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