Path 2- Hemolymphatic System- 4

kelseyfmeyer's version from 2015-08-16 23:27


Question Answer
He listed 6 responses RBCs can have to injury. What are they?(1) Increased 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 componentsnormally sequestered on the inner leaflet of the CM, dec deformability, binding of IgG and/or Complement, and oxidative damage (heinz bodies)
an example of immune-mediated hemolysis would be..IMHA, NI (Neonatal isoerythrolysis)
what are some infections which can cause hemolysis?protozoa, rickettsia, bacteria, viruses
which nutritional deficiency can cause hemolysis?lack of iron
how do levels of phosphorus affect hemolysis?Hypophosphatemia---->hemolysis
which enzymes can you be deficient in, leading to hemolysis?porphyrias, PK, PFK
Immune-mediated hemolytic anemia (IMHA)--> how does this occur? how common in who? explain the pathogenesisinc 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.
descibe 1* IMHA vs 2* IMHA1*- idiopathic. 2*- IgGs end up on RBCs because of.... infection, drug administration: antibiotics (cephalosporins, penicillin, sulfonamides), levamisole, chemicals(propylthiouracil, insecticide pirimicarb), vx, neoplasia, bee sting envenomation
explain what is happening in drug-induced IMHAdrug or drug metabolite interacts with 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), and mAbs react against its own RBCs. Common in horses. ((the maternal Abs against the foals blood could happen in these ways: transplacental exposure to fetal blood during pregnancy or mixing of maternal and 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 cause?lives inside RBCs! INTRACELLULAR! causes IV and EV hemolysis. Does direct damage to the erythrocyte by protozoal proteases, causes oxidative damage, and immune-mediated destruction of the RBC it occupies
what are the main gross lesions caused by babesia?(1) SPLENOMEGALY (causes congestion, cut surface will ooze blood), jaundice, HBuria, and swollen hemoglobin-stained kidneys
Cytauxzoon affects who? where is it, usually? what are the two phases it goes through? describe the anemiasevere, fatal disease in cats. common in the South Central US esp. during summer months. There are 2 phases: (1) schizogenous phase (infects macrophages...they can enlarge and occlude veins to cause ischemia) (2) erythrocytic phase (after schizonts develop into merozoites, host cell rupture and enter the blood). IV merozoites infect variable numbers of RBCs, which leads to immune-mediated destruction of parasitized erythrocytes. The resulting anemia is-- normocytic, normochromic, nonregenerative
anaplasma is what kinda critter/thing? where does it live? what does it cause, in who?it is a Rickettsial agent. they infect RBCs intracellularly. hemolytic anemia (immune-mediated EV hemolysis) in cattle (ana had a cow with rick, inside they destroyed things with their blood)
Hemotropic mycoplasma species or hemoplasmas is what kinda critter/thing? where dos it live? What happens upon infection with these?BACTERIA which likes to live on the SURFACE (epicellular) of RBCs. They can cause hyperbilirubinemia ±icterus, pallor, SPLENOMEGALY, distended gallbladder
Leptospira is a what, and causes hemolytic anemia in who? (HOW is it causing the hemolysis?)bacteria, causes hemolysis in calves, lambs, pigs, and black rhinoceros. (immune-mediated (IgM cold agglutinin) EV hemolysis, and enzymatic (phospholipase produced by the organism) IV hemolysis)
**Q: (not bolded on outline but emphasized) What is clostridium? how does it cause hemolytic anemia? how dangerous is it? what dz does it cause in cattle?bacterial agent which causes a FATAL hemolytic anemia. This happens because **bacterial toxin** (phospholipase C or lecithinase) enzymatically degrades cell membranes >> acute IV hemolysis. In cattle, it causes redwater dz (liver flukes cause hepatic necrosis, the anaerobuc enviro encourages colostrum to proliferate, and they release hemolytic toxins) (in the red closet)
*Q: What are the three 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) decreased 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 infection)
***Q: (not in ppt but marked as Q) what is the charateristic(s) of the anemia caused by EIA?goes in a CYCLIC pattern, so there will be bouts of REGNERATIVE AND NONREGENERATIVE ANEMIA
**Q: what kinda anemia does FeLV cause?NON REGENERATIVE (infects hematopoietic precursor cells, so can't regenerate blood properly)
what are some clinical signs youd see with EIA? how do you dx?Icterus! petechia! widespread hemorrhages! spleen and liver are enlarged, dark and turgid. fever/depression/LN enlargement+edema. COGGINS TEST (testing for presence of Abs against the virus)
FeLV affects the blood how? How does it cause anemia? explain what's going on. (describe the anemia)oncogenic and immunosuppressive virus. It can infect hematopoietic precursor cells, and there is continued replication in hematopoietic and lymphatic tissue of animals that remain persistently viremic. This leads to immunosuppression, infections, BM disorders, and lymphosarcoma. The direct effects of the virus on infected erythroid cells lead to a NONREGENERATIVE ANEMA
explain how FIV and anemia relate!FIV does not directly cause anemia. However, there will be anemia in a minority of infected cats, because FIV leads to immunosuppression and then another dz such as FeLV or hemotropic mycoplasma, or malignancies cause the anemia
explain how oxidative damage can cause hemolysis, and give examples of oxidative agentsIt can cause EV hemolysis via phagocytosis of damaged RBCs by splenic macrophages, OR it can cause 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 and garlic, Brassicaspp., rye grass, acetaminophen, vitamin K, zinc, etc.
which nutritional defeciency is the most common cause of nutritional deficiency anemia? explain what is happeningIRON! usually 2º to depletion of Fe stores via chronic hemorrhage (rather than a1º nutritional deficiency)
Hypophosphatemic hemolytic anemia happens in who, when, and 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 membrane and cytoskeletal integrity--> oxidative mechanisms. IV HEMOLYSIS OCCURS
explain how water intoxication can lead to anemia, and who does this occur in most often?usually calves, will drink excessive water and 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, and other heme proteins. Bc of this, there is an accumulation of toxic porphyrin compounds.... which leads to red-brown discoloration of teeth, bones, and urine from accumulation of porphyrins, photosensitization of nonpigmented skin, and HEMOLYTIC ANEMIA (from accumulation of XS prophyrins in developing and mature RBCs)
congenital porphyria (NOT congenital erythropoietic porphyria) affects WHO?DSH and siamese cats! it resembles congenital erythropoietic porphyria in cattle, and affected cats have brown teeth, photosensitization, and hemolytic anemia (in case he asks, it was pointed out to be important that the cattle one DOESNT 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) and cats (Abysisinian, Somali, DSH). PK, the glycolytic isoenzyme, that normally catalyzes the last ATP-generating reaction in glycolysis is deficient in RBCs of affected animals. Dec production of ATP >> loss of normal membrane function and dec 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 with osteosclerosis; favorable prognosis (PK chu hates cats and 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 and American cocker spaniel dogs. It is a autosomal recessive deficiency of RBC glycolytic enzyme (PFK) (also deficient in mm tissue). In this condition, RBCs have ↓ATP and 2,3-diphosphoglycerate production and ↑ fragility under alkaline conditions. (The english and americans are total fruits. They can't handle a basic bitch)
**Q: in a Phosphofructokinase (PFK) deficiency, what kinda anemia do you see in the [what animal] affected?DOGS affected. because the lack of enzyme causes inc RBC membrane fragility(esp in ALKALINE ENVIRO), you will see chronic EV hemolysis with marked reticulocytosis(affected dogs are **not anemic**) <---so, trick question. No anemia but there is EV hemolysis.....however, acute IV hemolysis may occur with hyperventilation and resulting alkalemia

Granulocyte, Monocyte/Macrophagedisorders

Question Answer
Granulocytic ehrlichiosis--> what is the causative agent? what is the thing called that is actually living in the granulocyte? what are the three major pathologies caused by this agent, in general?Ehrlichiae are small, pleomorphic, gram-negative, obligate intracellular bacteria transmitted by tick vectors. What we see is the morulae within the cytoplasm of neutrophils of affected animals. Major results of the ehrlichia infection are: (1) neutropenia (inconsistent finding) (2) thrombocytopenia (3) arthritis
Anaplasma phagocytophila is the new name of what dz? who does it affect, and what would the dz look like?AKA Equine granulocytic ehrlichiosis (EGE), affects horses. It causes 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 caused by what? what are the clinical signs you will see?Caused by Ehrlichia ewingii (rickettsiales bacteria), the ehrlichia infects the granulocytes and they adhere to endothelium --> vasculitis, platelet consumption. The infection will cause fever, lethragy, anorexia, weight loss, vomiting, diarrhea, thrombocytopenia, and non regenerative anemia
Leukocyte adhesion deficiency (LAD) Affects who? and how do they get it?inherited fatal autosomal recessive condition of Holstein cattle (bovine LAD [BLAD]) and Irish setter dogs.
What is the inherited defect associated with LAD (leukocyte adhesion deficiencies), and what is the sequale of this? what is the hallmark clinical sign, and the sad result?deficiency of the β2 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, and the animal will die young from infections
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 clinical signs 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
what is Chédiak-Higashi syndrome (CHS)?a GRANULOCYTE disorder which is a autosomal recessive condition...mutated gene encodes a protein called beige or LYST (lysosome trafficking regulator) (not sure how it all works tho, he said)
Who can inherit chediak-higashi syndrome?cattle, persian cats, blue and silver foxes, Aleutian mink, albino killer whale, beige mutant mice and rats, and ppl
what are the problems caused by Chédiak-Higashi syndrome (CHS), and what are the sequelae?you will see recurrent pyogenic infections, bleeding tendencies, ocular and cutaneous hypopigmentation, and cytoplasmic inclusions in blood cells. The sequelae will be severely impaired cellular innate immunity from neutropenia, impaired chemotaxis, and impaired killing by granulocytes and cytotoxic lymphocytes. Major-in-short version (because he loves to just keep putting more crap) Neutropenia, Thrombocytopenia, ↑ susceptibility to infections, ↓ immunity