Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
167 Cards in this Set
- Front
- Back
|
Processed peptides bound to MHC molecules
|
T cell antigens
|
|
|
Recognition by T cells of peptides bound to one’s own MHC
molecules |
MHC restriction
|
|
|
Cells that capture and present peptides to T cells
|
Antigen-presenting cells
(APC) |
|
|
Dendritic cells, macrophages, B cells
|
Professional APC’s
|
|
|
Another name for immature dendritic cell in the skin
|
Langerhans cell
|
|
|
Transports antigen from epithelia to draining lymph node
|
Dendritic cells
|
|
|
Destination of antigens captured in epithelia and sub-epithelial
tissues |
Lymph nodes, MALT, GALT,
BALT |
|
|
Destination of blood-borne antigens
|
Spleen
|
|
|
Microbial-induced activators of dendritic cells
|
TNF, IL-1, TLR signaling
|
|
|
Chemical signal that attracts activated dendritic cells to
draining lymph node |
Chemokines that bind to
CCR7 on dendritic cell |
|
|
Afferent lymphatic vessel—lymph node---efferent lymphatic
vessel |
Flow of lymph through a
draining lymph node |
|
|
Human Major Histocompatibility Complex (MHC) proteins
|
Human Leukocyte Antigens
(HLA) |
|
|
Genes that encode the Class I MHC moleculese
|
HLA-A, B, C
|
|
|
Cells that express Class I MHC molecules
|
All nucleated cells
|
|
|
Genes that encode the Class II MHC molecules
|
HLA-DP, DQ, and DR
|
|
|
Cells that express Class II MHC molecules
|
Professional APC’s
|
|
|
Set of MHC alleles present on each chromosome
|
MHC haplotype
|
|
|
MHC molecules that are recognized by CD8+ T cells
|
Class I
|
|
|
MHC molecules that are recognized by CD4+ T cells
|
Class II
|
|
|
Domains of peptide-binding groove of MHC Class I molecules
|
Alpha 1 and Alpha 2
|
|
|
CD8 binding site of MHC Class I molecule
|
Alpha 3
|
|
|
Domains of peptide-binding groove of MHC Class II molecules?
|
Alpha 1 and Beta 1
|
|
|
CD4 binding site of MHC Class II molecule
|
Beta 2
|
|
|
Source of antigens for MHC Class I molecules
|
Endogenous cytosolic proteins
|
|
|
Source of antigens for MHC Class II molecules
|
Endosomes/Lysosomes
|
|
|
Site of peptide loading for MHC Class I molecule
|
Endoplasmic reticulum
|
|
|
Site of peptide loading for MHC Class II molecule
|
Vesicle
|
|
|
Enzymes that generate peptides for MHC Class I molecules
|
Proteasome
|
|
|
Enzymes that generate peptides for MHC Class II molecules
|
Proteases in vesicles
|
|
|
T cell population that responds to peptide: MHC Class II
molecules |
CD4+ T cells
|
|
|
T cell population that responds to peptide: MHC Class I
molecules |
CD8+ T cells
|
|
|
(1) Edema?
|
The accumulation of excess fluid in cells or tissues
|
|
|
(2) Intracellular edema reflects?
|
cellular injury
|
|
|
(3) Interstitial Edema reflects what 2 possibilities?
|
a disturbance of normal hemodynamic forces, or endothelial injury
|
|
|
(4) Which hemodynamic force is greater on the arteriole side?
|
hydrostatic pressure
|
|
|
(5) Which force is greater on the venous side?
|
osmotic pressure
|
|
|
(6) Excess fluid remaining in interstitial tissue after circulation goes where?
|
The lymphatic system.
|
|
|
(7) Increased osmotic pressure of the interstitial fluid can cause?
|
generalized edema
|
|
|
(8) What 3 things can usually cause an increase of calcim levels leading to an increase of interstitial osmotic pressure?
|
1. Increased tubular sodium absorption
2. imparied renal tubular sodium excretion 3. excessice salt intake |
|
|
(9) A decrease in oncotic pressure leading to generalized edem is usually caused by?
|
a decrease in serum albumin.
|
|
|
(10) An increase of venous hydrostatic pressure causes?
|
a localized edema
|
|
|
(11) When lymph isdrainage is blocked, what usually occures?
|
localized edema.
|
|
|
(12) Increased capilary permiability will cause?
|
localized edema
|
|
|
What 3 things can cause localized edema?
|
1. An increase of venous hydrostatic pressure.
2. When lymph isdrainage is blocked 3. Increased capilary permiability |
|
|
What 2 things can cause generalized edema?
|
1. Increased osmotic pressure of the interstitial fluid
2. Decreased oncotic pressure of the plasma protien. |
|
|
(13) Transudate Fluid?
|
Protein poor fluid
|
|
|
(14) What generaly causes a buildup of transudate fluid?
|
Imbalances in the normal hydrodynamic forces. congestive heart faliur, liver, renal and GI disorders
|
|
|
(15) Exudate Fluid?
|
Protein rich fluid
|
|
|
(16) What causes exudate fluid?
|
endothelial damage and alteration of vascular permeability.
|
|
|
(17) Vascular Congestion?
|
a decrease in blood flow in the veins and capilaries.
|
|
|
(18) Chronic congestion leads to?
|
impaired pxygenation and necrosis
|
|
|
(19) Vascular hypermia?
|
An increase in blood flow.
|
|
|
(20) 3 normal reasons for vacular hypermia
|
1. flow to inflammed areas
2. tissues in need of more oxygen 3. heat dissipation |
|
|
(21) Heart faliure?
|
When the heat is no longer able to maintain adequate cardiac output.
|
|
|
(22) Left-sided heart faliure?
|
When the left ventricle is unable to maintain adequate cardiac output.
|
|
|
(23) Why does pulminary edem result in left-sided heart faliure?
|
the increased hydrostatic pressure that is created by the left ventricle is trasmitten backward into the pulminary venous circulation. Transudative fluid escapes and whent the lyphatic system is overloaded pulmonary edema results.
|
|
|
(24) "Heart Faliure Cells"
|
Upon pulminary capilary hemorrages, red blood cells comes into aveolar spaces and are phagocitized my macrophages. The macrophages break down the hemoglobin and become a brownish color.
|
|
|
(25) 5 vclinical signs of left-sided heart failure?
|
1. easy fatigability
2. shortess of breath 3. paroxymal nocturnal dyspnea 4. orthopnea 5. cough |
|
|
(26) Right-Sided Heart Failure?
|
When the right side of the heart is unable to maintain ventricular output
|
|
|
(27) 3 reasons why there might be increased vasticular resistance causing right-sided heart faliure?
|
1. vasticular obstruction or obliteration
2. vasoconstriction 3. increased flow |
|
|
(28) 5 clinical results of right-sided heart failure?
|
1.Engorgement and distention of neck veins
2. Passive congestion of the liver 3. Portal hypertention 4. Dependent pitting edema 5. Increased body weight |
|
|
(29) Hemorrage?
|
active bleeding into extravascular tissues
|
|
|
(30) Petechiae ?
|
a pin point hemorrage
|
|
|
(31) Purpura?
|
a hemoragge that is <1 cm
|
|
|
(32) Ecchymoses?
|
> 1 cm
|
|
|
(33) An extravascular blood clot?
|
hematoma
|
|
|
(34) A blood clot in the nose?
|
epistaxis
|
|
|
(35) hemoptysis?
|
coughing of blood from the lungs
|
|
|
(36) vomiting of blood?
|
hematemesis
|
|
|
(37) melena?
|
dark blood in the stool
|
|
|
(38) bright red blood in the stool?
|
hematochezia
|
|
|
(39) 3 things that determine blood loss significance?
|
1. amount
2. location 3. rate |
|
|
(40) Hemostasis?
|
refers to the body's intrinsic ability to slow down or stop hemorrhage
|
|
|
(41) an intravascular blood clot?
|
thrombus
|
|
|
(42) what is a blood clot?
|
formation of an extravascular blood coagulation or postortem intravascular coagultion formed only from the plasma coagulation factors.
|
|
|
(43) Primary hemostasis?
|
Platlet binding to injured tissue via von willebrand factor
|
|
|
(44) What is the factor order of the intrinsic coagulation cascade?
|
XII - XI- IX- X
|
|
|
(45) What is the main factor in the extrisinc pathway?
|
VII activates X
|
|
|
(46) The pathway that involves activation of factor XII?
|
Intrinsic pathway
|
|
|
(47) How is the Intrinsic pathway measured?
|
Partial thromboplastin time (PTT)
|
|
|
(48) The pathway that is stimulated by substances released by damages tissue?
|
The Extrinsic pathway through factor VII
|
|
|
(49) How is the Extrinsic pathway measured?
|
Prothrombin time (PT)
|
|
|
(50) What is the common pathway?
|
X - thrombin- fibrogen
|
|
|
(51) Functions of antithrombin III?
|
has a negative feedback effect on thrombin, deactivates Xa and to a less ectent XIIa XIa and IXa
|
|
|
(52) What activates protein C?
|
endothelial cell receptor called thrombomodulin
|
|
|
(53) What inactivated Va and VIIIa?
|
Protein C
|
|
|
(54) What activates realase of urokinase and tPA?
|
Excess thrombin in the presence of fibrogen and fibronectin
|
|
|
(55) tPA?
|
activates plasmin
|
|
|
(56) Plasmin?
|
Cuts fibrin
|
|
|
(57) How does the D-dimer test work?
|
measures the cut pieces of fibrin by plasmin.
|
|
|
(58) Virchow's Triad?
|
# things that affect predisposition to thrombosis:
1.Alteration of Vasular Endothelium 2. Alteration of Blood Flow 3. Alterations of Blood Components |
|
|
(59) Where to arterial Thombi most often form?
|
Area's of atherosclerotic damage, the heart or area's of privious myocardial infarction
|
|
|
(60) Which vessles are most often occlusive in arterial thombi?
|
Small vessels
|
|
|
(51) Functions of antithrombin III?
|
has a negative feedback effect on thrombin, deactivates Xa and to a less ectent XIIa XIa and IXa
|
|
|
(52) What activates protein C?
|
endothelial cell receptor called thrombomodulin
|
|
|
(53) What inactivated Va and VIIIa?
|
Protein C
|
|
|
(54) What activates realase of urokinase and tPA?
|
Excess thrombin in the presence of fibrogen and fibronectin
|
|
|
(55) tPA?
|
activates plasmin
|
|
|
(56) Plasmin?
|
Cuts fibrin
|
|
|
(57) How does the D-dimer test work?
|
measures the cut pieces of fibrin by plasmin.
|
|
|
(58) Virchow's Triad?
|
# things that affect predisposition to thrombosis:
1.Alteration of Vasular Endothelium 2. Alteration of Blood Flow 3. Alterations of Blood Components |
|
|
(59) Where to arterial Thombi most often form?
|
Area's of atherosclerotic damage, the heart or area's of privious myocardial infarction
|
|
|
(60) Which vessles are most often occlusive in arterial thombi?
|
Small vessels
|
|
|
(61) What gies a srteriol thombosis it's grey color?
|
alternating layers of fibrin and aggregated platlets (lines of Zahn)
|
|
|
(62) What is the most clinicly significant venous thrombi?
|
thrombi that form in the deep leg veins
|
|
|
(63) What cause venous thombi most often?
|
Slugish blood flow
|
|
|
(64) What gives venous thombi it's dark red blue color?
|
trapped red blood cells
|
|
|
(65) what cause capilary thombi?
|
local endothelial damage
|
|
|
(66) How does the body get rid of Thombi?
|
Trapped neutrophiles and moncytes will degrade them and phagocytize them. Plue cells from underlying vasculature wll infultrate them
|
|
|
(67) Why do previous thombi predispose you to more?
|
They tend to build on themselves
|
|
|
(68) Thromboembolus?
|
a pice or whole thombis that has come detached and is circulating the blood stream.
|
|
|
(69) 4 characteristics to a postmortem thombosis?
|
1. for a perfect cast of the vessel
2. do not for lines of zahn 3. are not firmly attached to the vessel 4. have a "chicken fat" appearance. |
|
|
(70) Infarction?
|
tissue necrosis secondary to an abrupt reduction in tissue oxygen
|
|
|
(71) What is the pathological appearance of an infarction?
|
pale area othen wedge shaped with the apex at the point of obstruction.
|
|
|
(72) Disseminated Intravascular Coagulation? (DIC)
|
It is a coagulation abnormality involving the coagulation factors and platelts
|
|
|
(74) What are some test results that would indicate DIC?
|
decreased platlets, increased bleeding time, increased PT, increased aPTT, decreased fibrigen and increased FSP
|
|
|
(75) Embolization?
|
process in which a free floating mass is carried though the vascular system to a point distant to it's insertion.
|
|
|
(76) What are the vast majority of emboli?
|
fragments of preexisting thombi
|
|
|
(77) What makes up 80-85% of systemic Emboli?
|
mural thrombi in the left ventricle or left atrial appendage
|
|
|
(78) What are major impact sites of systemic emboli? 4 things
|
lower extremities, brain, kidneys, and spleen
|
|
|
(79) What is the 3rd most common cause of sudden death?
|
Pulmonary Emboli
|
|
|
(80) Recurent showers of small pulmonary emboli result in?
|
reduction of perfusable pulmonary vascular bed and give rise to pulmonary hypertension
|
|
|
(81) What are the most clinicly significant pulmonary emboli?
|
Larger ones that originate from thombi in the femoral/iliac veins
|
|
|
(82) Pulmonary emboli are almost always pathologicly seen as?
|
Ischemic coagulation necrosis of lung parenchyma
|
|
|
(83) Where are pulmonary infarctions more commonly seen?
|
lower lobes and more often in the right lung
|
|
|
(84) The clinical traid for pulmoary infactions?
|
1. dyspnea
2. hemoptysis 3. pleuritic chest pain |
|
|
(85) What is the classical rule-out test for pulmonary emboli?
|
D- dimer test
|
|
|
(86) How are pulmonary emboli treated?
|
heparin
|
|
|
(87) 3 prevention meathods for pulmonary emboli?
|
1. pneumatic boots
2. low molecular weight heparin 3. inferior vena cava filter |
|
|
(88) Fat emboli commonly occure when?
|
long-bone trauma when marrow fat cells are exposed to vasculature
|
|
|
(89) A large air emboli can cause?
|
an "air lock" in the right heart
|
|
|
(90) Shock?
|
inadequate perfusion and resultant hypoxia of body tissues
|
|
|
(91) Hypovolemic shock?
|
acute loss of blood or fluid from circulation.
|
|
|
(92) Cardiogenic Shock?
|
inability of the heart to maintain output
|
|
|
(93) Vscular shock is caused by?
|
pooling of blood
|
|
|
(94) Septic Shock?
|
Sever gram-negative bacterial infections may produce endotoxins that cause peripheral vasular pooling
|
|
|
(95) Anaphylactic Shock?
|
Hypersensitivity rreactions may lead to widepread vasodialation and increased capilary permeability causing pooling
|
|
|
(96) 3 kinds of vascular shock?
|
1. meurogenic
2. septic 3. anaphylactic |
|
|
(97) 4 clinical signs of Shock?
|
1. Cariac Output
2. Blood Volume 3. Blood Flow 4. Acid/Base |
|
|
How do t-cells see antigen?
|
on MHC molecules
|
|
|
After a langerhans cell captures a microb, where does it go?
|
The lymph node
|
|
|
What are the three forms of MHC II molecules?
|
DP, DQ, and DR
|
|
|
What are the 3 classes of MHC I molecules?
|
A, B and C
|
|
|
Class 3 HLAs are?
|
All diffent kinds of immune protiens and receptors
|
|
|
2 cells that do not have MHC A B or C?
|
Sperm and cell with no nuclei
|
|
|
Which MHC is made of 2 chains?
|
MHC II
|
|
|
Which MHC has just 1 chain?
|
MHC I
|
|
|
Whci MHC grove is open at both ends?
|
MHC II
|
|
|
What is the small additiional chain on the MHC I?
|
The beta 2 chain
|
|
|
Which cells express MHC II?
|
phagocytic cells
|
|
|
What is the peptide lenge bound in a MHC class 1?
|
8-10 most often 9
|
|
|
What is the peptide length bound in a MHC class 2?
|
10-25
|
|
|
where are the peptide fragments achored?
|
at the two ends
|
|
|
The invarient chain?
|
It's a chaperone that hold MHC together before it is leaded. and filld the grove
|
|
|
Clip?
|
The end of the invarient chain that is clipped but still fills the MHC grove
|
|
|
Where do Class one's get loaded?
|
The ER
|
|
|
Tap?
|
transports peptide fragments to the ER
|
|
|
DM?
|
another MHC class II chaperone protien. loads MHC II with peptides.
|
|
|
What percentage of our body is water?
|
60%
|
|
|
Anasarca?
|
generalized edema
|
|
|
what is the arteriole hydrostatic, oncotic and osmotic pressure?
|
35mm Hg out. 5mm HG out and 20mm Hg in
|
|
|
What is the venuole hydrostatic, oncotic and osmotic pressure?
|
15mm HG out, 2mm Hg out and 30 mm Hg in
|
|
|
Where does generalized edema usually show up first?
|
loose tissue
|
|
|
Largest circulating protien?
|
albumin
|
|
|
pitted edema?
|
an edem that can leave inpressions when touched
|
|
|
One way to treat for edema?
|
dirruetics
|
|
|
"nut meg" liver?
|
chronic congestion due to right heart failure.
|
