Hemostasis, Hemodynamic Disorders, And Shock - Singh Flashcards
edema
fluid in interstitial space
Effusion
fluid in pleural, peritoneal = ascites, pericardial, joint spaces
Hyperemia
too much blood arriving (normal, like exercise)
= physiological and ARTERIAL, regulated by precapillary sphincter*
= can lead to some edema
Congestion
Not enough blood is leaving
= pathologic and VENOUS not draining fast enough, no regulation or sphincter
= can cause edema
how does heart failure lead to something else
heart failure leads to:
- high Pcap = edema
- low BF —-> renin activation —-> increase BV = edema
- kidney failure since renin is constantly needed and making conditions worse (retention of NA and H2O)
heart failure is what type of effusion
transudate fluid effusion
heart failure causes what edema
- pitting edema : press down on skin and its like a foam pillow
- Pulmonary edema
what can liver failure cause
edema and ascites due to low albumin production + Portal HTN**
jaundice, testicular atrophy
how does low albumin cause edema
low oncotic P in capillaries
how does portal HTN cause edema
causes CONGESTION (high Pcap) Liver cant process all the venous return from hepatic vein = blood backs up to portal vein and peritoneal cavity
2 ways you can get edema from renal disease
retention of h2o and NA = increase Pcap
2. Nephrotic syndrome = excess protein loss in urine (lower PIcap)
Kwashiorkor
low Protein in diet and malnutrition = edema
giant swollen in one leg like elephant looking
due to Lymphatic obstruction from worm parasites in the lymph causing lymph to not take up fluid (Filariasis)
swollen arm can happen after what surgery
removing breast LNs (especially axillary LN)
what causes exudate effucsion
inflammation
burns
sepsis
chronic congestion leads to
edema —-> Hemosiderosis (RBC leave capillaries) —-> tissue damage and necrosis
hemoosiderin- laden macrophages
heart failure cells
in the alveoli or chronic congestion
what can heart failure do to liver
hepatic congestion
Central Vein has low BF rate back to heart since RV is backing up
= nutmeg liver (centrilobular necrosis)
what besides heart failure can cause congestion in liver
hepatic congestion can happen from obstruction or thrombus in the central vein or portal vein
= nutmeg liver and centrilobular necrosis
portal HTN leads to what
cirrhosis
hemostasis
blood during injury
1st step in hemostasis
vasoconstriction (endothelin) to reduce SA and BF to the area injured
2nd step in hemostasis
Platelet plug (adhesion, activation, aggregation)
platelet adhesion involves what
vWF (uncurled form) on endothelium (Weibel Palade bodies = curled form) and GpIb on platelets
activation of platelets involves
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)
X vWF
Von Willebrand disease
X GpIb
Bernard Soulier Syndrome
=Giant platelets, that are size of RBCs
aggregation of platelets involves
bivalent fibrinogen binding to GpIIb-IIIa and cross linking
X GpIIb-IIIa
Glanzmann thrombasthenia
primary hemostasis
platelet plug formation
clinical signs if something is not right with primary hemostasis
Mucocutaneous bleeding (nose and mouth), excessive period bleeding
thrombocytopenia can lead to
hemorrhage
if someone has primary hemostasisi problem what labs should you do
CBC (platelet quantity)
Flow cytometry or PFA-100 looks at adhesion and aggregation (Platelet quality and function)
Thrombocytopenia
what happens
what do labs show
low or no platelet production
CBC low for platelets
Flow cytometry shows platelets aggregate and adhesion
Von Willebrand disease
what happens
what do labs show
X vWF
CBC shows normal platelet count
Flow cytometry shows NO platelet adhesion, YES agreggation
Bernard Soulier Disease
what happens
what do labs show
X GpIb
CBC shows normal to low platelet count
FC shows platelets NO adhesion, YES aggregation + abnormal large size
Glanzmann’s thrombasthenia
what happens
what do labs show
X GpIIb-IIIa
CBC shows normal platelet count
FC shows YES adhesion, NO aggregation
3rd step in hemostasis
coagulation cascade
Intrinsic and extrinsic
intrinsic pathway
F12–> F11–> F9–> F8 = aPartial Thromboplastin Time**
GOES TO COMMON pathway by activating F10
Extrinsic Pathway
Tissue Factor –> F7 = Prothrombin Time
GOES TO COMMON pathway by activating F10
Common pathway
- F10 activated, activated thrombin (F2a) with F5 and Ca+2 and Lipids
- Thrombin (F2a) binds to fibrinogen and forms Fibrin clot (F13)
Fibrinogen is what factor
F1
Prothrombin is what factor
F2
Antihemophilic A factor (AHF) is what factor
F8
function of thrombin
- stabilize fibrin
- activate platelets
- activate inflammatory cells and endothelium (N)
- Anti-thrombotic function when binding to (Thrombomodulin)
VIT K dependent factors
cant bind to CA+2 so they need VIT K:
F2, F7, F9, F10
(Warfarin, Coumadin inhibits these)
Secondary hemostasis is what
stabilize the clot then break it down
Secondary hemostasis problems show up as what
red dots on skin 1. Petechiae (small <3mm) 2. Purpura (large) 3. Ecchymosis (large and palpable, solid feeling) visceral and intracranial bleeding Hemarthrosis
visceral and intracranial bleeding happens from
factor deficiency or thrombocytopenia
when do you see Hemarthrosis
Factor deficiency**
blooding in the synovial joint
how to check aPTT
for intrinsic pathway
ADD NEGATIVE Ca+2 (should be 32-45 sec), not longer
how to check PT
for extrinsic pathway
ADD TISSUE FACTOR (should be 10-14sec), not longer
both PT and aPPT prolonged can mean
vit k deficiency liver disease anticoagulant medication dysfibrinogenemia (F10,5,2) disseminated intravascular coagulation
4th step of Hemostasis
Fibrinolysis
stop clot
resorption of clot
tissue repair
how to stop coagulation
- BF : washed away factors
- remove platelet adhesion surface
- Plasmin made by t-PA (breaks fibrin)
tPA
plasminogen —-> plasmin (break fibrin)
what does a normal not injured endothelium have on teh surface `
- Adenosine diphophatase
- Prostacyclin (PGl2), NO
= inhibit aggregation* - Thrombomodulin
Thrombin in anticoagulation
bind to Thrombomodulin causing Protein C to be active when Protein S is there = X F5a and F8a
Heparin function
blood thinner
it binds to anti-thrombin 3 = inactivated thrombin and F9a and 10a
Tissue Factor pathway inhibitor function
X F7a
examples of intrinsic pathway
inside vascular lumen injury exposing negative surface on platelets
examples of extrinsic pathway
injury outside BV and activated the tissue factor
Thrombus vs embolic
thrombus is the clot forming in a location
embolic is when a clot is traveling and then settles down some place
Virchow’s triad
- Endothelial injury : inflammation, Hypercholesterolemia
- Abnormal BF : stasis (afib, turbulence, bedrest), atherosclerosis (BV narrowing), dilated vessels(aneurism, hemorrhoids), heart failure
- Hypercoagulability : Inherited (Factor 5 Leiden), cancer
= all lead to thrombus
Endothelial injury leads to
Endothelial dyfunction = lowers NO
causing endothelial activtation (adhesion molecules for platelets)
what is down regulated in prothrombic state
Thrombomodulin, Protein C activated, Plasminogen (by Plasminogen activator inhibitor)
when can BF become turbulent
when P increases too high , happens nautraly at all bifurcations
how has aneurisms and hemorrhoids cause BF changes
it dilates the vessel
internal obstruction and change in BF
plaque buildup (atherosclerosis)
External interference, compression changing BF how
dead myocardium that is non-contractile
inadequate heart chamber function and change in BF
Atrial Fibrillation with stasis (inadequate pumping)
Factor 5 Leiden happens due to what mutation and how to test for it
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)
Prothrombin mutation leads to what
increased prothrombin levels
first place an Embolus goes and most common place it came from
where does it go if you have a foramen ovale
form popliteal fossa through the right heart to the lung pulmonary artery
if foramen ovale it goes to the brain
if thrombus presents in a person younger then 40 then what is it most likely
genetic factors
or something they did or use causing hypercoagulatory state
Heparin - induced thrombocytopenia
the patient has antibodies against heparin
- PF4 from platelet bound to heparin (anticoag usually)
- B-cells recognize this PF4-heparin
- IgG binds and cross linking on platelet (looks like fibrin cross link = PLATELET ACTIVATED)
- more PF4 released from platelets and binds to heparin causing
- platelet plug = thrombosis**
- M come to eat these IgG tagged = low platelet count**
how to test for HIT
- pt on heparin
- Labs show thrombocytopenia leading to thrombosis
- PF4 Abs are present**
- Platelets aggregate and get eaten
= can cause black fingers and toes = necrosis thrombus
Antiphospholipid Ab syndrome
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
how to fibrolyze a clot in someone in the brain area
- give chewed asprin before the travel to EM
- give exogenous t-PA** (within 6hr on symptoms) before liqueficous necrosis starts that can cause hemorrhage if BF returns
4 things that can happen when there is a thrombus
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
5 types of emboli
- thromboemboli (blood)
- Fat or Marrow
- Air
- Amniotic fluid
- Septic
emboli at saddle bifurcation on pulmonary artery
smaller emboli to periphery
very small emboli
- instantaneous fatal (due to Right Heart Failure)
- SOB + low O2 sat
- asymptotic
Lines of Zhan
tell you RED thrombus happened when pt was alive
= white (platelet + fibrin) and Red (RBCs) alternating stripes
*cause of death
Postmortem clots
pooled blood coagulated after death = look like chunky blackish jelly
fat emboli
from fracture of a bone going into circulation = mental changes + respiratory distress SOB
= can happen from resuscitation (chest compressions)
Air embolism
- can happen from cardiac catheterization introducing air in —-> usually goes to coronary artery
- 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
Amniotic Fluid embolism
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
Septic embolism
bloodborne infective tissue causing embolism
= can happen in endocarditis valve breaks off
Septic embolism SX:
SX: skin microemboli = Janeway lesions (purpuric) Retinal emboli (roth spots) Vascular damage on nail beds (splinter hemorrhage)
White thrombus
WHAT
EX:
TX:
ARTERIAL (coronary, cerebral) thrombus high platelets from high sheer stress EX: atheroscleorosis* TX: anti-platelet therapy
RED thrombus
WHAT
EX:
TX:
VENOUS
high RBCs
EX: Stasis**, DVT
Lower Extremities usually
RED infarct
tissue depend on many blood supplies
Lung, liver, GI
White infract
tissue depends on 1 vessel
Spleen
what can prevent a tissue to get an infarct from a thrombus
if thrombus grows slowly enough that collaterals can be made
tissue most vulnerable to hypoxia
brain , high change for infarct if thrombus
when does shock happen
O2 and nutrients to tissues are not met
- low BV or cardiac failure
- systemic inflammation when body need more
- hypovolemic (fluid loss)
- decreased resistance from IgE or X ANS during shock
steps in how shock happens
up to endothelial cell dysfunction and activation
- PAMPs —-> TLRs
- innate IS
- IL1, IL12, IL!8, IFN-g, TNF
- complement activated
- endothelial cells activate and some dysfunction
steps in how shock happens
after endothelial cell dysfunction and activation
- endothelial cells activate and some dysfunction
- fluid spills out = edema and hypovolemia
- vasodilation from NO (lower resistance)
- dyfunctional endothelium causes prothrombotic factors to come (F7, tissue factor), low Protein C and antithrombin
- Hypotention, hypovolemia, thrombosis, low O2 sat + low nutrients delivered
signs of shock
Hypotention, hypovolemia, thrombosis, low O2 sat + low nutrients delivered
