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Pathology > 4.8 Homeostasis > Flashcards

4.8 Homeostasis Flashcards

1
Q

Edema

A

accumulation of fluid in interstitial space - several causes

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2
Q

Hydrothorax

A

collections of fluids - low protein (basically water) so not an infection

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3
Q

Ascites

A

peritonial cavity fluid acumulation - abdomen

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4
Q

Anasarca

A

whole body edema

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5
Q

Transudate

A

low protein fluid that leaks out (mostly water)

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6
Q

Exudate

A

high protein fluid leaking out

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7
Q

Effusion

A

collection of fluid in the cavity

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8
Q

Hyperemia

A

increased dialation of vessels, an active process caused by mediators

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9
Q

Congestion

A

blood can’t get out of vessels and looks red, caused by blockage

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10
Q

Hemorrhage

A

beeding

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11
Q

Hematoma

A

collection of fluid in tissue

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12
Q

tissue hydrostatic pressure, oncotic pressure, and tissue compliance affct the

A

vessel and amout of resistance

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13
Q

Pc

A

capillary pressure

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14
Q

Pa

A

arterial end pressure

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15
Q

Pv

A

venous end pressure

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16
Q

Ra

A

arterial end resistance

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17
Q

Rv

A

venous end resistance

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18
Q

thigns that increase pressure at capilary level induce

A

lots of fluid leaving

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19
Q

what will change the rate of fluid leaving most drastically

A

venous block - increase in venous pressure will cause over a 5 forld increase in fluid leaving due to the increased hydrostatic pressure.
With hypertension you don_t see puffy faces, but with venous block you’ll have inc fluid in tissues. bc Ra > Rv inc in Pa has less of an effect on Pc than inc in Pv

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20
Q

Pc formula

A

Pc = ((Rv/Ra)Pa + Pv) / (1 + (Rv/Ra) )

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21
Q

Tissue hydrostatic pressure (Pt) formula

A

Pt = Tf x Tc

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22
Q

Tf

A

tissue fluid

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23
Q

Tc

A

tissue compliance

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24
Q

Pt is usually near

A

0

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25
Q

Tc is usually

A

low

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26
Q

inc in Tf causes

A

inc in Pt

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27
Q

inc in Pt

A

usually timints Tf

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28
Q

where is Tc very high and what is the effect?

A

lungs bc there is air surrounding capllaries so no back pressure,
so in congestive heart failure when there is an increase in pulmonary aretery pressure,
you’ll see pulmonary edema

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29
Q

osmotic/oncotic pressure (Pcos)

A

capilary osmotic/oncotic pressure due to proteins

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30
Q

Pcos is determined by

A

permeabiity of endothelium to proteins and amount of fluid vs protein

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31
Q

Permeabiity to proteins is determined by

A

type of capillary and physiology of endothelium

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32
Q

Most oncotic pressure is from

A

albumin__salt doesn’t really matter with respect to vessels

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33
Q

tissue oncotic pressure is determined by

A

tissue protein and fluid concentrations

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34
Q

inc capillary filtration of low pretein and fluid

A

decreases tissue oncotic pressure

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35
Q

filtration of high protein fluid

A

increases tissue oncotic pressure

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36
Q

causes of edema

A

increased intravascular hydrostatic pressure,
decreased intravascular osmotic pressure - won’t pull fluid in so it tends to go out,
lymphatic obstruction,
sodium retention,
inflammation

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37
Q

increased hydrostatic pressure due to

A

impaired venous flow,

arteriolar dilatation

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38
Q

imaired venous flow can be caused by

A

thrombosis,
heart failure,
pressure,
scarring

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39
Q

arteriolar dilatation

A

heat,

inflammation

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40
Q

decreased osmotic pressure

A

decreased protien in plasma

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41
Q

decreased protein in plasma is due to

A

lose it or don’t make it - glomerular nephritis,
liver disease,
nutritional deficiencies

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42
Q

glomerular nephritis

A

protein is not supposed to leave but if glomerulus gets damaged you can drop protein levels quickly

43
Q

liver disease

A

when you have end stage chirrosis you see dropped albumin and clotting factors bc you can’t make as much .terminal at this point..ince edema with reduced albumin you’ll see anasarca

44
Q

lymphatic obstruction can be caused by

A 
neoplasia, 
surgery, 
radiation, 
infection/inflammation, 
special infections like filaria (elephantitis)
45
Q

salt retention results from

A

renal dysfunction -renin angiotensin dysfn?

46
Q

salt retention causes

A

bon increased hydrostatic pressure and decreased osmotic pressure

47
Q

heart failure

A

inability of heart to pump out everything it receives - heart can only pump the blood it recieves up to its physiological limit

48
Q

inability to perfuse tissues

A

cadiogenic schock

49
Q

why is heart stupid

A

bc it just recives blood and when it can’t then there is failure

50
Q

closed hydraulic loop

A

heart,
lungs,
vessels

51
Q

which side heart failure is more common

A

left sided bc that’s where you have heat attacks, this is the ventricle that has to pump out blood and this is the one that can die, commonly due to ischemia

52
Q

common cause of right sided heart failure

A

left sided heart failure bc the pressure that cant be dealt with in the left is transmitted to the lungs where pulmonary edema will be seen and also back to the right ventricle

53
Q

what vessels see increased pressure in rigth ventricular failure

A

the venacava pressure goes up and you’ll see pedal edema bc getting blood back from the extermities is already hard and with inc pressure to fight against, it will be even harder. May also see jugular distension

54
Q

what other complications do you see with heart failure

A

kidneys - the low cardiac output stimulates the kidney activate the renin-angiotensin-aldosterone system causing: increase Na and water retention, increased blood volume, and increased volume returing to the failing heart (cycle of doom)

55
Q

morphology and distribution of Edema

A 
localized vs anasarca, 
dependent, 
pitting, 
periorbital, 
pulmonary, 
brain
56
Q

non pitting edema

A

in hyper thyroid problems where large polysaccharides leak fluid

57
Q

why does brain swelling last for a long time

A

brain doesn_t have lymphatics

58
Q

fluid from lung in heart failure

A

just transudate, low protein

59
Q

fluid from lung in hyperemia

A

high protein content due to dialation and leaky endotheial vessesl

60
Q

what transmits more pressure to the capilaries

A

congestion transmits more pressure to the capillaries than inflammation or dialation of arteriole

61
Q

hemorrhage

A

petechiae, purpura, ecchymosis, hemothorax, hematoma

62
Q

petechiae

A

1-3mm

63
Q

purpura

A

> 3mm <1-2cm

64
Q

ecchymosis

A

> 1-2cm

65
Q

rapid loss of up to ___. of blood volume or slow losses of more can be tolerated by young healthy individuals

A

20%

66
Q

epidural bleeds are

A

areterial

67
Q

subdural bleeds are

A

venous

68
Q

Hemostasis

A

maintainance of flow and generation of hemostatic plug at sites of hemorrhge

69
Q

clot

A

coagulated blood

70
Q

thrombus

A

coagulated blood inside of a vascular space - almost always pathological

71
Q

normal endothelium secretes

A

antiplatelet PGI2 that keeps flow gowing

72
Q

anti-thrombin III

A

inactivates thrombin and other activated factors

73
Q

heparin-like molecules also promote

A

flow

74
Q

thrombomodulin

A

converts thrombin into an activator of protein C

75
Q

Protein C cleaves

A

factors 5a and 8a (Va and VIIIa)

76
Q

Prtein C needs

A

protein S form endothelial cell

77
Q

t-PA

A

tissue plasminogen activator makes plasmin to promote flow

78
Q

NO

A

nitric oxide keeps vessesl open constitutively mad by endothelial cells

79
Q

laminar flow favours flow by

A

keeping cells away from cell walls

80
Q

Most potent stimulus for coagulation

A

collagen bc you don’t normally see collagen in your vessels

81
Q

if there is a chunck of endothelial cell loss then

A

collagen is exposed to plasma promoting coagulation

82
Q

platelets cannot bind collagen without

A

vonWillebrand factor - that factor has receptors for platelets and ECM__allows for aggregation activation and secretion of platelets

83
Q

tissue factor

A

extrinsic pathway activated by LPS and cytokines induce endothelial cells to produce TF (DIC)

84
Q

On injury endothelial cells change phenotype

A

form proflow to pro thrombotic – stop secreting prostacylin and mitric oxide and secrete procoagulation things instead

85
Q

Injured tissues releases

A

tissue factor to start the coagulation path

86
Q

platelet functions

A

adhesion,

secretion

87
Q

adhesion

A

vWF binds to collagen and platelets

88
Q

secretion

A

alpha granules, dense bodies

89
Q

alpha granules

A

fibrinogen, PDGF, TGF-b, vWF, platelet factors IV

90
Q

Dense bodies

A

ADP, Ca2+, histamine, serotonin, epinephrine, TXA2, and phospholipid complex

91
Q

primary coagulation

A

aggregation induced by ADP and TXA2 - primary hemostatic plug, coagulation cascade is initiated making thrombin

92
Q

secondary hemostatic plug

A

thrombin with ADP and TXA2 induces tighter aggregation to irreversibly fused mass of platelets - secondary hemostatic plug

93
Q

primary coagulation stops you from bleeding but

A

if you distrupt it you’ll bleed

94
Q

how do you find out pure platelet fn

A

form a regulated cut and using a stop watch wait till it stops bleeding - this is the formation of the primary hemostatic plug

95
Q

Platelet binding and aggregation

A

platelets bind to vWF via surface Gp1b

96
Q

Gp1b deficiency

A

Bernard - Soulier syndrome

97
Q

adp binds to its receptor and induces platelet aggregation via change in

A

confromation of Gp2bIIIa

98
Q

Gp2bIIIa bind to

A

noncleaved fibrinogen and that all liks the platelets together

99
Q

Gp2bIIIa deficiency

A

Glanzmann thrombasthenia

100
Q

adp receptor antagonsit

A

clopidogrel (plavix)

101
Q

Plavix

A

inhibits platelet aggregation via inhibition of the induced conformational change in Gp2bIIIa

102
Q

asprin inhibits

A

thromboxane production

103
Q

can you give asprin and plavix at the same time

A

no

Pathology (26 decks)

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