Hemodynamic Disorders Flashcards
___% lean body weight is due to water
___intracellular; ___ extracellular
___ %intravascular (in plasma)
The rest is in the interstitial space
60% lean body weight is due to water
2/3 intracellular; 1/3 extracellular
5% intravascular (in plasma)
The rest is in the interstitial space
Enumerate Starling forces
- Intravascular Hydrostatic Pressure
2. Plasma colloid oncotic pressure / Intravascular oncotic pressure
If imbalance is not corrected, there will be too much
for the lymphatics to clear, leading to
EDEMA
[Type of edema: Transudate/exudate : Protein Rich/Poor:Specific gravity]
Inflammatory: _________ : ________ : ________
Inflammatory: Exudate:ProteinRich:>1.020
[Type of edema: Transudate/exudate : Protein Rich/Poor:Specific gravity]
NonInflammatory: _________ : ________ : ________
NonInflammatory:Transudate:ProteinPoor:<1.012
Mechanisms of Edema
- Increased intravascular hydrostatic pressure
- Decreased plasma oncotic pressure
- Lymphatic drainage obstruction
- Increased Sodium and Water Retention
- Increased capillary permeability
In the ff conditions, decrease plasma oncotic pressure will be observed EXCEPT in
a. Congestive Heart Failure
b. Severe Liver Disease
c. Nephrotic Syndrome
d. Protein Malnutrition
A
In the ff. conditions, there is systemic increase in intravascular hydrostatic pressure except
a. Congestive Heart failure
b. Leg vein thrombosis
A; Leg vein thrombosis cause local increase
Lymphedema may be secondary to (3)
radiation, scarring post-surgery, filariasis
What does periorbital edema indicate
severe renal disease
accumulation of clear fluids in
the tunica vaginalis
Testicular hydrocoele
Local increase in the volume of blood within a
particular tissue
Hyperemia or congestion
Manifests with bluish discoloration from deoxygenated
blood; Morphology: Cyanosis;Brought about by obstruction along venous end; Prolonged congestion leads to tissue hypoxia and cell death
Congestion
Manifests with redness from oxygenated blood
Morphology: Erythema
Brought about by arteriolar dilatation (exercise)
Physiologic response to increased functional demand
Hyperemia
Hemosiderin-laden macrophages are a.k.a
heart failure cells
Characterized by scarring and fibrosis and heart failure cells
a. Acute congestion
b. Chronic congestion
B
______________
o Thickened; fibrotic alveolar septa
o Contain heart failure cells (hemosiderin-laden
macrophages; appear brown)
Chronic Passive Congestion of the Lung
morphology of CPC liver
Nutmeg liver with centrilobular necorsis
[size]
petechiae
1-2mmq
[size]
purpura
> 3mm
[size]
Ecchymoses
> 1cm
Occurs due to
o Trauma
o Vasculitides
Purpura
Occurs due to
o Chronic congestion
o Platelet disorders
o Clotting factor defects
o These are not only seen in the skin, it can also be
seen on organ surfaces like those of the heart.
Petechiae
Hypovolemic shock happens when how much of blood is lost?
20% of blood volume
ventricles supposedly filled with cerebrospinal fluid are
filled with blood
intraventricular hemorrhage
hemorrhagic stroke (differentiate from ischemic stroke), neural deficits depend on area of hemorrhage
Intraparenchymal hemorrhage
usually hemorrhage of a meningeal artery (usually the middlemeningeal), manifests rapidly, unlike subdural
hematoma
Epidural hematoma
usually due to venous
rupture; there is a delay in the manifestation of
symptoms; may happen in the very young or
the very old
Subdural hematoma
What is a thrombosis?
abnormal clotting
Participants in normal hemostasis include
endothelium
platelets
coagulation factors
Steps in vasoconstriction in normal hemostatic process
Vascular injury ->neurogenic reflex + endothelin ->
transient vasoconstriction of the arteriole -> Exposure of
subendothelial tissue
Steps in primary hemostasis
Platelet adhesion
Platelet aggregation
Platelet secretion
Steps in secondary hemostasis
Release of tissue factor (Factor III/Thromboplastin)
Release of phospholipid complex
Coagulation cascade – results in formation of
thrombin that converts fibrinogen to fibrin (forms secondary hemostatic plug)
Un-injured state of endothelium
a. anti-thrombic plug predominates
b. pro-thrombic plug predominates
A
Counter-regulatory mechanisms to stop plug
formation and necessary to stop clotting and prevent blocking of blood vessels
tissue plasminogen activator
[Pro-thrombotic Function of the Endothelium]
exposure attracts platelets
Sub-endothelial collagen
allows plateletcollagen binding, allows platelet-ECM binding
Von Willebrand factor (VIII)
what activates the extrinsic pathway
Factor III (tissue factor)
[Function ]
Prostacyclin (PGI2) and Nitric oxide (NO)
stops endothelial injury
give (2) anticoagulants that are involved in anti-thrombic function of the endothelium
Heparin-like molecules
Thrombomodulin
binds to thrombin, stops pro-thrombotic properties, potent anticoagulant
Thrombomodulin
FibronectinFactor V, Factor VII,Platelet factor 4, TGF-beta are degraded by
tPA
What is the only known way to stabilize initial
platelet adhesion against high shear forces of
flowing blood ?
Von Willebrand Factor – glycoprotein-Ib interaction
describe Bernard-Soulier syndrome
no Glycoprotein 1b receptor
describe von Willebrand disease
no vWF
What is the function of TXA2 and ADP
platelet aggregation
Participation of thrombin and fibrin
a. Primary hemostatic plug
b. Secondary hemostatic plug
B
[Disease]
Deficient/Inactive GpIIB, II-a
Glanzmann thrombasthenia
Extrinsic pathway proteins
VII,X,V,II.I
Intrinsic pathway proteins
XII,XI,IX,VIII,X,V,II,I
What does Prothrombin Time test?
Protein function of extrinsic pathway
How is PT assesed?
add TISSUE FACTOR and PHOSPHOLIPIDS to citrated plasma and initiate coagulation by adding exogenous CALCIUM
What is Partial Thromboplastin Time for?
assess protein function of intrinsic pathway
Enumerate Virchow’s Triad
Endothelial Injury
Blood Flow
Blood hypercoagulability
What are the causes of endothelial injury
Atherosclerosis Hemodynamic stress (e.g. HPN) Inflammation Endotoxins Hypercholesterolemia Homocysteinuria Trauma
What is the end result of endothlial injury?
Exposure of subendothelial collagen matrix
Give clinical settings where normal blood flow is altered
Atherosclerotic plaques Aneurysms Infarcted myocardium Polycythemia vera Sickle cell anemia
Note: all leads to stasis except atherosclerotic plaques
Mutant factor V making it resistant to cleavage by protein C is a.k.a
Leiden Mutation
[Function]
Protein C and S
inactivate Va and VIIIa
[Function]
Plasmin system
breaks down fibrin
[Function]
Anti-thrombin III
inactivates thrombin, IXa, Xa, XIa, XIIa (9,10,11,12)a
The ff can cause secondary hypercolaguability EXCEPT
a. Prolonged bed rest/immobilization
b. MI, atrial fibrillation
c. Disseminated malignancy
d. Smoking and obesity
e. Anti-phospholipid antibody syndrome (APAS)
f. AOTA
g. NOTA
G
Easily detached
a. Thrombus
b. Postmortem clot
B
Adherent to wall
a. Thrombus
b. Postmortem clot
A
lines of ZAHN
a. Thrombus
b. Postmortem clot
A
Firm consistency
a. Thrombus
b. Postmortem clot
A
Takes the shape of the vessel
a. Thrombus
b. Postmortem clot
B
Gelatinous
a. Thrombus
b. Postmortem clot
A
Common sites of arterial thrombi
coronaries, cerebral, femoral arteries
thrombi in heart chambers are called
mural thrombi
embolus at the bifurcation of vessels, causing sudden death
saddle embolus
T/F Venous thromboses, especially in superficial leg veins, commonly embolize
F; venous thrombosis usually embolize but not in superficial leg veins. usually involves deep veins
What is Trosseau syndrome
inflammation of vein with formation and migration of thrombus (Migratory thrombophlebitis)
What are the fates of a thrombus?
Lysis Propagation organization Canalization Embolization
[Identify] Not a disease, complication/endpoint of many
conditions Characterized by widespread thromboses – forms thrombus which disseminates throughout the body
Disseminated Intravascular Coagulation
T/F DIC begins as a thrombotic disorder but ends up with serious bleeding
T
How does consumptive coagulopathy in DIC lead to thrombocytopenia?
In disseminated intravascular coagulation, disseminated thrombi attract more and more platelets causing decrease in platelets in the blood.
The ff can embolize
a. detached thrombi
b. fat
c. gas
d. tumor
e. AOTA
E
What is the most important cause of sudden death in immobilized post-operative patient with Congestive Heart failure?
Pulmonary embolism due to DVT
The ff increases risk of DVT and pulmonary embolism EXCEPT
a. Inactivity
b. Trauma
c. Surgery
d. Burns
e. Injury to vessels
f. Procoagulant substance from tissue
None of the above
Give complications of Pulmonary embolism
Sudden death due to dyspnea
Right heart failure
Pulmonary infarction
Pulmonary hypertension
Systemic embolism usually arise from
a. DVT
b. SVT
c. Mural thrombus
C
Left atrium mural thrombi associated with
a. mitral stenosis
b. atrial fibrillation
c. myocardial infarction
d. a and b
e. b and c
D
If emoboli lodge at branches of the carotid artery esp. middle cerebral artery, the result will be
cerebral infarction
If emoboli lodge at branches of the mesenteric artery esp. middle cerebral artery, the result will be
hemorrhagic infarction of the intestine
If emboli lodge at branches of the renal artery the result will be
Infarction of the renal cortex
left-sided emboli that originate in the venous
circulation that gain access to the arterial circulation
through a right to left shunt, most often through a
patent foramen ovale or atrial septal defect
Paradoxical emboli
[Identify]
Fracture of long bones
Particles of bone marrow and other fatty intraosseous
tissue that enter the circulation as a result of severe
fractures
Lodge in lungs, brain, kidneys, and other organs
Fat embolism
How much air is required for a gas embolism to have a clinical effect?
1cc
Formation of gas bubbles in skeletal muscles
and joints
Bends
chronic form of decompression
sickness, may lead to ischemic necrosis
Caisson disease
What complications can arise from amniotic fluid embolism?
activation of coagulation leading to Disseminated Intravascular Coagulation and sudden death
Causes of infarction
arterial thromboembolism (99%) vasospasm external compression (tumor) torsion (volvolus) septic infarct
True of red or hemorrhagic infarcts EXCEPT
a. arterial occlusions
b. happens in organs with loose tissue support - lungs
c. organs with dual circulation - small intestines, lungs
d. AOTA
e. NOTA
A
White infarcts can most likely happen to (give more than one answer)
a. lungs
b. small intestine
c. spleen
d. kidneys
e. heart
c-e
________ happens when infected heart valve vegetations embolize or when microbes seed the area of necrosis and infarct becomes an abscess
septic infarct
Factors affecting development of infarcts
Nature of vascular supply
Rate of development of occlusion
Tissue vulnerability to hypoxia
Oxygen content of blood
What are the causes of cardiogenic shock?
o Myocardial infarction
o Ventricular arrhythmias
o Extrinsic compression
o Outflow obstruction (e.g. saddle embolus)
