Path 2 - Hemolymphatic System 4

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


Question Answer
He listed 6 responses RBCs can have to injury. What are they?(1) ↑ Destruction (e.g., hemolysis)
(2) Hemorrhage (especially erythrocytes)
(3) Consumption (platelets)
(4) Neoplasia
(5) Altered distribution
(6) Abnormal fxn
Normal turnover of RBCs occurs mainly by...? How is the mechanism triggered?EV hemolysis (senescent RBCs phagocytosed by macrophages in the spleen, liver, bone marrow). These places know to do EV hemolysis usually due to exposure of membrane components normally sequestered on the inner leaflet of the CM, ↓ deformability, binding of IgG &/or Complement & oxidative damage (Heinz bodies)
An example of immune-mediated hemolysis would be...IMHA, NI (Neonatal Isoerythrolysis)
What are some infxns which can cz hemolysis?Protozoa
Which nutritional deficiency can cz hemolysis?Iron Def
How do levels of phosphorus affect hemolysis?HypOphosphatemia → hemolysis
Which enzymes can you be deficient in, leading to hemolysis?Porphyrins
PK (Pyruvate Kinase)
PFK (Phosphofructokinase)
Immune-Mediated Hemolytic Anemia (IMHA) → How does this occur? How common in who? Explain the pathogenesis↑ Destruction (via EV hemolysis) of RBCs due to binding of Ig (IgG!!!!!!!!!!) to cell surface antigens. Common life-threatening condition in dogs. Clinically it is seen as an acute onset severe anemia.
Describe 1° IMHA vs 2° IMHA1° Idiopathic
2° IgGs end up on RBCs

Due to:
Drug administration: ABx (Cephalosporins, Penicillin, Sulfonamides), Levamisole
Chemicals (propylthiouracil, insecticide pirimicarb)
Bee sting envenomation
Explain what is happening in drug-induced IMHADrug or drug metabolite interacts w/ the RBC plasma membrane. (It could also be binding of drug-Ab immune complexes to the RBC membrane, or induction of a true autoantibody directed against a RBC antigen)
What is Neonatal Isoerythrolysis (NI)? Explain what is going on. Who is it common in?A form of IMHA where newborn has colostrum-derived maternal antibodies (mAbs) & mAbs react against its own RBCs. Common in horses. (The maternal Abs against the foal’s blood could happen in these ways: transplacental exposure to fetal blood during pregnancy or mixing of maternal & fetal blood during parturition or a mismatched blood donation)
Infectious disorders of RBCs → protozoal agents → babesia. Where does babesia live? What kind of problems does it cz?Lives inside RBCs! INTRACELLULAR! Czs IV & EV hemolysis. Does direct damage to the erythrocyte by protozoal proteases, czs oxidative damage & immune-mediated destruction of the RBC it occupies
What are the main gross lesions czd by babesia?(1) SPLENOMEGALY (bloody) (czs congestion, cut surface will ooze blood)
(2) Jaundice
(3) Hburia & swollen Hb-stained kidneys
Cytauxzoon affects who? Where is it, usually? What are the 2 phases it goes through? Describe the anemiaSevere, fatal dz in CATS. Common in the South Central US esp. during summer months.
There are 2 phases:
(1) Schizogenous phase (infects macrophages...they can enlarge & occlude veins to cz ischemia)
(2) Erythrocytic phase (after schizonts develop into merozoites, host cell rupture & enter the blood). IV merozoites infect variable numbers of RBCs, which leads to immune-mediated destruction of parasitized erythrocytes (EVH). The resulting anemia is-normocytic, normochromic, nonregenerative
Anaplasma is what kinda critter/thing? Where does it live? What does it cz, in who?It is a Rickettsial agent. They infect RBCs intracellularly. Hemolytic anemia (immune-mediated EV hemolysis) in cattle (ana had a cow w/ rick, inside they destroyed things w/ their blood)
Hemotropic Mycoplasma species or hemoplasmas is what kinda critter/thing? Where does it live? What happens upon infxn w/ these?BACTERIA which likes to live on the SURFACE (epicellular) of RBCs

They can cz:
Hyperbilirubinemia ± icterus
Distended gallbladder
Leptospira is a what & czs hemolytic anemia in who? (HOW is it causing the hemolysis?)Spirochete Bacteria, czs hemolysis in calves, lambs, pigs & black rhinoceros. (Immune-mediated (IgM cold agglutinin) EV hemolysis & enzymatic (phospholipase produced by the organism) IV hemolysis)
(Giemsa Stain)
**What is Clostridium? How does it cz hemolytic anemia? How dangerous is it? What dz does it cz in cattle?Bacterial agent which czs a FATAL Hemolytic Anemia. This happens bc **bacterial toxin** (Phospholipase C or Lecithinase) enzymatically degrades cell membranes → acute IV hemolysis. In cattle, it czs Redwater dz (liver flukes cz hepatic necrosis, the anaerobic enviro encourages Colostrum to proliferate & they release hemolytic toxins) (cows die in the red closter)
*What are the 3 major effects EIA (Equine Infectious Anemia) has on the blood? WHAT IS IT INFECTING? (Explain a little bit for each)Infects cells of the Mononuclear Phagocyte System (MPS)
(1) Immune-mediated hemolysis (typically EV but also IV during the acute phase)
(2) ↓ Erythropoiesis (direct suppression of early-stage erythroid cells by the virus, +anemia of inflammation)
(3) Thrombocytopenia (2º immune-mediated destruction is a classic feature of acute EIAV infxn)
***What is the characteristic(s) of the anemia czd by EIA?Goes in a CYCLIC pattern, so there will be bouts of REGNERATIVE & NONREGENERATIVE ANEMIA
**What kinda anemia does FeLV cz?NON REGENERATIVE (infects hematopoietic precursor cells, so can't regenerate blood properly)
What are some CS youd see w/ EIA? How do you dx?Icterus!
Widespread hemorrhages!
Spleen & liver are enlarged, dark & turgid
LN enlargement + edema
COGGINS TEST (testing for presence of Abs against the virus)
FeLV affects the blood how? How does it cz anemia? Explain what's going on. (Describe the anemia)Oncogenic & immunosuppressive virus. It can infect hematopoietic precursor cells & there is continued replication in hematopoietic & lymphatic tissue of animals that remain persistently viremic. This leads to immunosuppression, infxns, BM disorders & lymphosarcoma. The direct effects of the virus on infected erythroid cells lead to a NONREGENERATIVE ANEMA
Explain how FIV & anemia relate!FIV does not directly cz anemia. However, there will be anemia in a minority of infected cats, bc FIV leads to immunosuppression & then another dz such as FeLV or Hemotropic Mycoplasma, or malignancies cz the anemia
Explain how oxidative damage can cz hemolysis & give examples of oxidative agentsIt can cz EV hemolysis via phagocytosis of damaged RBCs by splenic macrophages, OR it can cz IV hemolysis, if the oxidative damage was extensive.
Some causative agents are:
Red Maple Toxicity
Phenothiazine (Acepromazine is in this class, for instance, these are TRANQS...)
Onions & Garlic
Brassica spp.
Rye Grass
Vitamin K
Which nutritional deficiency is the most common cz of nutritional deficiency anemia? Explain what is happeningIRON! Usually 2º to depletion of Fe stores via chronic hemorrhage (rather than a 1º nutritional deficiency)
Hypophosphatemic Hemolytic Anemia happens in who, when & why? Explain what happens (describe the hemolysis)LOTS OF P IN MILK....SO! Dairy cows! IV hemolytic anemia seen in postparturient dairy cows. No P, ↓ RBC production of ATP → compromised membranes & cytoskeletal integrity → oxidative mechanisms. IV HEMOLYSIS OCCURS
Explain how water intoxication can lead to anemia & who does this occur in most often?Usually calves, will drink excessive water & plasma becomes hypotonic → osmotic IV hemolysis. Will often see Hburia in affected calves
Metabolic disorders → enzyme deficiencies → Erythropoietic Porphyrias. What is happening here? What kinda anemia?Inherited defects of enzymes involved in the synthesis of porphyrins, precursors of Hb & other heme proteins. Bc of this, there is an accumulation of toxic porphyrin compounds.... which leads to red-brown discoloration of teeth, bones & urine from accumulation of porphyrins, photosensitization of nonpigmented skin & HEMOLYTIC ANEMIA (from accumulation of XS porphyrins in developing & mature RBCs)
Congenital Porphyria (NOT Congenital Erythropoietic Porphyria) affects WHO?DSH & Siamese cats! It resembles Congenital Erythropoietic Porphyria in cattle & affected cats have brown teeth, photosensitization & hemolytic anemia (in case he asks, it was pointed out to be important that Cattle CEP DOES NOT have anemia)
Pyruvate kinase (PK) deficiency affect who? What happens in this dz? Of the animals affected, who gets the better deal?Autosomal recessive condition in dogs (mostly Basenjis) & cats (Abyssinian, Somali, DSH). PK, the glycolytic isoenzyme that normally catalyzes the last ATP-generating rxn in glycolysis is deficient in RBCs of affected animals. ↓ Production of ATP → loss of normal membrane fxn & ↓ RBC life span. This leads to moderate to severe EV hemolytic anemia (strongly regenerative)
In DOGS, there is progressive myelofibrosis, osteosclerosis, hemosiderosis
In CATS, it is not associated w/ osteosclerosis; favorable prognosis (PK Chu hates cats & dogs, so he weakens their RBCs, but he hates dogs MORE so they get it worse)
Phosphofructokinase (PFK) deficiency affects who? What is happening/what does this enzyme do? When are the RBCs especially fragile when there is this condition?Deficiency happens in English Springer Spaniel & American Cocker Spaniel Dogs. It is an autosomal recessive deficiency of RBC glycolytic enzyme (PFK) (also deficient in mm tissue). In this condition, RBCs have ↓ ATP & 2,3-diphosphoglycerate production & ↑ fragility of the CM under alkaline conditions. (The English & Americans are total cockfruits. They can't handle a basic bitch)
**In a Phosphofructokinase (PFK) deficiency, what kinda anemia do you see in the [what animal] affected?DOGS affected. Bc the lack of enzyme czs ↑ RBC membrane fragility (esp in ALKALINE ENVIRO), you will see chronic EV hemolysis w/ marked reticulocytosis (affected dogs are **not anemic**) ← so, trick question. No anemia but there is EV hemolysis.... however, acute IV hemolysis may occur w/ hyperventilation & resulting alkalemia

Granulocyte, Monocyte/Macrophage disorders

Question Answer
Granulocytic Ehrlichiosis → what is the causative agent? What is the thing called that is actually living in the granulocyte? What are the 3 major pathologies czd by this agent, in general?Ehrlichiae are small, pleomorphic, gram-negative, obligate intracellular bacteria xmitted by tick vectors. What we see is the morulae w/in the cytoplasm of neutrophils of affected animals

Major results of the Ehrlichia infxn are:
(1) Neutropenia (inconsistent finding)
(2) Thrombocytopenia
(3) Arthritis
Anaplasma Phagocytophila is the new name of what dz? Who does it affect & what would the dz look like?AKA: Equine Granulocytic Ehrlichiosis (EGE), affects horses. It czs seasonal necrotizing vasculitis (edema, icterus, petechiae) seen in N. California, suspected to be tick borne. To dx, youll see inclusion bodies in neutrophils, icterus, petechiae, undulating fever (horses phago dick.)
Canine Granulocytic Ehrlichiosis (CGE) is czd by what? What are the CS you will see?Czd by Ehrlichia ewingii (Rickettsiales bacteria), the Ehrlichia infects the granulocytes & they adhere to endothelium → vasculitis, platelet consumption. The infxn will cz fever, lethargy, anorexia, weight loss, vomiting, diarrhea, thrombocytopenia & non regenerative anemia
Leukocyte Adhesion Deficiency (LAD) affects who? & how do they get it?Inherited fatal autosomal recessive condition of Holstein cattle (Bovine LAD [BLAD]) & Irish setter dogs.
What is the inherited defect associated w/ LAD (Leukocyte Adhesion Deficiencies) & what is the sequale of this? What is the hallmark clinical sign & the sad result?Deficiency of the β-2 chain (CD18 molecule) of leukocyte integrins → severely impaired ability of leukocytes to migrate from blood into tissue. So, you will see VERY high levels of neutrophils in the blood & the animal will die young from infxns
What is the Pelger-Huët anomaly (PHA)? Explain what's going on.Lack of normal segmentation of the nuclei of mature APPEARS like a left shift, but the animals do not have CS or laboratory results which indicate inflammation
How can you tell if the granulocyte looks immature as a result of Pelger-Huët anomaly (PHA), or if it is indeed a left shift?PHA cells can be distinguished from immature forms of normal granulocytes on the basis of their mature chromatin pattern.
PHA Band
What is Chédiak-Higashi syndrome (CHS)?A GRANULOCYTE disorder which is an autosomal recessive condition...mutated gene encodes a protein called Chédiak-Higashi or LYST (lysosome trafficking regulator) (not sure how it all works tho, he said)
Who can inherit Chédiak-Higashi syndrome?Cattle, Persian cats, Blue & Silver foxes, Aleutian mink, Albino killer whale, Beige mutant mice & rats & ppl
What are the problems czd by Chédiak-Higashi syndrome (CHS) & what are the sequelae?You will see recurrent pyogenic infxns, bleeding tendencies, ocular & cutaneous hypopigmentation & cytoplasmic inclusions in blood cells. The sequelae will be severely impaired cellular innate immunity from neutropenia, impaired chemotaxis & impaired killing by granulocytes & cytotoxic lymphocytes.
Major CS:
↑ susceptibility to infxns
↓ immunity