Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MOD 1 > chapter 4 > Flashcards

chapter 4 Flashcards

1
Q

increased hydrostatic pressure is from what disorders

2 categories

A

ones that impair venous return

localized: DVT

Systemic: congestive heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what can cause reduced plasma osmotic pressure

A

loss of albumin

neprotic syndrome
cirrhosis
protein malnutrition
protein losing gastroenterophathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

diminished due to dilution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what kind of edema is characteristic of renal dysfunction

A

periorbital edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

brain edema features

A

narrowed sulci and disteneded gyri

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

systemic congestion and localized

A

systemic: cardiac failure
localized: isolated venous obstruction

both lead to edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

chronic passive congestion leads to

A

chronic hypoxia–> ischemia tissue injury and scarring

  • hemorrhagic foci
  • hemosiderinladen macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

reddish-blue, cyanosis

A

morphology of congested tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

enlarged alveolar caps
alveolar septal edema
focal intralveolar hemorrhage

A

morphology of acute pulmonary congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

from CHF
septa thickened and fibrotic
heart failure cells

A

morphology of chronic pulmonary congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

morph of acute hepatic congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

centrilobular regions grossly red-brwon, slightly depressed

uncongested tan liver on outside part (nutmed liver)

A

chronic passive hepatic congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

primary hemostasis

A

formation of primary platelet plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what acts to limit clotting to site of injury

A

T-PA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

a granules of platelets have what selectin on their membrane

A

p selectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is contained inside alpha granules

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

B or dense granules in platelts contain

A

calcium
ADP
Serotonin
epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what on the platelet binds to vWF

A

GP1b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

deficient GP1b is what disease

A

bernard-soulier syndrome

bleeding disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what causes platelets to change shape

A

translocation of negatively charged phospholipids to platelet surface which bind calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how are platelets activated

A

thrombin cleaves PAR to activate it

ADP release gives rise to additional rounds of platelet activation called recruitment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

deficiency of GpIIb/IIIa called

A

glanzmann thrombasthenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what does GpIIb/IIIa usually do

A

connects platelets through fibrinogen linking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

assembly of clotting cascade reaction complexes depsends on _____ binding ____ on what factors

A

calcium binding y-carboxylated lutamic acid on
2,7,9,10

enzyme that y-carboxylates these factors uses vitamin K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

PTT what pathway and factors

A

intrinsic
8-12, II, V, firbrinogen

and negative cahgreged particle to active XII together with phospholipids and calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

PT pathway and factors

A

II,V,VII,X and TF, phospholipids, and calcium added

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

deficiency of what factors leads to moderate to severe bleeding disorders

A

5,7,8,9,10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what factor deficiency leads to mild bleeding

A

XI

-lose ability of clot amplification from thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what factor deficiency leads to people who don’t bleed and susceptible to what

A

XII and thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

thrombin has a positive feedback that amplifies clotting on what factors

A

5,8,11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

thrombin stabilizes the secondary hemostatic plug by activation what factor which covalently cross-links fibrin

A

13

37
Q

thrombin on normal endothelium

A

anti-coagulant

38
Q

clotting in vivo

A

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
Q

clotting in lab intrinsic

A

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
Q

clotting in lab extrinsic

A

1) TF and VII activate X

2) X and Va activate thrombin

41
Q

fibrinolysis limits size of clot and contributes to its later dissolution
-largely accopmlised by enzyme activity of

A

plasmin

-breaks down fibrin

42
Q

elevation of D-dimers means what

A

marker of several thrombotic states

43
Q

how is plasminogen converted to plasmin

A

by factor XII (no bleeding disease)

t-PA

44
Q

t-PA

A

synthesized by endothelium and most active when bound to fibrin

45
Q

what limits plasmin

A

a2 plamsmin inhibitor

46
Q

platelet inhibitory effects of normal endothelium

A

PGI2
NO
ADPtase

47
Q

thrombomodulin

A

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
Q

antithrombin III

A

bind heparin like molecules on surface of endothelium and inhibit:
thrombin
factors: 9-12

49
Q

tissue factor pathway inhibitor requires what and does what

A

needs protein S

binds and inhibits Tf/VIIa complexes

50
Q

what are purpura

A

like petechiae but slightly larger

51
Q

defects of 2ndary hemostasis what is cause and where is leed

A

defect coag factors
bleedis into soft tissue like muscle or jionts
hemarthrosis

52
Q

generalized defects involving small vessels often presents with
can create what

A

palpable purpura and ecchymosies

-can create palpable mass of blood called hematoma

53
Q

what is the virchow triad in thrombosis

A

abnormal blood flow
endothelial injury
hypercoagulability

54
Q

injured endothelial cells secrete ____ which limits fibrinolysis and downregulates expression of t-PA

A

PAI

favors development of thrombi

55
Q

factor V point mutaions

increases what

A

factor V leiden
increases DVT
factor V is resistant to cleavage by protein C

56
Q

nucleotide change in 3’ UTR prothrombin gene

increases what

A

elevates prothrombin

3X increase in venous thrombosis

57
Q

elevated homocystein

increases what and can also cause what

A

arterial and venous thrombosis

atheroslerosis

58
Q

heparin induced thrombocytopenia syndrome

A

heparin and factor 4 bind and then go to platelet surface
Abs recognize this and bind
-activation, aggregation and consumption
-prothrombotic state

59
Q

antiphospholipid Ab syndrome

A

anticardriolipin Ab
recurrent vascular thrombossis
throbocytopenia
recurrent fetal loss

60
Q

presentaion of Antiphospholipid Ab syndrome

A

PMS bitch

pulmonary embolism
myocardial infarction
stroke
bowel infarction

61
Q

arterial or cardiac thrombi begin where and what travel

A

turbulence or endothelial injury

retrograde travel

62
Q

venous thrombi begin and goes

A

at stasis goes forward towards heart

63
Q

lines of zahn description and indication

A 
alternating red (RBCs) and tan (platelets and fibrin)
indicates thrombus formed in flowing blood
64
Q

mural thrombi occur where

A

in heart chambers or in aortic clumen

65
Q

arterial thrombi location

A

coronary
cerebral
femoral

66
Q

postmortem clots

A

gelatinous
dark red dependent portion
yellow chicken fat upper portion

67
Q

fate of thrombus

A

PEDO

68
Q

venous thrombi 2 types and can embolize where

A

superficial (rarely embolize)

DVT: large veins at or above knee, more often embolize to lung

69
Q

arterial and cardiac thrombosis from what (2)

A

MI and atherosclerosis

70
Q

vegetations from bacteria or fungi or previous damage can cause distrubed blood flow and induce formation of large thrombotic masses called

A

infective endocarditis

71
Q

what occurs when emboli obstruct ___ or more of pulmonary circulation

A

60%

death, Right side heart failure

72
Q

systemic thromboembolism are from

main spot it deposits

A

intracardiac mural thrombi

deposits in LE

73
Q

fat and marrow embolism

A 
after fracture of long bones
pulmonary insufficency
anemia
neurologic symptoms
thrombocytopenia
74
Q

air embolism

A

decompression sickness

caisson disaease

75
Q

amniotic fluid embolism

A

can cause death and 85% of time causes neurological damage to survivors
tear in placenta membrane or rupture of uterine veins

76
Q

infarcts caused by venous thrombosis more likely in what organs

A

with single efferent vein

-testis and ovary

77
Q

morphology of red infarct

-white

A

hemorrhagic

anemic

78
Q

where do red infarcts occur

A

venous occlusions (testicular torsion)
loose spongy tissue (lungs)
dual circulating tissue (lungs and SI)

79
Q

white infarcts occur

A

arterial occlusion ins solid organs with end artery supply like
heart, spleen, kidney

80
Q

metabolic abnormalities in septic shock

A

increased insulin resistance
-imparired GLUT-4

hyperglycemia

  • gluconeogenesis activated
  • accute glucocorticoid product followed by adrenal insufficiency
81
Q

adrenal necrosis due to intravascular dissemination is called

A

waterhouse-friederichsen syndrome

82
Q

stages of shock

A

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
Q

adrenal changes in shock

A

cortical cell lipid depletion

84
Q

kidneys in shock

A

acute tubular necrosis

85
Q

lungs in shock

A

if sepsis or trauma then diffuse alveolar damage

86
Q

systemic intracvasuclar affect of shock

A

petechial hemorrhages

87
Q

clinical consequence of hypovolemic and cardiogenic shock

A

hypotension, weak pulse, cool, clammy cyanotic skin

88
Q

clinical consequence of septic shock

A

initial warm skin bc of vasodilation

MOD 1 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions