2: Hemodynamics

Question 1

Edema vs effusion

Answer 1

Edema: abnl fluid in interstitial space
Effusion: abnl fluid in potential spaces / body cavities (pleural space, peritoneal space, pericardial space, joint space)

Question 2

Most important colloidal protein in oncotic pressure

Answer 2

Albumin

Question 3

Kwashiorkor and how it causes edema

Answer 3

Protein deficiency -> insufficient albumin -> reduced plasma oncotic pressure

Question 4

Three main mechanisms that lead to decreased protein -> decreased plasma oncotic pressure

Answer 4

1. Not enough ingested
2. Not enough produced by liver
3. Too much lost via kidney disease

Question 5

Possible differentials for lymphedema

Answer 5

Infection, inflammation, trauma, tumors, surgery, malformation, helminth infection by Filariasis

Question 6

Lymphedema in pt s/p breast cancer surgery and axillary dissection

Answer 6

Removing draining LNs from the breast can cause lymphedema -> edema in upper extremity on that side

Question 7

Chronic congestion and hemosiderosis

Answer 7

Chronic congestion can allow RBCs to escape vessels -> hemosiderin escapes and causes tissue damage

Question 8

Normal hepatic blood flow in the liver

Answer 8

From portal tract -> towards central vein

Question 9

Endothelial organelles that create vWF

Answer 9

Weibel Palade bodies

Question 10

Syndromes caused by lack of vWF vs lack of GpIb receptor

Answer 10

Lack of vWF: bon Willebrand disease

Lack of GpIb: Bernard Soulier syndrome

Question 11

What do ADP and thromboxane A2 do in primary hemostasis

Answer 11

ADP: increase platelet activation

Thromboxane A2: increase platelet aggregation

Question 12

What does Aspirin block?

Answer 12

Thromboxane A2

Question 13

Disorder caused by deficiency in GpIIb-IIIa

Answer 13

Glanzmann thrombasthenia

Question 14

S/S that point to possible primary hemostasis

Answer 14

Muco cutaneous bleeding (nose bleeds, gums bleeding), easy bruising, metromenorrhagia

Question 15

Lab testing to see if there is something wrong with primary hemostasis

Answer 15

1. CBC for platelet quantity
2. Platelet function studies
3. Flow cytometry
4. PFA-100: tests adhesion and aggregation

Question 16

Other name for factor I and II

Answer 16

I: fibrinogen
II: prothrombin

Question 17

Other name for factor III and VIII

Answer 17

III: tissue factor
VIII: antihemophilic A factor

Question 18

Four factors dependent on vitamin K

Answer 18

II, VII, IX, X (2, 7, 9, 10)

Question 19

S/S of a defect in hemostasis

Answer 19

1. Derm manifestations (petechiae, purpura, ecchymosis)
2. Visceral bleeding
3. Intracranial bleeding
4. Hemarthrosis

Question 20

Difference between petechiae, purpura, and ecchymosis

Answer 20

Petechiae: small spots <3mm
Purpura: larger spots
Ecchymosis: palpable bruise - an indurated/solid area

Question 21

What causes abnormal activated partial thromboplastin time (aPPT) vs abnormal prothrombin time (PT)?

Answer 21

APPT: intrinsic pathway factors

Prothrombin time: factor VII (extrinsic)

Question 22

What can cause endothelial activation in Virchow’s triad

Answer 22

Injury, infection, inflammatory mediators, hypercholesterolemia, smoking, turbulent flow

Question 23

Why is turbulent flow bad and could lead to thrombosis?

Answer 23

Mixes coagulation factors + injured endothelium

Question 24

Two common genetic hypercoagulopathies

Answer 24

Factor V Leiden mutation, Prothrombin mutation

Question 25

Strong risk factors for thrombosis

Answer 25

Prolonged bed rest, MI, AFib, tissue injury, CA

Question 26

Risk factors for DVT

Answer 26

Underlying genetic disorders, inactivity, injury, hormone replacement/contraceptives, smoking, pregnancy, CA, obesity

Question 27

What happens if a thrombus dislodges?

Answer 27

Can cause an embolus

Question 28

Hx that makes you suspect a primary hypercoagulable disorder

Answer 28

Initial event (DVT or PE) without any provoking factors, under age 40, or a strong FHx

Question 29

Tests for primary hypercoagulopathy

Answer 29

ATIII, Protein C, S, factor V mutation, prothrombin mutation

Question 30

Four fates of a thrombus

Answer 30

1. Propagation 2. Embolization 3. Dissolution 4. Organization/recanalization

Question 31

Two ways a thrombus can dissolve

Answer 31

1. Spontaneous due to endogenous fibrinolytic pathways | 2. Therapeutic: tPA

Question 32

How can you tell if a thrombus/embolus occurred during active blood flow (AKA before death) vs blood clot that occurs post-mortem?

Answer 32

Pre-Mortem: Lines of Zahn: alternating pale and red areas (platelets/fibrin and RBCs) Post-Mortem: jelly-like blood

Question 33

What type of emboli can be seen as a post-mortem finding and why?

Answer 33

Fat emboli due to CPR creating rib fractures -> fat emboli

Question 34

Three signs of septic emboli

Answer 34

1. Janeway lesion: skin microemboli 2. Roth spots: retinal microemboli 3. Splinter hemorrhage: vascular damage in nail bed

Question 35

White vs red thrombus: where they are commonly found

Answer 35

White: arteries - areas of high shear stress (atherosclerosis), typically in coronary and cerebral arteries Red: veins - areas of still blood/stasis, typically in LEs

Question 36

Composition of white vs red thrombus

Answer 36

White: platelet-rich Red: RBC rich

Question 37

Red vs white infarct

Answer 37

Red: infarct in an organ with dual blood supply (ex: lung, liver, intestine) White: infarct in an organ dependent on one vessel (ex: spleen)

Question 38

What happens if the rate of occlusion is slow?

Answer 38

Collateral circulation can make up for vascular obstruction -> less likely to lead to infarct

Question 39

Shock

Answer 39

Tissue oxygen and nutrient delivery is inadequate to meet physiologic needs

Question 40

PTT vs PT times

Answer 40

PTT: 32-45 sec PT: 10-14 sec