagulation cascade

A

Ca++ important!!!
No Ca++ = no clotting

prothrombin –> thrombin –> polymerizes fibrinogen to fibrin strands

84
Q

fibrinolysis

A

plasmin breaks down fibrin

85
Q

thrombolysis

A

dissolves the fibrin-platelet thrombus after vessel healing

86
Q

prevent further hemostatis with ?

A

inhibition of thrombin

87
Q

What is DIC?

A

disseminated intravascular coagulation - uncontrolled coagulation throughout the body, causing widespread tissue damage

88
Q

2 potential outcomes of thrombi

A
  1. dissolution - the thrombis is broken down
  2. persistance
89
Q

thrombosis

A

persistent thrombi - pathologic formation of one or more intravascular thrombi that partially or fully occlude a vessel

90
Q

major determinants of thrombosis

A
  1. endothelial injury (most important)
  2. abnormal blood flow (turbulent flow, blood stasis)
  3. hypercoagulability (inflamm., loss of antithrombin III, increased platelet activation)
91
Q

main complications of thrombosis

A
  1. obstruction of blood flow (partial or complete)
  2. ischemia and infarction of local tissues
  3. increassed intravascular pressure
  4. embolization
92
Q

thromboemboli

A

whole or part of thrombus breaks loose and gets lodged in a vessel downstream

93
Q

embolism

A

a detatched intravascular solid, liquid, or gasseous mass that is carried by the blood to a site distant from its origin

94
Q

ischemia

A

reduced blood flow to an area

95
Q

example of a synthesized chemical mediator

A

arachidonic acid metabolites (PGE2)

96
Q

example of exogenous microbial products

A

lipopolysaccharide, peptidoglycan..

97
Q

preformed chemical mediators

A

histamine, serotonin, kinins

98
Q

pus

A

exudate composed largely of neutrophils

99
Q

purulent/suppurative

A

composed of pus

100
Q

abscess

A

a pocket of pus

101
Q

chemoattractants of eosinophils

A

parasites, mast cells (histamine, eotaxin)

102
Q

eosinophils degranulate to release ..?

A

major basic protein

103
Q

granulomatous

A

largely macrophages surrounding, enclosing, and phagocytizing with granuloma formation

104
Q

granulomatous inflammation - lesions grow quickly or slowly?

A

slowly - can take weeks to months

105
Q

When do lymphocytes arrive to the inflamm site?

A

24-48 hrs
(last to arrive)

106
Q

lymphoplasmacytic inflammation

A

largely lymphocytes and plasma cells responding to chronic antigenic stimulation

107
Q

fibrinous inflammation

A

fibrin comprises large part of visible inflammation

108
Q

catarrhal inflammation

A

excessive mucus production

109
Q

proliferative inflammation

A

seems to be forming more tissue

110
Q

4 phases of healing after tissue injury

A
  1. hemostasis
  2. acute inflammation
  3. proliferation
  4. remodeling
111
Q

2 main mechanisms of tissue repair (proliferation)

A

regeneration - same cells
replacement - replaced cells

112
Q

what cell produces collagen

A

fibroblasts

113
Q

presence of fibrin means the inflamm is acute/chronic?

A

acute

114
Q

presence of collagen means inflamm is acute/chronic?

A

chronic

115
Q

fibrosis - acute or chronic?

A

chronic

116
Q

permanent cell

A

cells are terminally differentialted and have little to no ability to divide and regenerate

117
Q

examples of permanent cells

A

neurons, cardiomyocytes

118
Q

stable cells

A

cells normally exhibit low turnover, but will readily divide and regenerate if stimulated

119
Q

examples of stable cells

A

hepatocytes, renal tubular epithelial cells, osteoblasts, fibroblasts

120
Q

labile cells

A

cells normally exhibit high turnover with constant division and regeneration

121
Q

examples of labile cells

A

keratinocytes, gastrointestinal epithelial cells, hematopoietic cells

122
Q

histologic evidence of regeneration

A
  • cells in mitosis
  • hypertrophy
  • hyperplasia
  • karyomegaly
  • bi- or multinucleated cells
  • cytoplasmic basophilia
  • attenuation

Gen Path (3 decks)

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