4.8 Homeostasis Flashcards Preview

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Flashcards in 4.8 Homeostasis Deck (103):
1

Edema

accumulation of fluid in interstitial space - several causes

2

Hydrothorax

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

3

Ascites

peritonial cavity fluid acumulation - abdomen

4

Anasarca

whole body edema

5

Transudate

low protein fluid that leaks out (mostly water)

6

Exudate

high protein fluid leaking out

7

Effusion

collection of fluid in the cavity

8

Hyperemia

increased dialation of vessels, an active process caused by mediators

9

Congestion

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

10

Hemorrhage

beeding

11

Hematoma

collection of fluid in tissue

12

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

vessel and amout of resistance

13

Pc

capillary pressure

14

Pa

arterial end pressure

15

Pv

venous end pressure

16

Ra

arterial end resistance

17

Rv

venous end resistance

18

thigns that increase pressure at capilary level induce

lots of fluid leaving

19

what will change the rate of fluid leaving most drastically

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

20

Pc formula

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

21

Tissue hydrostatic pressure (Pt) formula

Pt = Tf x Tc

22

Tf

tissue fluid

23

Tc

tissue compliance

24

Pt is usually near

0

25

Tc is usually

low

26

inc in Tf causes

inc in Pt

27

inc in Pt

usually timints Tf

28

where is Tc very high and what is the effect?

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

29

osmotic/oncotic pressure (Pcos)

capilary osmotic/oncotic pressure due to proteins

30

Pcos is determined by

permeabiity of endothelium to proteins and amount of fluid vs protein

31

Permeabiity to proteins is determined by

type of capillary and physiology of endothelium

32

Most oncotic pressure is from

albumin__salt doesn't really matter with respect to vessels

33

tissue oncotic pressure is determined by

tissue protein and fluid concentrations

34

inc capillary filtration of low pretein and fluid

decreases tissue oncotic pressure

35

filtration of high protein fluid

increases tissue oncotic pressure

36

causes of edema

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

37

increased hydrostatic pressure due to

impaired venous flow,
arteriolar dilatation

38

imaired venous flow can be caused by

thrombosis,
heart failure,
pressure,
scarring

39

arteriolar dilatation

heat,
inflammation

40

decreased osmotic pressure

decreased protien in plasma

41

decreased protein in plasma is due to

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

42

glomerular nephritis

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

43

liver disease

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

lymphatic obstruction can be caused by

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

45

salt retention results from

renal dysfunction -renin angiotensin dysfn?

46

salt retention causes

bon increased hydrostatic pressure and decreased osmotic pressure

47

heart failure

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

48

inability to perfuse tissues

cadiogenic schock

49

why is heart stupid

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

50

closed hydraulic loop

heart,
lungs,
vessels

51

which side heart failure is more common

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

common cause of right sided heart failure

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

what vessels see increased pressure in rigth ventricular failure

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

what other complications do you see with heart failure

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

morphology and distribution of Edema

localized vs anasarca,
dependent,
pitting,
periorbital,
pulmonary,
brain

56

non pitting edema

in hyper thyroid problems where large polysaccharides leak fluid

57

why does brain swelling last for a long time

brain doesn_t have lymphatics

58

fluid from lung in heart failure

just transudate, low protein

59

fluid from lung in hyperemia

high protein content due to dialation and leaky endotheial vessesl

60

what transmits more pressure to the capilaries

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

61

hemorrhage

petechiae, purpura, ecchymosis, hemothorax, hematoma

62

petechiae

1-3mm

63

purpura

>3mm <1-2cm

64

ecchymosis

>1-2cm

65

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

20%

66

epidural bleeds are

areterial

67

subdural bleeds are

venous

68

Hemostasis

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

69

clot

coagulated blood

70

thrombus

coagulated blood inside of a vascular space - almost always pathological

71

normal endothelium secretes

antiplatelet PGI2 that keeps flow gowing

72

anti-thrombin III

inactivates thrombin and other activated factors

73

heparin-like molecules also promote

flow

74

thrombomodulin

converts thrombin into an activator of protein C

75

Protein C cleaves

factors 5a and 8a (Va and VIIIa)

76

Prtein C needs

protein S form endothelial cell

77

t-PA

tissue plasminogen activator makes plasmin to promote flow

78

NO

nitric oxide keeps vessesl open constitutively mad by endothelial cells

79

laminar flow favours flow by

keeping cells away from cell walls

80

Most potent stimulus for coagulation

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

81

if there is a chunck of endothelial cell loss then

collagen is exposed to plasma promoting coagulation

82

platelets cannot bind collagen without

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

83

tissue factor

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

84

On injury endothelial cells change phenotype

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

85

Injured tissues releases

tissue factor to start the coagulation path

86

platelet functions

adhesion,
secretion

87

adhesion

vWF binds to collagen and platelets

88

secretion

alpha granules, dense bodies

89

alpha granules

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

90

Dense bodies

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

91

primary coagulation

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

92

secondary hemostatic plug

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

93

primary coagulation stops you from bleeding but

if you distrupt it you'll bleed

94

how do you find out pure platelet fn

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

95

Platelet binding and aggregation

platelets bind to vWF via surface Gp1b

96

Gp1b deficiency

Bernard - Soulier syndrome

97

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

confromation of Gp2bIIIa

98

Gp2bIIIa bind to

noncleaved fibrinogen and that all liks the platelets together

99

Gp2bIIIa deficiency

Glanzmann thrombasthenia

100

adp receptor antagonsit

clopidogrel (plavix)

101

Plavix

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

102

asprin inhibits

thromboxane production

103

can you give asprin and plavix at the same time

no