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Pathology Block 1 > Block 1 Hemodynamics > Flashcards

Block 1 Hemodynamics Flashcards

1
Q

Percent of body that is water, and distribution of water

A

60%

40% intracellular, 15% intercellular, 5% intravascular

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2
Q

Causes of edema

A

Increased hydrostatic pressure, decreased osmotic pressure, lymphatic obstruction, increased sodium, inflammation

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3
Q

Nephrotic syndrome symptoms

A

Proteinuria, hypoalbuminemia, periorbital and ankle edema, hyperlipidemia;

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4
Q

Nephrotic syndrome causes

A

Focal segmental glomerulo-sclerosis or -nephritis (minimal change or membranous); SLE, HBV, HCV, HIV, DM, malignancy

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5
Q

Filariasis

A

Worm that obstructs lymphatics -> elephantiasis

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6
Q

Hyperemia vs. congestion

A

H: active process like inflammation or exercise -> redness
C: passive process due to outflow obstruction (local or CHF) -> loss of oxygen

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7
Q

Nutmeg liver

A

Sign of passive congestion due to blood collecting around central veins in liver (not portal areas)

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8
Q

Plain film signs of CHF

A

Pulmonary edema, Kerley B lines (manifestation of pulm edema)

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9
Q

Histological signs of pulmonary edema

A

Proteinaceous fluid in alveolar spaces, engorged capillaries with RBCs (pulmonary congestion), hemosiderin-laden MFs

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10
Q

Transudate vs. exudate

A

T: low protein content, SG 1.020, inflammatory; suppurative, serosanguinous, or hemorrhagic

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11
Q

Anasarca

A

Generalized edema, due to low serum albumin (liver disease)

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12
Q

Petechiae

A

1-2 mm hemorrhages of skin, serial surfaces, due to thrombocytopenia (or aspirin)

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13
Q

Purpura

A

> 3 mm hemorrhages, due to trauma, vasculitis

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14
Q

Ecchymoses

A

> 1-2 cm bruise, blood in soft tissue

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15
Q

Hematoma

A

Larger collection of blood; hemarthrosis, hemothorax, etc.

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16
Q

Factors that stop hemostasis

A

Anticlotting: AT3 (inh thrombin), protein C/S
Fibrinolysis: plasmin

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17
Q

Mechanism of protein C, S

A

Thrombin + TM activates protein C, with protein S -> proteolysis of Va, VIIIa

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18
Q

Mechanism of AT3

A

Binds heparin-like molecules to inactivate thrombin, Xa, IXa

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19
Q

Mechanism of tissue factor pathway inhibitor

A

Inactivates tissue factor-VIIa complexes

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20
Q

Factors produced by endothelium to inhibit thrombosis & mechanism

A

PGI2, NO, ADP -> inhibit platelet aggregation

tPA -> activates fibrinolytic cascade

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21
Q

Pro-thrombosis mechanisms

A

Platelet adhesion held together by fibrinogen (on vWF on collagen)
Exposure of membrane-bound TF -> extrinsic coagulation sequence

22
Q

Virchow’s triad

A

Causes of thrombosis: altered endothelium, blood flow, or coagulability

23
Q

Inherited hypercoagulable states

A

Factor V Leiden mut, prothrombin G20210A mut
Rare: AT3, protein C, S deficiencies
Very rare: homozygous homocysteinuria

24
Q

Leiden mutation

A

Factor V resistant to protein C cleavage -> always active -> thrombus formation

25
Q

Cause of venous vs. arterial thromboses

A

V: all hyper coagulable states except…
A: homozygous homocysteinuria

26
Q

Antithrombin 3, protein C, protein S deficiency

A

No inactivation of thrombus formation = formation of blood clot

27
Q

Acquired hypercoagulable states

A

Prolonged bed rest, tissue injury, cancer (myeloma), HITS, anti-PL Abs, drugs (estrogen), smoking

28
Q

HITS

A

Large molecular weight heparin may induce Ab formation against platelet factor 4 = cross-linking = low platelet count

29
Q

Anti-PL antibodies

A

In connective tissue disease, causes recurrent pregnancy loss

30
Q

Estrogen & hypercoagulable state

A

Increased risk of clot because of increased synthesis of coagulation factors

31
Q

Smoking & hypercoagulable state

A

Endothelial damage

32
Q

Clinical warning signs of hypercoagulable states

A

Repeated miscarriages, stroke in young person, recurrent thrombosis/emboli (in odd places, like upper limb), resistance to anticoagulation

33
Q

Lines of Zahn

A

Layering of fat with RBCs = red lines, alternating with tan lines (platelets, fibrin)

34
Q

White thrombi

A

In faster moving flows, more fibrin and platelets

35
Q

Red thrombi

A

In slower moving flows/veins, more time for RBCs to become enmeshed

36
Q

Chicken fat clots

A

Post-mortem clots

37
Q

Saddle embolus

A

Blood clot that occupies both left and right main pulmonary arteries

38
Q

Fates of thrombi

A

Dissolution, organization & recanalization, propagation (enlargement), embolization

39
Q

Mural thrombus

A

Attached to the wall of a cavity

40
Q

Embolism & types

A

Detached intravascular mass that is carried by blood to distant site
Blood, fat, air, amniotic fluid (1/40k), tumor

41
Q

Infarction & red vs. white infarct locations

A

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)

42
Q

Clinical symptoms of shock

A

Sys BP

43
Q

Types of shock

A

Anaphylactic, cardiogenic, hypovolemic, neurogenic, septic

44
Q

Cardiogenic shock causes

A

Myocardial pump failure or MI

45
Q

Hypovolemic shock causes

A

Loss of blood or plasma

46
Q

Septic shock causes

A

Systemic microbial infection; vasodilation, peripheral pooling of blood; systemic reaction to bacterial or fungal infection

47
Q

Anaphylactic shock causes

A

IgE-mediated hypersensitivity, vasodilation and permeability

48
Q

Neurogenic shock causes

A

Loss of vascular tone

49
Q

Stages of shock

A

Non-progressive, progressive, irreversible

50
Q

Morphology of shock

A

Hypoperfusion; fibrin microthrombi of brain, heart, kidney, adrenals, GI; adrenocortical lipid depletion; diffuse alveolar damage (“shock lung”)

51
Q

Shock lung/DAD

A

Decreased perfusion to hyaline membrane, alveolar spaces, injured pneumocytes slough off -> plasma proteins in alveolar spaces -> ARDS d/t damage of hyaline membranes

52
Q

Changes in metabolism from non-progressive to progressive shock

A

Switch from aerobic to anaerobic, causing lactic acidosis; change in pH inactivates the enzymes that would clear things out

Pathology Block 1 (12 decks)

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