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chapter 4 Flashcards

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1
Q

increased hydrostatic pressure is from what disorders

2 categories

A

ones that impair venous return

localized: DVT

Systemic: congestive heart failure

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2
Q

what can cause reduced plasma osmotic pressure

A

loss of albumin

neprotic syndrome
cirrhosis
protein malnutrition
protein losing gastroenterophathy

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3
Q

when sodium and water are retained what happens to colloid osmotic pressure

A

diminished due to dilution

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4
Q

subcutaneous edema is in regions with what and distribution often influenced by what

-depending on position person is in called what

A

hydrostatic pressure, gravity

  • legs when standing
  • sacrum when recumbent

-dependednt edema

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5
Q

what kind of edema is characteristic of renal dysfunction

A

periorbital edema

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6
Q

describe the lungs in pulmonary edema

A

lungs are 2-3X normal weight and yield frothy, blood tinged fluid
-air, edema, and extravasated red cells

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7
Q

brain edema features

A

narrowed sulci and disteneded gyri

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8
Q

what would a peritoneal effusion caused by lymphatic blockage look like
-main cause

A

milky due to presence of lipids absorbed from gut

-from portal hypertension

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9
Q

systemic congestion and localized

A

systemic: cardiac failure
localized: isolated venous obstruction

both lead to edema

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10
Q

chronic passive congestion leads to

A

chronic hypoxia–> ischemia tissue injury and scarring

  • hemorrhagic foci
  • hemosiderinladen macrophages
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11
Q

reddish-blue, cyanosis

A

morphology of congested tissue

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12
Q

enlarged alveolar caps
alveolar septal edema
focal intralveolar hemorrhage

A

morphology of acute pulmonary congestion

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13
Q

from CHF
septa thickened and fibrotic
heart failure cells

A

morphology of chronic pulmonary congestion

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14
Q

central vein and sinusoids distended
centrolobular area hepatocytes necrotic
periportal hepatocytes may only develop fatty change

A

morph of acute hepatic congestion

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15
Q

centrilobular regions grossly red-brwon, slightly depressed

uncongested tan liver on outside part (nutmed liver)

A

chronic passive hepatic congestion

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16
Q

primary hemostasis

A

formation of primary platelet plug

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17
Q

secondary hemostasis

A

deposition of fibrin

TF exposed on surface of subendothelial cells (SM and fibroblasts)

  • binds and activates factor VII
  • leads to thrombin generation and fibrin
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18
Q

what acts to limit clotting to site of injury

A

T-PA

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19
Q

what is the last step in hemostasis

A

clot stabilization and resoprtion

-polymerized fibrin and platelet aggregates undergo contraction to form solid permanent plug

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20
Q

a granules of platelets have what selectin on their membrane

A

p selectin

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21
Q

what is contained inside alpha granules

A

factor 4 and 5, fibrinogen, vWF, TGF-B, PDGF

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22
Q

B or dense granules in platelts contain

A

calcium
ADP
Serotonin
epinephrine

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23
Q

what on the platelet binds to vWF

A

GP1b

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24
Q

deficient GP1b is what disease

A

bernard-soulier syndrome

bleeding disorder

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25
what causes platelets to change shape
translocation of negatively charged phospholipids to platelet surface which bind calcium
26
how are platelets activated
thrombin cleaves PAR to activate it | ADP release gives rise to additional rounds of platelet activation called recruitment
27
deficiency of GpIIb/IIIa called
glanzmann thrombasthenia
28
what does GpIIb/IIIa usually do
connects platelets through fibrinogen linking
29
assembly of clotting cascade reaction complexes depsends on _____ binding ____ on what factors
calcium binding y-carboxylated lutamic acid on 2,7,9,10 enzyme that y-carboxylates these factors uses vitamin K
30
PTT what pathway and factors
intrinsic 8-12, II, V, firbrinogen and negative cahgreged particle to active XII together with phospholipids and calcium
31
PT pathway and factors
II,V,VII,X and TF, phospholipids, and calcium added
32
deficiency of what factors leads to moderate to severe bleeding disorders
5,7,8,9,10
33
what factor deficiency leads to mild bleeding
XI | -lose ability of clot amplification from thrombin
34
what factor deficiency leads to people who don't bleed and susceptible to what
XII and thrombosis
35
thrombin has a positive feedback that amplifies clotting on what factors
5,8,11
36
thrombin stabilizes the secondary hemostatic plug by activation what factor which covalently cross-links fibrin
13
37
thrombin on normal endothelium
anti-coagulant
38
clotting in vivo
1) TF activates VII to VIIa 2) TF and VIIa activate IX 3) IX and VIII activate X 4) X and V activate thrombin 5) thrombin converts fibrinogen to fibrin and also amplifies V,VIII,XI
39
clotting in lab intrinsic
1) neg charged surface glass beads activate 12 2) 11 activated 3) 9 activated 4) 8 and 9 activate 10 5) 10 and 5 activate thrombin
40
clotting in lab extrinsic
1) TF and VII activate X | 2) X and Va activate thrombin
41
fibrinolysis limits size of clot and contributes to its later dissolution -largely accopmlised by enzyme activity of
plasmin | -breaks down fibrin
42
elevation of D-dimers means what
marker of several thrombotic states
43
how is plasminogen converted to plasmin
by factor XII (no bleeding disease) | t-PA
44
t-PA
synthesized by endothelium and most active when bound to fibrin
45
what limits plasmin
a2 plamsmin inhibitor
46
platelet inhibitory effects of normal endothelium
PGI2 NO ADPtase
47
thrombomodulin
inhibits thrombin make it cleave and activate protein C which then inactivates factors Va and VIIIa -requires protein S to work -also vitamin K
48
antithrombin III
bind heparin like molecules on surface of endothelium and inhibit: thrombin factors: 9-12
49
tissue factor pathway inhibitor requires what and does what
needs protein S | binds and inhibits Tf/VIIa complexes
50
what are purpura
like petechiae but slightly larger
51
defects of 2ndary hemostasis what is cause and where is leed
defect coag factors bleedis into soft tissue like muscle or jionts hemarthrosis
52
generalized defects involving small vessels often presents with can create what
palpable purpura and ecchymosies | -can create palpable mass of blood called hematoma
53
what is the virchow triad in thrombosis
abnormal blood flow endothelial injury hypercoagulability
54
injured endothelial cells secrete ____ which limits fibrinolysis and downregulates expression of t-PA
PAI | favors development of thrombi
55
factor V point mutaions | increases what
factor V leiden increases DVT factor V is resistant to cleavage by protein C
56
nucleotide change in 3' UTR prothrombin gene | increases what
elevates prothrombin | 3X increase in venous thrombosis
57
elevated homocystein | increases what and can also cause what
arterial and venous thrombosis | atheroslerosis
58
heparin induced thrombocytopenia syndrome
heparin and factor 4 bind and then go to platelet surface Abs recognize this and bind -activation, aggregation and consumption -prothrombotic state
59
antiphospholipid Ab syndrome
anticardriolipin Ab recurrent vascular thrombossis throbocytopenia recurrent fetal loss
60
presentaion of Antiphospholipid Ab syndrome
PMS bitch pulmonary embolism myocardial infarction stroke bowel infarction
61
arterial or cardiac thrombi begin where and what travel
turbulence or endothelial injury | retrograde travel
62
venous thrombi begin and goes
at stasis goes forward towards heart
63
lines of zahn description and indication
``` alternating red (RBCs) and tan (platelets and fibrin) indicates thrombus formed in flowing blood ```
64
mural thrombi occur where
in heart chambers or in aortic clumen
65
arterial thrombi location
coronary cerebral femoral
66
postmortem clots
gelatinous dark red dependent portion yellow chicken fat upper portion
67
fate of thrombus
PEDO
68
venous thrombi 2 types and can embolize where
superficial (rarely embolize) | DVT: large veins at or above knee, more often embolize to lung
69
arterial and cardiac thrombosis from what (2)
MI and atherosclerosis
70
vegetations from bacteria or fungi or previous damage can cause distrubed blood flow and induce formation of large thrombotic masses called
infective endocarditis
71
what occurs when emboli obstruct ___ or more of pulmonary circulation
60% | death, Right side heart failure
72
systemic thromboembolism are from | main spot it deposits
intracardiac mural thrombi | deposits in LE
73
fat and marrow embolism
``` after fracture of long bones pulmonary insufficency anemia neurologic symptoms thrombocytopenia ```
74
air embolism
decompression sickness | caisson disaease
75
amniotic fluid embolism
can cause death and 85% of time causes neurological damage to survivors tear in placenta membrane or rupture of uterine veins
76
infarcts caused by venous thrombosis more likely in what organs
with single efferent vein | -testis and ovary
77
morphology of red infarct | -white
hemorrhagic | anemic
78
where do red infarcts occur
venous occlusions (testicular torsion) loose spongy tissue (lungs) dual circulating tissue (lungs and SI)
79
white infarcts occur
arterial occlusion ins solid organs with end artery supply like heart, spleen, kidney
80
metabolic abnormalities in septic shock
increased insulin resistance -imparired GLUT-4 hyperglycemia - gluconeogenesis activated - accute glucocorticoid product followed by adrenal insufficiency
81
adrenal necrosis due to intravascular dissemination is called
waterhouse-friederichsen syndrome
82
stages of shock
initial nonprogressive phase -reflex compensatory mech activated, perfusion to vital organs maintained progressive stage -tissue hypoperfusion and lactic acidosis irreversible stage -cell survival not possible, lysosomal enzyme leak, organ failure
83
adrenal changes in shock
cortical cell lipid depletion
84
kidneys in shock
acute tubular necrosis
85
lungs in shock
if sepsis or trauma then diffuse alveolar damage
86
systemic intracvasuclar affect of shock
petechial hemorrhages
87
clinical consequence of hypovolemic and cardiogenic shock
hypotension, weak pulse, cool, clammy cyanotic skin
88
clinical consequence of septic shock
initial warm skin bc of vasodilation

MOD 1 (6 decks)

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