2: Hemodynamics Flashcards

1
Q

Edema vs effusion

A

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

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2
Q

Most important colloidal protein in oncotic pressure

A

Albumin

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3
Q

Kwashiorkor and how it causes edema

A

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

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4
Q

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

A
  1. Not enough ingested
  2. Not enough produced by liver
  3. Too much lost via kidney disease
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5
Q

Possible differentials for lymphedema

A

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

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6
Q

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

A

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

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7
Q

Chronic congestion and hemosiderosis

A

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

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8
Q

Normal hepatic blood flow in the liver

A

From portal tract -> towards central vein

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9
Q

Endothelial organelles that create vWF

A

Weibel Palade bodies

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10
Q

Syndromes caused by lack of vWF vs lack of GpIb receptor

A

Lack of vWF: bon Willebrand disease

Lack of GpIb: Bernard Soulier syndrome

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11
Q

What do ADP and thromboxane A2 do in primary hemostasis

A

ADP: increase platelet activation

Thromboxane A2: increase platelet aggregation

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12
Q

What does Aspirin block?

A

Thromboxane A2

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13
Q

Disorder caused by deficiency in GpIIb-IIIa

A

Glanzmann thrombasthenia

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14
Q

S/S that point to possible primary hemostasis

A

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

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15
Q

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

A
  1. CBC for platelet quantity
  2. Platelet function studies
  3. Flow cytometry
  4. PFA-100: tests adhesion and aggregation
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16
Q

Other name for factor I and II

A

I: fibrinogen
II: prothrombin

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17
Q

Other name for factor III and VIII

A

III: tissue factor
VIII: antihemophilic A factor

18
Q

Four factors dependent on vitamin K

A

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

19
Q

S/S of a defect in hemostasis

A
  1. Derm manifestations (petechiae, purpura, ecchymosis)
  2. Visceral bleeding
  3. Intracranial bleeding
  4. Hemarthrosis
20
Q

Difference between petechiae, purpura, and ecchymosis

A

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

21
Q

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

A

APPT: intrinsic pathway factors

Prothrombin time: factor VII (extrinsic)

22
Q

What can cause endothelial activation in Virchow’s triad

A

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

23
Q

Why is turbulent flow bad and could lead to thrombosis?

A

Mixes coagulation factors + injured endothelium

24
Q

Two common genetic hypercoagulopathies

A

Factor V Leiden mutation, Prothrombin mutation

25
Q

Strong risk factors for thrombosis

A

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

26
Q

Risk factors for DVT

A

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

27
Q

What happens if a thrombus dislodges?

A

Can cause an embolus

28
Q

Hx that makes you suspect a primary hypercoagulable disorder

A

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

29
Q

Tests for primary hypercoagulopathy

A

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

30
Q

Four fates of a thrombus

A
  1. Propagation
  2. Embolization
  3. Dissolution
  4. Organization/recanalization
31
Q

Two ways a thrombus can dissolve

A
  1. Spontaneous due to endogenous fibrinolytic pathways

2. Therapeutic: tPA

32
Q

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

A

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

33
Q

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

A

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

34
Q

Three signs of septic emboli

A
  1. Janeway lesion: skin microemboli
  2. Roth spots: retinal microemboli
  3. Splinter hemorrhage: vascular damage in nail bed
35
Q

White vs red thrombus: where they are commonly found

A

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

36
Q

Composition of white vs red thrombus

A

White: platelet-rich
Red: RBC rich

37
Q

Red vs white infarct

A

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

38
Q

What happens if the rate of occlusion is slow?

A

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

39
Q

Shock

A

Tissue oxygen and nutrient delivery is inadequate to meet physiologic needs

40
Q

PTT vs PT times

A

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