Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

77 Cards in this Set

  • Front
  • Back
Where do emboli in the venous circulation usually get stuck?
in the pulmonary capillaries
Flow of blood:
RA --> tricuspid --> RV -> pulmonary valve --> pulmonary circulation --> LA --> mitral valve --> LV --> aortic valve --> aorta
What is the starling hypothesis?
fluid movement across capillaries is dependent on hydrostatic and oncotic pressure
What is the amount of fluid that the lymph carries away normally?
2 ml/min in 1 gram of tissue
What does cerebral edema often lead to?
subfalacine herniation, uncinate herniation, or tonsillar herniation
What can cause CPC of the liver, (chronic passive congestion), and what are some features of it?
Cirrhosis of the liver often leads to it, and you get the classic nutmeg liver.
The lits of hemorrhage types:
1) petichiae - 1-2 mm, due to platelets
2) Purpura - greater than 3 mm
3) Ecchymoses (1-2 cm) - bruise basically
What is called when entire heart fills up with thrombus, usually after an MI
Mural thrombus
What are the classic feature of a thrombus where you see rings or lines?
Lines of Zahn - alternating layers of pale (platelets/fibrin) and red (RBC/WBC) regions
When the antithrombotic system of the body kicks in to get rid of thrombus, what is this called?
What can you inject in person to increase resolution of thrombus?
streptokinase, urokinase
what can cause plumonary thromboembolism?
sitting in a plane too long, leading to thrombi formation near valves of leg veins
what is it called when a thrombus gets stuck where the pulmonary artery bifurcates to each lung?
saddle thrombus
What can cause a systemic thrombi?
1) most common - mural thrombus after MI
2) atherosclerotic emboli on aorta, can get lodged in renal artery or others
3) bacterial endocardinitis - can form chunks of material on mitral valve
2 types of infarcts
white infarct - not much blood present
red infarct - often seen in lung, where you have 2 circulations
What is ARDS?
diffuse alveolar damage of lung from systemic shock, almost always fatal
What is low number of platelets called?
thrombocytopenia (also the most common cause for bleeding)
The glue that keep platelets bound to damaged vessel wall?
von Willebrand factor
What receptor for vWF are found on platelets?
Glycoprotein Ib-9
What granules in the platelets hold vWF?
alpha granules
What is found in dense granules?
S - serotonin
C - calcium
Bernard Soulier Syndrome (BSS)?
Missing vWF receptor.
Glanzmann's Thrombobasthenia?
Missing Glycoprotein IIb receptor on platelets - a receptor for fibrinogen/fibronectin, and vWF
When tissue is injured, tissue factor is released and binds with what? This complex then goes on to do what?
Tissue Factor binds with Factor VII(7)

TF/VII will go on to activate Factors IX(9) and X(10)
After the TF/VII(7) complex activates factos IX(9) and X(10), what do those two factors do?
Factor IX(9) combines with VIII(8). IX/VIII will then activate more X(10)

Factor X(10) combines with V(5). X/V converts Prothrombin to thrombin.
The most common hereditary coagulation factor deficiency?
Hemophilia A (deficiency in Factor VIII(8).
What can you use to chelate calcium and keep blood from clotting in test tube?
Sodium Citrate
Thrombin does a lot. In addition to activating fibrin, and the cross linking of fibrin (XIII(13)), what else does it activate?
Thrombin also activates the "cofactors" in the coagulation cascade --> VIII(8) and V(5) and XI(11)
So when Factor VII(7) binds with Tissue Factor, it acts as the "spark" that activates Factor (X)10 and IX(9). But the TF/VII complex will "die away" because why?
Tissue Factor Pathway Inhibitor (TFPI) will inhibit TF/VII. So now, the way that coagulation continues on is newly formed thrombin will "go back" and active Factor XI(11), which ultimately activates X(10). AND thrombin will activate VIII(8), which binds to X(10) as a cofactor. Sort of a feedback mechanism.
Thrombin activates what factor which helps cross links the fibrin monomers?
What are the Contact coagulation factors that we don't really need, are serine proteases?
XII(12) and XI (11)
What are the "Fibrinogen" group coagulation factors involved where fibrin forms?
I(1) - Fibrinogen
V(5) and VIII(8) and XIII (13)
All these are consumed during clotting, and it looks like they are what thrombin will activate (minus 11 i think)
What are the "Prothrombin" group coagulation factors? What is their significance?
II(2), VII(7), IX (9), and X(10).
All these are dependent on Vitamin K, so they will be reduced in patients on Coumadin.
What does antithrombin block?
Xa (10), thrombin, IXa(9), and a few others not worth memorizing.
What do protein C and protein S do?
Work together as the "APC complex", this complex forms when thrombin binds to thrombomodulin on healthy endothelial cells. The APC will inhibit factor VIII(8) and V(5).
What is Factor V Leiden?
Its a mutation in Factor V(5), so that the APC complex, that normally inhibits further clot formation, can't bind to V(5) to inhibit it, so V(5) keeps "clotting" so to speak.
Ok, so Factor XII(12) apparently doesn't play a big role in coagulation, but this intrinsic pathway is through to act in what way that's important?
Factor (XII), after forming on damaged endothelium, will convert prekallikrein to kallikrein, which enhances the activity of the plasminogen activator, activating plasmin. Plasmin will in turn activate more Factor XII(12), in sort of a positive feedback. It all sort of keeps the clot from spreading.
What does plasmin do to fibrin?
It breaks it down into Fibrin Degradation Products (FDPs) like X, Y, D, and E.
how does a deficiency in secondary hemostasis (coagulation factors) manifest itself clinically?
soft tissue (hematoma), joint, or body cavity injury.
What deficiency would you think present in a patient who doesn't bleed bad after surgery, but days later you notice a large hematoma?
Deficiency in Factor XIII (13) or they have hyperfibrinolysis (overactive, trigger happy plasmin)
What is the highest antibody secreting area of tissue in the body?
intestinal tract
What do we use to treat patients with IV of Abs that have been isolated?
Cohn alcohol fractionation
How much do the chains of Ab weigh?
2 H-chains (50kDa each)
2 L-chains (25kDa each)
150 kDa total
What fragments does papain produce in Abs?
2 Fab fragments (identical)
1 Fc fragment
What fragments does pepsin produce in Abs?
1 (Fab)2 fragment
1 Fc fragment
What od patients with multiple myeloma often secrete in their urine?
Bence-Jones proteins (BJP) - excess of light chain gamma globulins.
Uniform colonies of bacteria found in the guy, aggregated due to antibody binding.
How do Abs enhance innate factors?
they form complexes with things like peroxidases and lysozymes so that they are directed towards bacteria
Which light chain is more common in humans, kappa or lambda?
kappa (70% are this in humans)
The most common IgG subtype in the serum?
IgG1 (IgG itself is the most common Ab found in the serum)
Ab with the longest half-life?
IgG (3 weeks)
Where is IgG secreted exernally?
male and female genital tract excretions. Some in the milk too but it's not absorbed in baby's circulation.
What antibody crosses the placental barrier?
When does a baby start producing IgG?
about 5-6 months after birth
What is the most potent complement activator of the IgG subclasses?
Which IgG is an anti-polysacharride antibody?
Which IgG does not cross the placental barrier?
What protects the J domain on IgA antibodies from degradation by proteolytic digestion?
the SC (secretory component) between the dimeric Abs.
Where is IgA commonly found?
In secretions - tears, saliva, milk, and intestinal fluid
Which antibody is produced the most?
Does IgA bind complement?
What bacteria can produce proteases to IgA?
Strep. pneumoniae, gonococcus, meningococcus, covering the Ab with monovalent fragments with no Fc region, so it actually protects the Ab
When are adult levels of IgA achieved?
In secretions? - 6 to 12 months
In serum? - not until puberty
What antibody is the "secondary response" antibody?
Which antibody has 4 constant domains on their heavy chain, rather than 3?
What antibody is extremely sensitive to proteolytic enzymes?
What antibody functions in the primary Ab response?
When do you find high concentration of IgM in secretions?
When a person has an IgA deficiency.
What is the phylogenetically oldest Ab?
Does IgM have complement activation?
yes, "tremendous"
Where do you find IgD?
It's most important as a receptor on maturing B cells, to differnetiate or activate them.
What do you see in heavy chain gene rearrangment that is different than light.
There is a VDJ rearranemnt in heavy, there is no "D" in light (just VJ)
What are the steps in heavy chain rearrangment?
1) DJ forms
2) Any V combines with VDJ
What kind of mutation occurs at junction between VJ or VDJ regions?
N nucleotide - when nucleotide is added
P nucleotide
How are different isotypes formed?
By alternative splicing (no DNA rearrangement i think)
What mediates class switching?
Activation-INduced Deaminase
What adds additional nucleotides to DNA strands before V/J segments join?
TdT (terminal deoxynucleotidytransferase)