Path 2- Hemolymphatic System- 3

kelseyfmeyer's version from 2015-08-16 23:26

Lymph nodes continued

Question Answer
how is the structure/composition of the LN affected by hyperplasia?large pale-to-dark red solid nodes. HOWEVER, LACK OF CAPSULAR INVASION, PRESERVATION OF LN ARCHITECHURE
***Q:what is the main way to tell a hyperplasia apart from a lymphoma, aside from the fact the cells look cancerous?lymphoma=CAPSULAR INVASION, LOSS OF STRUCTURE!!!
describe the difference between large and small cell lymphomassmall are SLOW proliferating but poorly responsive to chemo (small, slow, sucks), large are FAST proliferating, but very responsive to chemo
***Q: Enzootic bovine leukosis is caused by? affects what age? Where do the tumors usually end up?Caused by BLV (bovine leukemia virus) in ADULT cattle (usually 4-8yrs). The preferential sites are H.A.U.L.S.(R) (I'd haul-r ass away from a canerous cow) Heart, abomasum, uterus, LNs, spinal canal, retro-orbital space
**Q: sporatic cattle lymphoma happens at what age? what causes it?young animals. NOT associated with BLV, it is SPORATIC
calf/juvanile forms of bovine lymphoma (multicentric) occur at what age?up to 6mo
at what age does the thymic form of lymphoma affect cattle?1-2 years (when it's regressing, maybe? not sure)
at what age does the cutaneous form of lymphoma affect cattle?2-3yr old cattle (older than thymic type, thymus is reduced, and now the skin has been out in the sun for a while, is how im gonna think of it)
how does lymphoma present in the horse? what are some of the forms? (5)Variable presentation. Some of the forms include: multicentric, Alimentary: upper intestine, pancreas, cutaneous, splenic, abdominal
how common is lymphoma in dogs? is it caused by a virus? what are the forms usually seen?common, no viral etiology. Multicentric: most common form, alimentary/enteric, mediasteinal/thymic, cutaneous
how common is lymphoma in cats? is it caused by a virus? what are the forms usually seen?caused by FeLV, the cutaneous form is NOT common, however, all of the rest of these forms are common: multicentric, Alimentary/Intestinal/Enteric, Mediastinal/Thymic, Miscellaneous (renal, ocular, nasal, neural)

Bone marrow

Question Answer
*in hyperplasia of the bone marrow, what is the mechanism by which is it getting bigger?it is an INCREASE IN THE NUMBER OF CELLS
what would cause erythroid hyperplasia in the BM? lymphoid hyperplasia?erythroid: hypoxemia. Lymphoid: antigenic stim
reactive thrombocytosis is reacting to what, and results in what?reacts secondarily to inflammation, neoplasia, iron deficiency, asplenia, etc. and results in increased concentration of circulating platelets>> megakaryocytic hyperplasia
how do you know if the BM is hyperplastic?there will be RED marrow(active) where there is usually yellow(inactive, fatty)
aplasia is what, and refers to what part of the bone marrow?aplasia is the ABSENCE of normal growth, in this case the absence of bone marrow hematopoietic tissue of: a particular lineage OR all lineages (aplastic anemia!!)
what are the three different mechanisms for aplastic pancytopenia?(1) destruction of hematopoietic stem cells or progenitor cells (2) disruption of normal stem cell function due to mutation (3) perturbation of the hematopoietic microenvironment
what are some CHEMICALS which could cause aplasia of BM?chemo, bracken fern, estrogen, antimicrobial agents, phenylbutazone (horses, dogs), trichloroethylene (cattle, sheep), aflatoxin B1 (horses, cattle, dogs, pigs)
**Q: what are some INFECTIONS which could cause aplasia of the BM? How would you characterize the anemia?ehrlichiosis (dogs, cats), parvovirus (dogs, cats), FLV, FIV, EIA...all resulting in NON-REGENERATIVE ANEMIA
in which animals can aplasia of the BM be IDIOPATHIC?in horses, cattle, dogs, cats
what are the sequelae of aplasia of the BM? The order of the signs is noted heresevere neutropenia in the 1stweek >> infection, severe thrombocytopenia in the 2ndweek >> hemorrhage, anemia (dependent on rapidity of recovery and life span of RBCs)
**what are the two types of leukemia? explain their origin(1) lymphocytic (lymphoid): originate from outside the bone marrow, e.g., lymphosarcoma arising from lymphoid organs or tissues other than the bone marrow. (2) myelogenous (myeloid): leukemias of nonlymphoid origin
explain the difference between ACUTE leukemias, and CHRONIC leukemias (cells and their progression)ACUTE is poorly differentiated cells; aggressive clinical course. CHRONIC is well differentiated cells; slowly progressive disease
****Q: WHAT IS MYELOPTHISIS???replacement of hematopoietic tissue in the bone marrow can be replaced by fibrous tissue, malignant cells, etc..
Abnormal proliferation--> Serous atrophy of fat. WHAT causes this? what does it look like?CAUSED BY cachexia or starvation, negative energy balance. The fat is catabolilzed and the bone marrow + reticular cells produce a mucoid ground substance. The marrow is translucent, watery, pink. HOWEVER, Neither hematopoietic cells nor fat is absent from the bone marrow. So really, the better term is: “gelatinous transformation
Cyclic hematopoiesis occurs in who? aka? What is happening in this disease?"Lethal Grey collie dz" is a autosomal recessive trait in dogs (associated with dilute hair coat color, hence "grey") is a inherited disorder of pluripotent hematopoietic stem cells. predictable fluctuations in concentrations of blood cells occur in 14-day cycles (cyclic marked neutropenia, cyclic reticulocytosis, monocytosis, and thrombocytosis)
Cyclic hematopoiesis--> How many days is the "cycle"? Which blood cells are affected how?14 day cycle.. cyclic marked neutropenia (infections common), cyclic reticulocytosis, monocytosis(systemic amyloidosis (cyclic increases in the [acute phase proteins] during phases of monocytosis) ), and thrombocytosis(bleeding tendancy from defective platelet fxn) (neutrophils down, everything else go up except lymphocytes which don't seem to care)
*once again, what is PANCYTOPENIA? what is the etiology?(2)sustained decreased production of all three major bone marrow hematopoietic lineages: anemia, neutropenia, thrombocytopenia. Etiology: (1) myelophthisis (replacement of normal bone marrow tissue by abnormal cells-- malig or fibrous cells) (2) abnormality of hematopoietic cells
Aplastic cytopenia (aplastic anemia) results from what getting damaged?results from destruction of hematopoietic stem cells and progenitor cells
the pattern of aplastic pancytopenia depends on the normal lifespans of the blood cells. what are the lifespans of neutrophils? Platelets? erythrocytes?Neutrophils: Hours, so neutropenia develops within 1 week after cessation of granulopoiesis, after the bone marrow storage pool of neutrophils is depleted. Platelets: days, so thrombocytopenia develops in the 2nd week after cessation of thrombopoiesis. erythrocytes is months, so anemia develops much more slowly after the cessation of erythropoiesis, if at all, depending on how rapidly the marrow recovers from the insult and on species variation in the erythrocyte life span
what are drepanocytes?sickle shaped cells
what are poikilocytes?irregularly shaped cells
*What is the definition of anemia??DEC O2 CARRYING CAPACITY
*what is pseudoneutropenia? why does it happen?it looks like less neutrophils, but this is due to inc proportion of neutrophils in the marginated pool. Usually due to dec blood flow OR in response to endotoxemia (promoting interaction between neutrophils and endothelial cells)
what are the five reasons you'd see a neutropenia?(1) dec production (GRANULOCYTIC HYPOPLASIA) (could be due to chemicals, radiation, neoplasia, infection, fibrosis, immune-mediated neutropenia) (2) inc destruction (3) altered distribution (4) demand for neutrophils in inflamed tissue > the rate of granulopoiesis (5) inherited dz
Usually the WRI of a eosinophil can go down to zero. However, if you are able to actually a detect a eosinopenia, what does it mean?usually dec bc part of the STRESS LEUKOGRAM
what are the 5 mechanisms of thrombocytopenia?(1) ↓ production (megakaryocytic hypoplasia) (2) ↑ consumption in DIC: hypercoagulability followed by hypocoagulability & bleeding (3) altered distribution (4) hemorrhage: loss and consumption (5) immune-mediated
how does the spleen and platelets relate?the spleen normally contains a significant proportion of total platelet mass, so splenic abnormalities may result in changes in number of circulating platelets (congestion can lead to a penia, and contraction to a cytosis)
5 mechanisms behind lymphopenia?(1) mediated by endogenous glucocorticoid excess (2) altered distribution of lymphocytes (more in the lymphoid tissues) (3) lymphotoxicity (chemo, infectious agents) (4) loss of lymphocyte-rich lymphatic fluid (5) congenital disorders (hereditary immunodeficiencies like SCID, or thymic aplasia)
endogenous glucocorticoids have what effect on lymphocytes?lymphoPENIA, because: redistribution from the blood to lymphoid tissue/ direct lymphotoxic effects
which erythrocytosis has to do with EPO?2* (usually due to hypoxia or a EPO secreting tumor)
(eh.) what are some mechanisms of neutrophilia?(1) normal mvt into tissues (2) inc release of marrow storage pool cells (3) demargination of neutrophils (4) dec extravasation into tissues (5) expansion of marrow precursor pool
what are some things which might cause an inc release of marrow storage pool neutrophils?endotoxemia, acute infection, hypoxia, glucocorticoids
what are some things which might cause a demargination of neutrophils?acute infection, exercise, epinephrine, glucocorticoids
what causes a dec extravasion of neutrophils into the tissues?glucocorticoids
*what are the TWO MAIN CAUSES (not mechanisms) of neutrophilia? (two less emphasized?)(1) INFLAMMATION--> LEFT SHIFT. (2) STRESS LEUKOGRAM--> (glucocorticoid excess, mature neutrophilia) ( (3) epi release causes “physiological leukocytosis” with lymphocytosis (4) LADs (leukocyte adhesion deficiencies) impaired leukocyte migration)
persistent lymphocytosis (PL) occurs in who? why?cattle with BLV infection (↑in the blood [lymphocytes] above the reference interval for at least 3 months). remeber it is a NON-NEOPLASTIC HYPERPLASIA OF B-LYMPHOCYTES!! (Bovine, Blymphocytes)
how do akitas and shibas differ in their RBCs?RBCs are smaller than normal, RBCs have a high concentration of potassium
What does a Toxic neutrophil look like? (3 charateristics). what might it indicate?(1) increased cytoplasmic basophilia (2) presence of small blue-gray cytoplasmic inclusions (Döhle bodies); often noted incidentally in cats (3) cytoplasmic vacuolation (in severe cases).... generally the more marked the toxic change, the higher the index of suspicion for -infection or endotoxemia-
what is a Döhle body?small blue-gray cytoplasmic inclusions in toxic neutrophils (Dhole bananas are toxic)
explain how liver disease and hemostatic disorders relateliver dz can CAUSE hemostatic disorders, because decreased or defective synthesis of coagulation factors, AND impaired clearanceof fibrinolytic products that inhibit coagulation reactions and platelet function
What is the Pelger-Huët anomaly?lack of normal SEGMENTATION of the nuclei of mature granulocytes. STILL FUNCTIONAL (in heterozygous state, since it is a resessive inherited trait) (not broken up so can still peg it)
primary hemostatic disorders result in _[size]_ bleeds, such as...[small], petechiation, mild ecchymosis (subcutaneous purpura (extravasation of blood) larger than 1 centimeter), bleeding from mucous membranes, bleeding immediately after venipuncture
secondary hemostatic disorders result in _[size]_ bleeds, such as...[large], hemorrhage into body cavities/joints, marked ecchymosis, large hematomas, delayed bleeding after venipuncture