Path 2 - Hemolymphatic System 3

drraythe's version from 2016-02-09 01:03

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
***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 btwn large & small cell lymphomasSmall are SLOW proliferating but poorly responsive to chemo (small, slow, sucks)
Large are FAST proliferating, but very responsive to chemo
***Enzootic Bovine Leukosis is czd by? Affects what age? Where do the tumors usually end up?Czd by BLV (Bovine Leukemia Virus) in ADULT cattle (usually 4-8yrs). The preferential sites are HAULS-R (I'd haul-r ass away from a cancerous cow) Heart, Abomasum, Uterus, LNs, Spinal canal, Retro-orbital space
**Sporadic Cattle Lymphoma happens at what age? What czs it?Young animals. NOT associated w/ BLV, it is SPORADIC
Calf/juvenile 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 & 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 incld:
Alimentary: Upper intestine, Pancreas, Cutaneous, Splenic, Abdominal
How common is lymphoma in dogs? Is it czd by a virus? What are the forms usually seen?Common, no viral etiology
Multicentric = most common form
How common is lymphoma in cats? Is it czd by a virus? What are the forms usually seen?Czd by FeLV
Common Forms:
Miscellaneous (Renal, Ocular, Nasal, Neural)
The Cutaneous form is NOT common

Bone Marrow

Question Answer
*In hyperplasia of the bone marrow, what is the mechanism by which is it getting bigger?It is an ↑ IN THE NUMBER OF CELLS
What would cz erythroid hyperplasia in the BM? Lymphoid hyperplasia?Erythroid: Hypoxemia
Lymphoid: Antigenic stim
Reactive thrombocytosis is reacting to what & results in what?Reacts secondarily:
Iron deficiency
Asplenia, etc.
Results in: ↑ 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) (in adults)
Aplasia is what & 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 3 different mechanisms for aplastic pancytopenia?(1) Destruction of hematopoietic stem cells or progenitor cells
(2) Disruption of normal stem cell fxn due to mutation
(3) Perturbation of the hematopoietic microenvironment
What are some CHEMICALS which could cz aplasia of BM?Chemo
Bracken fern
Antimicrobial agents
Phenylbutazone (horses, dogs)
Trichloroethylene (cattle, sheep)
Aflatoxin B1 (horses, cattle, dogs, pigs)
**What are some INFXNS which could cz aplasia of the BM? How would you characterize the anemia?Ehrlichiosis (dogs, cats)
Parvovirus (dogs, cats)
In which animals can aplasia of the BM be IDIOPATHIC?Horses
What are the sequelae of aplasia of the BM? The order of the signs is noted hereSevere neutropenia in the 1st week → infxn, severe thrombocytopenia in the 2nd week → hemorrhage, anemia (dependent on rapidity of recovery & life span of RBCs)
**What are the 2 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 btwn ACUTE leukemias & CHRONIC leukemias (cells & their progression)ACUTE is poorly differentiated cells; Aggressive clinical course
CHRONIC is well differentiated cells; Slowly progressive Dz
****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 czs this? What does it look like?CZD BY cachexia or starvation, negative energy balance. The fat is catabolized & 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 dz?"Lethal Grey Collie Dz" is an autosomal recessive trait in dogs (associated w/ dilute hair coat color, hence "grey") is an 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 & thrombocytosis)
Cyclic hematopoiesis → How many days is the "cycle"? Which blood cells are affected how?14 day cycle. Cyclic marked neutropenia (infxns common)
Cyclic reticulocytosis
Monocytosis (Systemic amyloidosis (cyclic ↑ in the [acute phase proteins] during phases of monocytosis) )
Thrombocytosis (Bleeding tendency 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 ↓ production of all three major bone marrow hematopoietic lineages: Anemia, Neutropenia, Thrombocytopenia.
(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 & 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 w/in 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: 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 & 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??↓ O2 CARRYING CAPACITY
*What is Pseudoneutropenia? Why does it happen?It looks like less neutrophils, but this is due to ↑ proportion of neutrophils in the marinating pool. Usually due to ↓ blood flow OR in response to endotoxemia (promoting interaction btwn neutrophils & endothelial cells)
What are the 5 reasons you'd see a neutropenia?(1) ↓ production (GRANULOCYTIC HYPOPLASIA) (could be due to chemicals, radiation, neoplasia, infxn, fibrosis, immune-mediated neutropenia)
(2) ↑ destruction
(3) Altered distribution
(4) Demand for neutrophils in inflamed tissues ↑ the rate of granulopoiesis
(5) Inherited dz
Usually the WRI of an eosinophil can go down to zero. However, if you are able to actually a detect an eosinopenia, what does it mean?Usually ↓ 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 & consumption
(5) Immune-mediated
How does the spleen & 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 & 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, bc redistribution from the blood to lymphoid tissue = direct lymphotoxic effects
Which erythrocytosis has to do w/ EPO?(usually due to hypoxia or an EPO secreting tumor)
What are some mechanisms of neutrophilia?(1) Normal mvt into tissues
(2) ↑ release of marrow storage pool cells
(3) Demargination of neutrophils
(4) ↓ extravasation into tissues
(5) Expansion of marrow precursor pool
What are some things which might cz an ↑ release of marrow storage pool neutrophils?Endotoxemia
Acute infxn
What are some things which might cz a demargination of neutrophils?Acute infxn
What czs a ↓ extravasation of neutrophils into the tissues?Glucocorticoids
*What are the 2 MAIN CZS (not mechanisms) of neutrophilia? (2 less emphasized?)(1) INFLAMMATION → LEFT SHIFT
(2) STRESS LEUKOGRAM → (glucocorticoid excess → demargination → mature neutrophilia)
(3) Epi release czs “physiological leukocytosis” w/ lymphocytosis
(4) LADs (Leukocyte Adhesion Deficiencies) impaired leukocyte migration)
Persistent Lymphocytosis (PL) occurs in who? Why?Cattle w/ BLV infxn (↑ in the blood lymphocytes above the reference interval for at least 3 months)
Remember it is a NON-NEOPLASTIC HYPERPLASIA OF B-LYMPHOCYTES!! (Bovine, Blymphocytes)
How do Akitas & 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 characteristics). What might it indicate?(1) ↑ 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 infxn or endotoxemia
What is a Döhle body?Small blue-gray cytoplasmic inclusions in toxic neutrophils (Dohle bananas are toxic)
Explain how Liver Dz & hemostatic disorders relateLiver dz can cz hemostatic disorders, bc a ↓ in or defective synthesis of coagulation factors & impaired clearance of fibrinolytic products that inhibit coagulation rxns & platelet fxn
What is the Pelger-Huët anomaly?Lack of normal SEGMENTATION of the nuclei of mature granulocytes. STILL FXNAL (in heterozygous state, since it is a recessive inherited trait) (not broken up so can still peg it)
1⁰ Hemostatic Disorders result in _[size]_ bleeds, such as...Small
Mild ecchymosis (subcutaneous purpura (extravasation of blood) larger than 1 centimeter)
Bleeding from mucous membranes
Bleeding immediately after venipuncture
2⁰ Hemostatic Disorders result in _[size]_ bleeds, such as...Large
Hemorrhage into body cavities/joints
Marked ecchymosis
Large hematomas
Delayed bleeding after venipuncture