Block 1 Hemodynamics Flashcards
Percent of body that is water, and distribution of water
60%
40% intracellular, 15% intercellular, 5% intravascular
Causes of edema
Increased hydrostatic pressure, decreased osmotic pressure, lymphatic obstruction, increased sodium, inflammation
Nephrotic syndrome symptoms
Proteinuria, hypoalbuminemia, periorbital and ankle edema, hyperlipidemia;
Nephrotic syndrome causes
Focal segmental glomerulo-sclerosis or -nephritis (minimal change or membranous); SLE, HBV, HCV, HIV, DM, malignancy
Filariasis
Worm that obstructs lymphatics -> elephantiasis
Hyperemia vs. congestion
H: active process like inflammation or exercise -> redness
C: passive process due to outflow obstruction (local or CHF) -> loss of oxygen
Nutmeg liver
Sign of passive congestion due to blood collecting around central veins in liver (not portal areas)
Plain film signs of CHF
Pulmonary edema, Kerley B lines (manifestation of pulm edema)
Histological signs of pulmonary edema
Proteinaceous fluid in alveolar spaces, engorged capillaries with RBCs (pulmonary congestion), hemosiderin-laden MFs
Transudate vs. exudate
T: low protein content, SG 1.020, inflammatory; suppurative, serosanguinous, or hemorrhagic
Anasarca
Generalized edema, due to low serum albumin (liver disease)
Petechiae
1-2 mm hemorrhages of skin, serial surfaces, due to thrombocytopenia (or aspirin)
Purpura
> 3 mm hemorrhages, due to trauma, vasculitis
Ecchymoses
> 1-2 cm bruise, blood in soft tissue
Hematoma
Larger collection of blood; hemarthrosis, hemothorax, etc.
Factors that stop hemostasis
Anticlotting: AT3 (inh thrombin), protein C/S
Fibrinolysis: plasmin
Mechanism of protein C, S
Thrombin + TM activates protein C, with protein S -> proteolysis of Va, VIIIa
Mechanism of AT3
Binds heparin-like molecules to inactivate thrombin, Xa, IXa
Mechanism of tissue factor pathway inhibitor
Inactivates tissue factor-VIIa complexes
Factors produced by endothelium to inhibit thrombosis & mechanism
PGI2, NO, ADP -> inhibit platelet aggregation
tPA -> activates fibrinolytic cascade
Pro-thrombosis mechanisms
Platelet adhesion held together by fibrinogen (on vWF on collagen)
Exposure of membrane-bound TF -> extrinsic coagulation sequence
Virchow’s triad
Causes of thrombosis: altered endothelium, blood flow, or coagulability
Inherited hypercoagulable states
Factor V Leiden mut, prothrombin G20210A mut
Rare: AT3, protein C, S deficiencies
Very rare: homozygous homocysteinuria
Leiden mutation
Factor V resistant to protein C cleavage -> always active -> thrombus formation
Cause of venous vs. arterial thromboses
V: all hyper coagulable states except…
A: homozygous homocysteinuria
Antithrombin 3, protein C, protein S deficiency
No inactivation of thrombus formation = formation of blood clot
Acquired hypercoagulable states
Prolonged bed rest, tissue injury, cancer (myeloma), HITS, anti-PL Abs, drugs (estrogen), smoking
HITS
Large molecular weight heparin may induce Ab formation against platelet factor 4 = cross-linking = low platelet count
Anti-PL antibodies
In connective tissue disease, causes recurrent pregnancy loss
Estrogen & hypercoagulable state
Increased risk of clot because of increased synthesis of coagulation factors
Smoking & hypercoagulable state
Endothelial damage
Clinical warning signs of hypercoagulable states
Repeated miscarriages, stroke in young person, recurrent thrombosis/emboli (in odd places, like upper limb), resistance to anticoagulation
Lines of Zahn
Layering of fat with RBCs = red lines, alternating with tan lines (platelets, fibrin)
White thrombi
In faster moving flows, more fibrin and platelets
Red thrombi
In slower moving flows/veins, more time for RBCs to become enmeshed
Chicken fat clots
Post-mortem clots
Saddle embolus
Blood clot that occupies both left and right main pulmonary arteries
Fates of thrombi
Dissolution, organization & recanalization, propagation (enlargement), embolization
Mural thrombus
Attached to the wall of a cavity
Embolism & types
Detached intravascular mass that is carried by blood to distant site
Blood, fat, air, amniotic fluid (1/40k), tumor
Infarction & red vs. white infarct locations
Ischemic necrosis d/t occlusion of arterial supply or venous drainage
R: dual blood supply (liver, lung), hollow viscus (gut)
W: single blood supply, solid organ (heart, spleen, kidney)
Clinical symptoms of shock
Sys BP
Types of shock
Anaphylactic, cardiogenic, hypovolemic, neurogenic, septic
Cardiogenic shock causes
Myocardial pump failure or MI
Hypovolemic shock causes
Loss of blood or plasma
Septic shock causes
Systemic microbial infection; vasodilation, peripheral pooling of blood; systemic reaction to bacterial or fungal infection
Anaphylactic shock causes
IgE-mediated hypersensitivity, vasodilation and permeability
Neurogenic shock causes
Loss of vascular tone
Stages of shock
Non-progressive, progressive, irreversible
Morphology of shock
Hypoperfusion; fibrin microthrombi of brain, heart, kidney, adrenals, GI; adrenocortical lipid depletion; diffuse alveolar damage (“shock lung”)
Shock lung/DAD
Decreased perfusion to hyaline membrane, alveolar spaces, injured pneumocytes slough off -> plasma proteins in alveolar spaces -> ARDS d/t damage of hyaline membranes
Changes in metabolism from non-progressive to progressive shock
Switch from aerobic to anaerobic, causing lactic acidosis; change in pH inactivates the enzymes that would clear things out
