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MOD Midterm > Hemostasis, Hemodynamic Disorders, And Shock - Singh > Flashcards

Hemostasis, Hemodynamic Disorders, And Shock - Singh Flashcards

1
Q

edema

A

fluid in interstitial space

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2
Q

Effusion

A

fluid in pleural, peritoneal = ascites, pericardial, joint spaces

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3
Q

Hyperemia

A

too much blood arriving (normal, like exercise)
= physiological and ARTERIAL, regulated by precapillary sphincter*
= can lead to some edema

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4
Q

Congestion

A

Not enough blood is leaving
= pathologic and VENOUS not draining fast enough, no regulation or sphincter
= can cause edema

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5
Q

how does heart failure lead to something else

A

heart failure leads to:

  1. high Pcap = edema
  2. low BF —-> renin activation —-> increase BV = edema
  3. kidney failure since renin is constantly needed and making conditions worse (retention of NA and H2O)
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6
Q

heart failure is what type of effusion

A

transudate fluid effusion

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7
Q

heart failure causes what edema

A
  1. pitting edema : press down on skin and its like a foam pillow
  2. Pulmonary edema
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8
Q

what can liver failure cause

A

edema and ascites due to low albumin production + Portal HTN**
jaundice, testicular atrophy

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9
Q

how does low albumin cause edema

A

low oncotic P in capillaries

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10
Q

how does portal HTN cause edema

A 
causes CONGESTION (high Pcap)
Liver cant process all the venous return from hepatic vein = blood backs up to portal vein and peritoneal cavity
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11
Q

2 ways you can get edema from renal disease

A

retention of h2o and NA = increase Pcap

2. Nephrotic syndrome = excess protein loss in urine (lower PIcap)

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12
Q

Kwashiorkor

A

low Protein in diet and malnutrition = edema

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13
Q

giant swollen in one leg like elephant looking

A

due to Lymphatic obstruction from worm parasites in the lymph causing lymph to not take up fluid (Filariasis)

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14
Q

swollen arm can happen after what surgery

A

removing breast LNs (especially axillary LN)

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15
Q

what causes exudate effucsion

A

inflammation
burns
sepsis

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16
Q

chronic congestion leads to

A

edema —-> Hemosiderosis (RBC leave capillaries) —-> tissue damage and necrosis

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17
Q

hemoosiderin- laden macrophages

A

heart failure cells

in the alveoli or chronic congestion

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18
Q

what can heart failure do to liver

A

hepatic congestion
Central Vein has low BF rate back to heart since RV is backing up
= nutmeg liver (centrilobular necrosis)

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19
Q

what besides heart failure can cause congestion in liver

A

hepatic congestion can happen from obstruction or thrombus in the central vein or portal vein
= nutmeg liver and centrilobular necrosis

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20
Q

portal HTN leads to what

A

cirrhosis

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21
Q

hemostasis

A

blood during injury

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22
Q

1st step in hemostasis

A

vasoconstriction (endothelin) to reduce SA and BF to the area injured

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23
Q

2nd step in hemostasis

A

Platelet plug (adhesion, activation, aggregation)

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24
Q

platelet adhesion involves what

A

vWF (uncurled form) on endothelium (Weibel Palade bodies = curled form) and GpIb on platelets

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25
Q

activation of platelets involves

A

conformational change so - charge surface of platelets
(GpIIb-IIIa** on platelet changes conformation) and fibrinogen binds to it = thrombin makes this secrete:
1. ADP (more activation)
2. Thromboxane A2 (aggregation, inhibited by asprin)

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26
Q

X vWF

A

Von Willebrand disease

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27
Q

X GpIb

A

Bernard Soulier Syndrome

=Giant platelets, that are size of RBCs

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28
Q

aggregation of platelets involves

A

bivalent fibrinogen binding to GpIIb-IIIa and cross linking

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29
Q

X GpIIb-IIIa

A

Glanzmann thrombasthenia

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30
Q

primary hemostasis

A

platelet plug formation

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31
Q

clinical signs if something is not right with primary hemostasis

A

Mucocutaneous bleeding (nose and mouth), excessive period bleeding

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32
Q

thrombocytopenia can lead to

A

hemorrhage

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33
Q

if someone has primary hemostasisi problem what labs should you do

A

CBC (platelet quantity)

Flow cytometry or PFA-100 looks at adhesion and aggregation (Platelet quality and function)

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34
Q

Thrombocytopenia
what happens
what do labs show

A

low or no platelet production
CBC low for platelets
Flow cytometry shows platelets aggregate and adhesion

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35
Q

Von Willebrand disease
what happens
what do labs show

A

X vWF
CBC shows normal platelet count
Flow cytometry shows NO platelet adhesion, YES agreggation

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36
Q

Bernard Soulier Disease
what happens
what do labs show

A

X GpIb
CBC shows normal to low platelet count
FC shows platelets NO adhesion, YES aggregation + abnormal large size

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37
Q

Glanzmann’s thrombasthenia
what happens
what do labs show

A

X GpIIb-IIIa
CBC shows normal platelet count
FC shows YES adhesion, NO aggregation

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38
Q

3rd step in hemostasis

A

coagulation cascade

Intrinsic and extrinsic

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39
Q

intrinsic pathway

A

F12–> F11–> F9–> F8 = aPartial Thromboplastin Time**

GOES TO COMMON pathway by activating F10

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40
Q

Extrinsic Pathway

A

Tissue Factor –> F7 = Prothrombin Time

GOES TO COMMON pathway by activating F10

41
Q

Common pathway

A
  1. F10 activated, activated thrombin (F2a) with F5 and Ca+2 and Lipids
  2. Thrombin (F2a) binds to fibrinogen and forms Fibrin clot (F13)
42
Q

Fibrinogen is what factor

A

F1

43
Q

Prothrombin is what factor

A

F2

44
Q

Antihemophilic A factor (AHF) is what factor

A

F8

45
Q

function of thrombin

A
  1. stabilize fibrin
  2. activate platelets
  3. activate inflammatory cells and endothelium (N)
  4. Anti-thrombotic function when binding to (Thrombomodulin)
46
Q

VIT K dependent factors

A

cant bind to CA+2 so they need VIT K:
F2, F7, F9, F10
(Warfarin, Coumadin inhibits these)

47
Q

Secondary hemostasis is what

A

stabilize the clot then break it down

48
Q

Secondary hemostasis problems show up as what

A 
red dots on skin 
1. Petechiae (small <3mm)
2. Purpura (large)
3. Ecchymosis (large and palpable, solid feeling)
visceral and intracranial bleeding
Hemarthrosis
49
Q

visceral and intracranial bleeding happens from

A

factor deficiency or thrombocytopenia

50
Q

when do you see Hemarthrosis

A

Factor deficiency**

blooding in the synovial joint

51
Q

how to check aPTT

A

for intrinsic pathway

ADD NEGATIVE Ca+2 (should be 32-45 sec), not longer

52
Q

how to check PT

A

for extrinsic pathway

ADD TISSUE FACTOR (should be 10-14sec), not longer

53
Q

both PT and aPPT prolonged can mean

A 
vit k deficiency 
liver disease
anticoagulant medication
dysfibrinogenemia (F10,5,2)
disseminated intravascular coagulation
54
Q

4th step of Hemostasis

A

Fibrinolysis
stop clot
resorption of clot
tissue repair

55
Q

how to stop coagulation

A
  1. BF : washed away factors
  2. remove platelet adhesion surface
  3. Plasmin made by t-PA (breaks fibrin)
56
Q

tPA

A

plasminogen —-> plasmin (break fibrin)

57
Q

what does a normal not injured endothelium have on teh surface `

A
  1. Adenosine diphophatase
  2. Prostacyclin (PGl2), NO
    = inhibit aggregation*
  3. Thrombomodulin
58
Q

Thrombin in anticoagulation

A

bind to Thrombomodulin causing Protein C to be active when Protein S is there = X F5a and F8a

59
Q

Heparin function

A

blood thinner

it binds to anti-thrombin 3 = inactivated thrombin and F9a and 10a

60
Q

Tissue Factor pathway inhibitor function

A

X F7a

61
Q

examples of intrinsic pathway

A

inside vascular lumen injury exposing negative surface on platelets

62
Q

examples of extrinsic pathway

A

injury outside BV and activated the tissue factor

63
Q

Thrombus vs embolic

A

thrombus is the clot forming in a location

embolic is when a clot is traveling and then settles down some place

64
Q

Virchow’s triad

A
  1. Endothelial injury : inflammation, Hypercholesterolemia
  2. Abnormal BF : stasis (afib, turbulence, bedrest), atherosclerosis (BV narrowing), dilated vessels(aneurism, hemorrhoids), heart failure
  3. Hypercoagulability : Inherited (Factor 5 Leiden), cancer
    = all lead to thrombus
65
Q

Endothelial injury leads to

A

Endothelial dyfunction = lowers NO

causing endothelial activtation (adhesion molecules for platelets)

66
Q

what is down regulated in prothrombic state

A

Thrombomodulin, Protein C activated, Plasminogen (by Plasminogen activator inhibitor)

67
Q

when can BF become turbulent

A

when P increases too high , happens nautraly at all bifurcations

68
Q

how has aneurisms and hemorrhoids cause BF changes

A

it dilates the vessel

69
Q

internal obstruction and change in BF

A

plaque buildup (atherosclerosis)

70
Q

External interference, compression changing BF how

A

dead myocardium that is non-contractile

71
Q

inadequate heart chamber function and change in BF

A

Atrial Fibrillation with stasis (inadequate pumping)

72
Q

Factor 5 Leiden happens due to what mutation and how to test for it

A

Arg to Gln = cant activate Protein C
TEST : genetic, APC resistance testing = measures clotting time when APC is added and not added(normal shows longer time to clot when APC is present)

73
Q

Prothrombin mutation leads to what

A

increased prothrombin levels

74
Q

first place an Embolus goes and most common place it came from
where does it go if you have a foramen ovale

A

form popliteal fossa through the right heart to the lung pulmonary artery
if foramen ovale it goes to the brain

75
Q

if thrombus presents in a person younger then 40 then what is it most likely

A

genetic factors

or something they did or use causing hypercoagulatory state

76
Q

Heparin - induced thrombocytopenia

A

the patient has antibodies against heparin

  1. PF4 from platelet bound to heparin (anticoag usually)
  2. B-cells recognize this PF4-heparin
  3. IgG binds and cross linking on platelet (looks like fibrin cross link = PLATELET ACTIVATED)
  4. more PF4 released from platelets and binds to heparin causing
    - platelet plug = thrombosis**
    - M come to eat these IgG tagged = low platelet count    **
77
Q

how to test for HIT

A
  1. pt on heparin
  2. Labs show thrombocytopenia leading to thrombosis
  3. PF4 Abs are present**
  4. Platelets aggregate and get eaten
    = can cause black fingers and toes = necrosis thrombus
78
Q

Antiphospholipid Ab syndrome

A

person has Lupus anticoagulant
= Abs against plasma proteins bound to phospholipids (so like proteins on cell membranes)
= Vascular throbosis HIGH
= unexplained miscarriage or still birth
= gangrene, ulcers, heart valve disease, adrenal thrombosis, chorea, pulmonary HTN , portal thrombosis

79
Q

how to fibrolyze a clot in someone in the brain area

A
  1. give chewed asprin before the travel to EM
  2. give exogenous t-PA** (within 6hr on symptoms) before liqueficous necrosis starts that can cause hemorrhage if BF returns
80
Q

4 things that can happen when there is a thrombus

A 
1. recanalization through the thrombus to find alternative ways to get blood to the area
collaterals
2. lysis and resolved
3. scar tissue 
4. embolism
81
Q

5 types of emboli

A
  1. thromboemboli (blood)
  2. Fat or Marrow
  3. Air
  4. Amniotic fluid
  5. Septic
82
Q

emboli at saddle bifurcation on pulmonary artery
smaller emboli to periphery
very small emboli

A
  • instantaneous fatal (due to Right Heart Failure)
  • SOB + low O2 sat
  • asymptotic
83
Q

Lines of Zhan

A

tell you RED thrombus happened when pt was alive
= white (platelet + fibrin) and Red (RBCs) alternating stripes
*cause of death

84
Q

Postmortem clots

A

pooled blood coagulated after death = look like chunky blackish jelly

85
Q

fat emboli

A

from fracture of a bone going into circulation = mental changes + respiratory distress SOB
= can happen from resuscitation (chest compressions)

86
Q

Air embolism

A
  1. can happen from cardiac catheterization introducing air in —-> usually goes to coronary artery
  2. Decombression illness BENDS, CAISSON D : N (high P) is breathed in under lowww depths and goes into BVs where there is lower P, ascending too fast makes N accumulate and not able to leave BV in time causing lung embolism
87
Q

Amniotic Fluid embolism

A

late preg or after just delivering baby
= sudden SOB, cyanosis, anaphylactic shock**, (pulmonary edema), hair, squamous cells, fat in BVs (FETUS MATERIAL forming embolism in lungs)
= leathal
= prolongerd aPTT and PT, and low fibrinogen, high fibrin, low O2 sat

88
Q

Septic embolism

A

bloodborne infective tissue causing embolism

= can happen in endocarditis valve breaks off

89
Q

Septic embolism SX:

A 
SX: skin microemboli = Janeway lesions (purpuric)
Retinal emboli (roth spots)
Vascular damage on nail beds (splinter hemorrhage)
90
Q

White thrombus
WHAT
EX:
TX:

A 
ARTERIAL (coronary, cerebral) thrombus
high platelets
from high sheer stress
EX: atheroscleorosis*
TX: anti-platelet therapy
91
Q

RED thrombus
WHAT
EX:
TX:

A

VENOUS
high RBCs
EX: Stasis**, DVT
Lower Extremities usually

92
Q

RED infarct

A

tissue depend on many blood supplies

Lung, liver, GI

93
Q

White infract

A

tissue depends on 1 vessel

Spleen

94
Q

what can prevent a tissue to get an infarct from a thrombus

A

if thrombus grows slowly enough that collaterals can be made

95
Q

tissue most vulnerable to hypoxia

A

brain , high change for infarct if thrombus

96
Q

when does shock happen

A

O2 and nutrients to tissues are not met

  1. low BV or cardiac failure
  2. systemic inflammation when body need more
  3. hypovolemic (fluid loss)
  4. decreased resistance from IgE or X ANS during shock
97
Q

steps in how shock happens

up to endothelial cell dysfunction and activation

A
  1. PAMPs —-> TLRs
  2. innate IS
  3. IL1, IL12, IL!8, IFN-g, TNF
  4. complement activated
  5. endothelial cells activate and some dysfunction
98
Q

steps in how shock happens

after endothelial cell dysfunction and activation

A
  1. endothelial cells activate and some dysfunction
  2. fluid spills out = edema and hypovolemia
  3. vasodilation from NO (lower resistance)
  4. dyfunctional endothelium causes prothrombotic factors to come (F7, tissue factor), low Protein C and antithrombin
  5. Hypotention, hypovolemia, thrombosis, low O2 sat + low nutrients delivered
99
Q

signs of shock

A

Hypotention, hypovolemia, thrombosis, low O2 sat + low nutrients delivered

MOD Midterm (9 decks)

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