2: Hemodynamics Flashcards
Edema vs effusion
Edema: abnl fluid in interstitial space
Effusion: abnl fluid in potential spaces / body cavities (pleural space, peritoneal space, pericardial space, joint space)
Most important colloidal protein in oncotic pressure
Albumin
Kwashiorkor and how it causes edema
Protein deficiency -> insufficient albumin -> reduced plasma oncotic pressure
Three main mechanisms that lead to decreased protein -> decreased plasma oncotic pressure
- Not enough ingested
- Not enough produced by liver
- Too much lost via kidney disease
Possible differentials for lymphedema
Infection, inflammation, trauma, tumors, surgery, malformation, helminth infection by Filariasis
Lymphedema in pt s/p breast cancer surgery and axillary dissection
Removing draining LNs from the breast can cause lymphedema -> edema in upper extremity on that side
Chronic congestion and hemosiderosis
Chronic congestion can allow RBCs to escape vessels -> hemosiderin escapes and causes tissue damage
Normal hepatic blood flow in the liver
From portal tract -> towards central vein
Endothelial organelles that create vWF
Weibel Palade bodies
Syndromes caused by lack of vWF vs lack of GpIb receptor
Lack of vWF: bon Willebrand disease
Lack of GpIb: Bernard Soulier syndrome
What do ADP and thromboxane A2 do in primary hemostasis
ADP: increase platelet activation
Thromboxane A2: increase platelet aggregation
What does Aspirin block?
Thromboxane A2
Disorder caused by deficiency in GpIIb-IIIa
Glanzmann thrombasthenia
S/S that point to possible primary hemostasis
Muco cutaneous bleeding (nose bleeds, gums bleeding), easy bruising, metromenorrhagia
Lab testing to see if there is something wrong with primary hemostasis
- CBC for platelet quantity
- Platelet function studies
- Flow cytometry
- PFA-100: tests adhesion and aggregation
Other name for factor I and II
I: fibrinogen
II: prothrombin
Other name for factor III and VIII
III: tissue factor
VIII: antihemophilic A factor
Four factors dependent on vitamin K
II, VII, IX, X (2, 7, 9, 10)
S/S of a defect in hemostasis
- Derm manifestations (petechiae, purpura, ecchymosis)
- Visceral bleeding
- Intracranial bleeding
- Hemarthrosis
Difference between petechiae, purpura, and ecchymosis
Petechiae: small spots <3mm
Purpura: larger spots
Ecchymosis: palpable bruise - an indurated/solid area
What causes abnormal activated partial thromboplastin time (aPPT) vs abnormal prothrombin time (PT)?
APPT: intrinsic pathway factors
Prothrombin time: factor VII (extrinsic)
What can cause endothelial activation in Virchow’s triad
Injury, infection, inflammatory mediators, hypercholesterolemia, smoking, turbulent flow
Why is turbulent flow bad and could lead to thrombosis?
Mixes coagulation factors + injured endothelium
Two common genetic hypercoagulopathies
Factor V Leiden mutation, Prothrombin mutation
Strong risk factors for thrombosis
Prolonged bed rest, MI, AFib, tissue injury, CA
Risk factors for DVT
Underlying genetic disorders, inactivity, injury, hormone replacement/contraceptives, smoking, pregnancy, CA, obesity
What happens if a thrombus dislodges?
Can cause an embolus
Hx that makes you suspect a primary hypercoagulable disorder
Initial event (DVT or PE) without any provoking factors, under age 40, or a strong FHx
Tests for primary hypercoagulopathy
ATIII, Protein C, S, factor V mutation, prothrombin mutation
Four fates of a thrombus
- Propagation
- Embolization
- Dissolution
- Organization/recanalization
Two ways a thrombus can dissolve
- Spontaneous due to endogenous fibrinolytic pathways
2. Therapeutic: tPA
How can you tell if a thrombus/embolus occurred during active blood flow (AKA before death) vs blood clot that occurs post-mortem?
Pre-Mortem: Lines of Zahn: alternating pale and red areas (platelets/fibrin and RBCs)
Post-Mortem: jelly-like blood
What type of emboli can be seen as a post-mortem finding and why?
Fat emboli due to CPR creating rib fractures -> fat emboli
Three signs of septic emboli
- Janeway lesion: skin microemboli
- Roth spots: retinal microemboli
- Splinter hemorrhage: vascular damage in nail bed
White vs red thrombus: where they are commonly found
White: arteries - areas of high shear stress (atherosclerosis), typically in coronary and cerebral arteries
Red: veins - areas of still blood/stasis, typically in LEs
Composition of white vs red thrombus
White: platelet-rich
Red: RBC rich
Red vs white infarct
Red: infarct in an organ with dual blood supply (ex: lung, liver, intestine)
White: infarct in an organ dependent on one vessel (ex: spleen)
What happens if the rate of occlusion is slow?
Collateral circulation can make up for vascular obstruction -> less likely to lead to infarct
Shock
Tissue oxygen and nutrient delivery is inadequate to meet physiologic needs
PTT vs PT times
PTT: 32-45 sec
PT: 10-14 sec
