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M1 FMK > Fluids and Hemodynamics > Flashcards

Fluids and Hemodynamics Flashcards

1
Q

Exudates

A

Caused by inflammation (aka inflammatory edema) that results from increased permeability of post-capillary venules (due to separation of endothelial junctions), commonly caused by histamine secretion from mast cells

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2
Q

Transudates

A

Results from abnormalities involving Starling forces acting at the capillary level (noninflammatory edema)

Elevated capillary hydrostatic pressure, decreased plasma oncotic pressure, and decreased lymphatic drainage - promote transudate formation

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3
Q

What initially offsets factors favoring edema during chronic heart failure?

A

In CHF, increased lymphatic drainage initially offsets factors favoring edema, temporarily delaying edema development

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4
Q

Causes of lymphatic obstruction

A

Lymphatic network dysgenesis and malignancy

Can result in nonpitting edema

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5
Q

Congenital lymphedema

A

Due to lymphatic network dysgenesis - common w/ Turner syndrome

Turner Syndrome - characteristically associated with webbed neck, horeshoe kidney, and nail dyslasia

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6
Q

Where do most pulmonary emobli arise?

A

DVT of the lower extremities

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7
Q

Where do DVTs typically originate

A

Calf veins, but PE-causing DVTs are much more likely to originate in the large proximal femoral veins

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8
Q

What is a large thromboembolism called that is lodged in the right pulmonary artery?

A

Saddle PE

Cause of sudden death

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9
Q

Sonographic findings that suggest thrombus

A

Noncompressible vein

Visible hyperechoic mass

and/or absent or abnormal venous flow

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10
Q

What is the test of choice for dx’ing DVT?

A

Compression US

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11
Q

What Pt’s should be evaluated for inherited hypercoagulability?

A

Pt’s younger than 50 y/o who present with thrombosis and no obvious explanation for an acquired prothrombotic state

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12
Q

Mutation of coagulation factor V

A

The Leiden mutation - most common inherited cause of hypercoagulable state

Resistance to degradation by activated protein C

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13
Q

Clinical manifestations of factor V Leiden

A

DVT (associated with PE)

Cerebral vein thrombosis

Recurrent pregnancy loss

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14
Q

Antiphospholipid syndrome

A

Secondary hypercoagulable disorder characterized by recurrent venous or arterial thrombi, repeated miscarriages, cardiac valvular vegetations (Libman-Sacks endocarditis), and thrombocytopenia

Characterized by formation of procoagulant antiphospholipid autoantibodies: anti-beta-2-glycoprotein antibodies, anticardiolilpin antibodies, and lupus anticoagulant

Lab findings: prolonged PTT w/ normal serum levels of anithrombin III, protein C, and protein S

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15
Q

Atheroembolic disease

A

Needle-shaped cholesterol clefts in affected vessels (cholesterol emboli) are diagnostic

Typically occurs after invasive vascular procedure (i.e. coronary angiography/aortic surgery), is most often associated with kidney injury.

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16
Q

Hemorrhagic necrosis of the lungs

A

Can appear due to PE from DVT

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17
Q

Fat embolism syndrome

A

Results from long-bone fracture

Acute-onset neurologic abnormalities, respiratory failure, and petechiae in a patient wiht a traumatic bone fracture

Sections of lung would reveal fat microglobules in pulmonary arteries

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18
Q

Amniotic fluid emboli

A

Are related to the rupture of uterine venous sinuses as a complication of childbirth (fetal squamous epithelial cells would be present in the blood vessels in lung of mom)

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19
Q

Bone marrow embolism

A

May be incidental finding due to CPR that fractures ribs or it may occur with fat embolism syndrome

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20
Q

White infarcts

A

Located in solid organs that lack a dual blood supply or collateral circulation such as the heart, spleen, and kidneys

Usually caused by arterial occlusion due to thrombosis or thromboembolism which may be seen with atrial fibrillation

Results in coagulative necrosis

21
Q

Red infarcts

A

Hemorrhagic infarcts

Can occur in organs with a dual blood supply - such as the lung, or in organs with extensive collateral circulation (i.e. small intestines and the brain)

Also can occur in organs in which the venous outflow is obstructed (venous occlusion) - such as with torsion of the ovary or testis

22
Q

Why are liver infarcts rare?

A

Becuase the liver has a dual blood supply: the portal vein and hepatic artery

23
Q

Hyperemia

A

Refers to excess amounts of blood within an organ (grossly a red color)

Active hyperemia- increased arterial supply

Passive hyperemia - impaired venous drainage

24
Q

Exmples of passive hyperemia

A

aka congestion - blue-red color grossly

Changes produced by CHF - chronic passive congestion of the lung or the liver

Lung - results from pulmonary hemorrhage (erythrocytes within alveoli) which can lead to hemoptysis and produce intra-alveolar, hemosiderin-ladien macrophages (heart failure cells)

Congestion in the liver is characterized by centrilobular congestion (congestion in acinar zone 3 of liver) which is seen grossly as a nutmeg appearance of the liver

25
Q

Heart failure cells

A

intra-alveolar, hemosiderin-laden macrophages, called heart failure cells. These are macrophages that have phagocytize the intra alveolar erythrocytes (note that the special stain for hemosiderin, which contains iron, is a Prussian blue stain).

26
Q

Increased capillary hydrostatic pressure

Causes

A

May result from:

  1. Arteriolar dilation
  2. Hypervolemia
  3. Increased venous pressure
27
Q

Hypervolemia

Downstream effect and potential cause

A

Increases hydrostatic pressure

May be caused by sodium retention (seen in renal disease)

28
Q

Increased venous hydrostatic pressure

A

Can be seen in venous thrombosis, CHF (most common), or cirrhosis

29
Q

Decreased plasma oncotic pressure

A

Results from decreased plasma albumin

May be caused by loss of albumin in the urine (seen with nephrotic syndrome) or by reduced synthesis (seen with chronic liver disease)

30
Q

Lymphatic obstruction

A

Caused by:

  1. Tumors (usually lymphoma)
  2. Surgery (axillary node dissection after mastectomy)
  3. Microfilaria infection - Wuchereria bancrofti - parasite that can cause lymphatic filariasis (humans are definitive host - mosquitoes are intermediate host)
31
Q

Elephantiasis

A

Caused by Muchereria bancrofti

causes lymphatic filariasis

Adult parasites live in lymphatics where they release microfilariae that enter bloodstreamand can be transferred into a mosquito where they mature into motile larvae. Mosquito bite can transfer these larve back to humans where they migrate to lymph nodes, pimarily in the legs and groin - maturing into adult worms

Obstruction of the lymphatics in these areas leads to massive swelling in the legs and genitals

32
Q

Hydrothorax

A

Fluid in the thorax

33
Q

Anasarca

A

Refers to extreme generalized edema involving the extracellular space in subcutaneous tissue, visceral organs, and body cavities

34
Q

Ascites

A

Refers to clinically apparent accumulation of fluid in the peritoneal cavity (may be due to cirrhosis)

35
Q

Mural thrombi

A

Associated with MIs and arrhythmias

36
Q

Thrombi within the aorta

A

Associated with atherosclerosis or aneurysmal dilatations

37
Q

Virchow’s triad

A
  1. Endothelial damage
  2. Abnormal blood flow
  3. Hypercoagulable states

Used to assess risk of thrombosis

38
Q

Causes of endothelial damage

A

Atherosclerosis (and causes of atherosclerosis)

Vasculitis

Elevated levels of homocysteine

39
Q

Primary hypercoagulable states

A
  1. Deficiencies of protein C or protein S
  2. Ledien mutation
  3. Deficiency of anithrombin III
40
Q

Functions of proteins C and S

A

C - inactivate factor Va

S - inactivate factor VIIIa

Therefore deficiency is associated with overactivity of factors Va and VIIIa - increases thromboses

41
Q

Warfarin

A

aka Coumadin

Inhibits the production of vitamin k-dependent coagulation factors and proteins C and S

Therefore initial Tx with warfarin may temporarily make clotting worse or precipitate skin necrosis

42
Q

What binds and inactivates thrombin and factor X

A

Antithrombin III (ATIII)

Deficiency of ATIII increases thrombin and factor X - increases risk of thrombosis - PTT does not rise with standard heparin therapy

43
Q

Anti-beta-2 glycoprotein antibodies

A

β2 glycoprotein, aka apolipoprotein H (apoH), is complex and includes regulating complement and coagulation.

β2 glycoprotein has both antithrombotic effects (anticoagulant and antiplatelet) and procoagulant effects. The balance between these opposing effects are dependent on
multiple factors.

Anti-β2 glycoprotein antibodies can increase the procoagulant effect of β2 glycoprotein, possibly by inhibiting the activation of protein C.

Note that the confirmatory test for the APS is the presence of these anti-β2 glycoprotein antibodies.

44
Q

Anticardiolipin antibodies

A

Cardiolipin in an anionic phospholipid that is similar to platelet factor 4 on platelets. Antibodies against cardiolipin can bind to the surface of platelets and make them sticky, leading to clot formation

45
Q

Lupus anticoagulant

A

Misnomer

Can artificially prolong PTT (prolonged PTT indicates a deficiency of one of the components of the intrinsic pathway - such as coagulation factor VIII)

46
Q

Anti-phospholipid syndrome (APS) most commonly occurs secondary to what?

A

Lupus erythematosus

Individuals with APS may have false positive lab tests - i.e. a false positive for rapid plasma reagin (syphylis)

47
Q

The pathogenesis of inflammatory edema (exudate) mainly involves increased permeability of post-capillary venules due to which one of the following?

A

C) Separation of endothelial junctions

Exudates are caused by inflammation (aka inflammatory edema) that results from increased permeability of post-capillary venules, due to separation of endothelial junctions, commonly caused by histamine secretion from mast cells.

48
Q

Arterial occlusion in solid organs lacking a dual blood supply or collateral circulation, such as the heart, spleen, and kidneys, is most likely to produce what type of infarct?

A

C) White infarct

White infarcts are located in solid organs that lack a dual blood supply or collateral circulation, such as the heart, spleen, and kidneys.

M1 FMK (55 decks)

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