Block 1 Hemodynamics

Question 1

Percent of body that is water, and distribution of water

Answer 1

60%

40% intracellular, 15% intercellular, 5% intravascular

Question 2

Causes of edema

Answer 2

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

Question 3

Nephrotic syndrome symptoms

Answer 3

Proteinuria, hypoalbuminemia, periorbital and ankle edema, hyperlipidemia;

Question 4

Nephrotic syndrome causes

Answer 4

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

Question 5

Filariasis

Answer 5

Worm that obstructs lymphatics -> elephantiasis

Question 6

Hyperemia vs. congestion

Answer 6

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

Question 7

Nutmeg liver

Answer 7

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

Question 8

Plain film signs of CHF

Answer 8

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

Question 9

Histological signs of pulmonary edema

Answer 9

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

Question 10

Transudate vs. exudate

Answer 10

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

Question 11

Anasarca

Answer 11

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

Question 12

Petechiae

Answer 12

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

Question 13

Purpura

Answer 13

> 3 mm hemorrhages, due to trauma, vasculitis

Question 14

Ecchymoses

Answer 14

> 1-2 cm bruise, blood in soft tissue

Question 15

Hematoma

Answer 15

Larger collection of blood; hemarthrosis, hemothorax, etc.

Question 16

Factors that stop hemostasis

Answer 16

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

Question 17

Mechanism of protein C, S

Answer 17

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

Question 18

Mechanism of AT3

Answer 18

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

Question 19

Mechanism of tissue factor pathway inhibitor

Answer 19

Inactivates tissue factor-VIIa complexes

Question 20

Factors produced by endothelium to inhibit thrombosis & mechanism

Answer 20

PGI2, NO, ADP -> inhibit platelet aggregation

tPA -> activates fibrinolytic cascade

Question 21

Pro-thrombosis mechanisms

Answer 21

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

Question 22

Virchow’s triad

Answer 22

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

Question 23

Inherited hypercoagulable states

Answer 23

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

Question 24

Leiden mutation

Answer 24

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

Question 25

Cause of venous vs. arterial thromboses

Answer 25

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

Question 26

Antithrombin 3, protein C, protein S deficiency

Answer 26

No inactivation of thrombus formation = formation of blood clot

Question 27

Acquired hypercoagulable states

Answer 27

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

Question 28

HITS

Answer 28

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

Question 29

Anti-PL antibodies

Answer 29

In connective tissue disease, causes recurrent pregnancy loss

Question 30

Estrogen & hypercoagulable state

Answer 30

Increased risk of clot because of increased synthesis of coagulation factors

Question 31

Smoking & hypercoagulable state

Answer 31

Endothelial damage

Question 32

Clinical warning signs of hypercoagulable states

Answer 32

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

Question 33

Lines of Zahn

Answer 33

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

Question 34

White thrombi

Answer 34

In faster moving flows, more fibrin and platelets

Question 35

Red thrombi

Answer 35

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

Question 36

Chicken fat clots

Answer 36

Post-mortem clots

Question 37

Saddle embolus

Answer 37

Blood clot that occupies both left and right main pulmonary arteries

Question 38

Fates of thrombi

Answer 38

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

Question 39

Mural thrombus

Answer 39

Attached to the wall of a cavity

Question 40

Embolism & types

Answer 40

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

Question 41

Infarction & red vs. white infarct locations

Answer 41

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)

Question 42

Clinical symptoms of shock

Answer 42

Sys BP

Question 43

Types of shock

Answer 43

Anaphylactic, cardiogenic, hypovolemic, neurogenic, septic

Question 44

Cardiogenic shock causes

Answer 44

Myocardial pump failure or MI

Question 45

Hypovolemic shock causes

Answer 45

Loss of blood or plasma

Question 46

Septic shock causes

Answer 46

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

Question 47

Anaphylactic shock causes

Answer 47

IgE-mediated hypersensitivity, vasodilation and permeability

Question 48

Neurogenic shock causes

Answer 48

Loss of vascular tone

Question 49

Stages of shock

Answer 49

Non-progressive, progressive, irreversible

Question 50

Morphology of shock

Answer 50

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

Question 51

Shock lung/DAD

Answer 51

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

Question 52

Changes in metabolism from non-progressive to progressive shock

Answer 52

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