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From Flashcardlet > Immune and Hemolymph and Cancer > Flashcards

Immune and Hemolymph and Cancer Flashcards

1
Q

MOA cyclosporine

A

CALCINEURIN INHIBITOR, inhibits T-cell activation and prevents synthesis of cytokines, esp IL-2; binds to cyclophilin, immunophilin in cytoplasm, binding and blocking fxn of calcineurin which is an enzyme necessary for T-cell activation

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2
Q

Side effects cyclosporine

A

Dose dependent nephrotoxicity, hepatic disorders, hypertension, gingival hyperplasia, weight loss, allergic reactions

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3
Q

MOA azathioprine

A

Antimetabolite, purine analog, acts on proliferating lymphocytes and induces both B-cell and T-cell lymphopenia, converted to 6-mercaptopurine in liver, specific to T-cells

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4
Q

Side effects azathioprine

A

liver failure, bone marrow suppression, pancreatitis, hepatotoxicity

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5
Q

MOA mycophenolate

A

Inhibits purine synthethesis in both T and B lymphs, 97% protein bound, acts on DNA metabolism by noncompetitive, reversible inhibition of inosine monophosphate dehydrogenase, which is needed for synthesis of guanosine triphosphate; blocks guanosine so more adenosine which blocks B cell lymph proliferation

Reduces NO and TNFalpha prod’n, reduces proliferation of B and T lymphs

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6
Q

Describe how lymphocyte purines are synthesized

A

2 types of purine synth: de novo and salvage. Lymphs only use de novo which is competitively regulated. Down regulated by adenosine nucleotides and up regulated by guanosine nucleotides. MMF works by blocking guanosine so more adenosine to down regulate.

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7
Q

Side effects of MMF

A

bone marrow suppression, GI upset, nausea, peripheral edema, infection, lymphoma, sepsis, hypertension, tremors, chronic heart failure, primary CNS lymphoma

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8
Q

Leflunomide MOA

A

isoxazol derivative, primary metabolite (A77 1726) inhibits T and B cell proliferation, suppresses Ig production, and interferes with cell adhesion

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9
Q

Cyclophosphamide MOA

A

alkylating agent, acts on DNA replication, RNA transcription and replication, to disrupt nucleic acid function and inhibit cell proliferation

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10
Q

Side effects of cyclophosphamide

A

bone marrow suppression, bladder toxicity, dose-related neoplasms

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11
Q

Tacrolimus MOA

A

macrolide compound isolated from Streptomyces tsukubanesis; acts on T helper cells to suppress production of cytokines, specifically IL-2

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12
Q

Etanercept MOA

A

soluble recombinant TNFalpha receptor Fc (a receptor found on cells that binds to antibodes)

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13
Q

Rituximab MOA

A

Monoclonal HUMAN anti-CD20 B-cell antibody that targets B cell activation, differentiation, and growth. It depletes B cells by complement mediated cytotoxicity and induces apoptosis.

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14
Q

What % of dogs with thymomas have MG?

A

30-50%

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15
Q

What is MG?

A

NM disorder caused by reduction in fxnal NICOTINIC receptors on the postsynaptic membrane of NM jxn

T-lymphocyte dependent dz (CD4+, T helper) and interaction with B lymphs

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16
Q

What is the difference in subunits b/t fetal and mature AChRs?

A

fetal: alpha1, gamma, alpha1, delta, beta1
mature: gamma replaced with epsilon

many dogs with MG have autoabs against fetal AChRs

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17
Q

What breeds are recognized with congential form of MG?

A

JRT, springer spaniel, smooth fox terrier, Gammel Dansk Honsehund

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18
Q

Most autoAbs to AChR directed against…

A

MIR (main immunogenic region), a conformation-dependent region located at exracellular tip of alpha1 subunits

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19
Q

What are the 3 mechanisms for loss of fxnal AChRs at NM jxn?

A
  1. Complement dependent lysis of post synaptic membrane caused by abs bound to AChRs
  2. Abs crosslink AChRs on surface causing internalization and decreased in receptor half life and total #s
  3. Abs directly inhibit AChR function
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20
Q

Ddx for MG?

A 
Hypothyroidism
Severe hypoglycemia
Diabetic neuropathy
Electrolyte abn
Polyradiculoneuritis
Polymyositis
Addisons
Tick paralysis
Botulism
OP tox
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21
Q

What is edrophonium chloride?

A

ultra short acting anticholinesterase

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22
Q

What is MuSK?

A

enzyme located near AChR, activated by agrin, induces acetylcholine clustering in post-synaptic membrane, MuSK ab detected in 70% AChR-ab negative humans with MG

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23
Q

What is RyR?

A

Calcium release channel in striated muscle that is needed for contraction

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24
Q

How do pyridostigmine and neostigmine work?

A

Inhibit hydrolysis of ACh by directly competing with ACh for attachement to AChE; pyridostigmine better tolerated than neostigmine

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25
Q

Adverse effects of pyrido and neo stigmine?

A

muscarinic - GI cramping, increased GI motility, diarrhea, abd pain, increase gastric acid secretion, salivation, lacrimation, bradycardia

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26
Q

hIVIG interrupts complement where?

A

C3 stage

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27
Q

What drugs should be avoided in MG patients?

A

aminoglycosides, ampicillin, lidocaine, propanolol, beta-blockers, quinidine, procainamide, penicillamine, magnesium, contrast agents

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28
Q

Half life of IVIG in dogs.

A

7-9 d

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29
Q

How does IVIG work?

A 
Blocks Fc receptors
Eliminates pathogenic autoabs
Modulates cytokine synthesis
Inhibits complement (C3 and C4)
Mediates Fas-Fas ligant interactions
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30
Q

What is the FasL responsible for

A

initiation of cellular death thru transduction of apoptotic signals to keratinocytes

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31
Q

IVIG has been used to treat what dz in vet med, which shows most promising…

A 
IMHA
ITP
Evan's
Cutaneous drug reactions
PF
SARDS
MG

ITP and skin dz most promising

32
Q

Dogs treated with IVIG initially with ITP left hospital 4 days earlier. T/F

A

T

33
Q

Adverse reactions to IVIG.

A 
Acute hypersensitivity
thromboembolism
renal failure
hypotension
aseptic meningitis
fluid overload
34
Q

L-asparginase MOA

A

Catalyzes the enzymatic hydrolysis of asparagine into aspartic acid and ammonia, causing depletion of serum asparagine, and subsequent inhibition of protein synthesis and lymphoblast cell apoptosis.

Lymphoma cells require asparagine but lack enzyme to make it…so dependent on serum levels

35
Q

What is the primary metabolic product of ammonia metabolism in the brain?

A

glutamine

36
Q

How does sodium benzoate work to trap ammonia?

A

forms hippurate with glycine and excreted in urine

37
Q

How does phylacetate work to trap ammonia?

A

forms phenylacetyl glutamine with glutamine and excreted in urine

38
Q

What formulas were best to predict post PCV with pRBC (est PCV 60%)? Short, JVECC, 2012

A
  1. 90 ml x kg patient x [wanted PCV-patient PCV/donor PCV]

2. 1.5 ml x %PCV increase wanted x kg patient

39
Q

Findings on carboplatin for OSA with limb spare, JAVMA, 2011.

A

Proteinuria preop decreased MST, (no other factors associated with survival), most common reason to d/c carbo was metastatic dz (not side effects), side effects were vomiting, diarrhea, neutropenia

Carbo is a cisplatin analog that is less emetogenic, nephrotoxic, ototoxic, and neurotoxic but more myelosuppressive than cisplatin. Not cardiotoxic or vessicant.

40
Q

What were findings from JAVMA, 2011 - Tx and predictors of outcome in dogs with IMT?

A
  1. Cockers overrepresented
  2. 84% survived
  3. 9% relapse (median interval to relapse 1743 d)
  4. Melena or high BUN on admission significantly correlated with decreased probability of survival
  5. Melena associated with more blood transfusions
41
Q

IMHA and hypercoagulable state, JAVMA, Fenty, 2011, findings.

A

Dogs were hypercoagulable before any treatment (lower K, higher alpha angle, higher MA, higher G; no change in R)
All dogs were hyperfibrinogenemic
10/11 elevated D-dimers

42
Q

Predictors of outcome with IM HSA, JAVMA, 2011

A

Nonmetastatic SC and IM HSA and small tumors (<4 cm) in which aggressive local control can be expected have improved outcome, OST 172 d, 25% alive at 1 y

Lameness - worse outcome

43
Q

High grade multicentric lymphoma outcome predictors, JAVMA, 2011, Marconato.

A

MST 914 d, 11/13 long term survivors had BW > 10 kg, PCV >35%, normal calcium, centroblastic lymphoma, immunophenotype B, no bone marrow involvement, lymphoma state I-IV, and did not receive steroids before treatement

3 long term survivors died from osteosarcoma

44
Q

Lymphoma stages

A
  1. single LN
  2. regional lymphadenopathy, one side of diaphragm
  3. generalized lymphadenopathy, crosses diaphragm
  4. spleen/liver +/- lymphadenopathy
  5. bone marrow, CNS, or extranodal sites

a. not sick
b. sick

45
Q

What is CHOP protocol?

A

cyclophosphamide
doxorubicin
vincristine
prednisone

remission 80% with first CHOP

Can redo CHOP and have good results (remission 214 d) if initial remission duration >289 d, but if first remisison < 289 d, results in 98 d remission, JAVMA 2011, Flory

46
Q

What is gemcitabine?

A

antimetabolite, GI and neutropenia, plts not affected much

Piroxicam + gemcitabine no more effective than other treatments for TCC, JAVMA 2011; side effects mostly GI 60-70%, neutropenia 26%

47
Q

Diagnostic accuracy of using erythrocyte indices and polychromasia to identify regenerative anemia in dogs. Findings? JAVMA, 2011, Hodges

A
  1. Polychromasia most accurate (77%)
  2. Only 11.8% dogs with regenerative anemia were macrocytic and hypochromic
  3. High MCV low MCHC sens 11%, specificity 98%, acc 70%
  4. polychromasia alone 77%
  5. polychromasia with high RDW 79%
48
Q

Factors associated with death generalized megaesophagus, JAVMA, 2011, McBrearty.

A

AP and >13 months neg associated with overall survival time

49
Q

Dogs with ____ splenic masses had a * higher mean mass-to-splenic volume ratio and higher mean splenic weight as a percentage of body weight than did dogs with ____. JAVMA, 2011, Mallinckrodt

A

benign, HSA

M:SV - 1.77 HSA, 5.09 benign
SWPBW - 2.92% HSA, 6.29% benign

other findings: hemoabd 80% with HSA, 60% benign

50
Q

What is HIF-1 alpha and HIF-2 alpha

A

hypoxia inducible transcription factor

51
Q

Fxn of HIF-1a during innate immunity

A

allows myeloid cells to generate ATP in oxygen deprived inflamed tissues; prolongs lifespan of neutrophils in hypoxic conditions by inhibiting apoptosis

52
Q

Myeloma related organ dysfunction includes (NEJM, 2011)

A

Hypercalcemia, renal insufficiency d/t proteinuria/ dehydration/nephrotoxic drugs/ hypercalcemia, anemia d/t myelophthesis, bone disease

53
Q

Mechanism of hypercalcemia from multiple myeloma.

A

increased osteoclast activity due to imbalance in ratio b/t receptor activator of NFkB (RANK) and osteoprotegerin (OPG) as a result of enhanced production of RANK ligand and reduced OPG

54
Q

What are two proteins regulated by HIF?

A

ET-1 and EPO

55
Q

Under aerobic conditions, HIF-1a is…

A

hydroxylated by prolyl hydroxylase domain proteins(PHDs) which use oxygen and alpha-ketoglutarate as substrates and contain Fe2+ in their catalytic center

56
Q

Under hypoxic conditions, HIF-1a

A

accumulates b/c hydroxylation is inhibited, regulated by FIG-1, an asparaginyl hydroxylase

57
Q

HIF-1 activates expression of..

A

lactate dehydrogenase A
pyruvate dehydrogenase kinase 1

Shifts from oxidative to anaerobic glycolysis

58
Q

Autoantibodies against ____ were found in 70-80% human patients with idiopathic membranous nephropathy.

A

PLA2R

59
Q

Tumor lysis syndrome

A

hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia

60
Q

Tumor lysis

A

Relase potassium, phosphorus, nucleic acids which are then metabolized to adenosine then inosine then hypoxanthine then xanthine, then uric acid

61
Q

What are thrombopeitin mimetics?

A

romiplostin and eltrombopag

binds to the thrombopoietin receptor and activates intracellular signaling pathways (the JAK-STAT and MAP kinase pathways)

62
Q

Histamine synthesized whre?

A

mast cells, basophils, platelets, histaminergic neurons, enterochromaffin cells

63
Q

What are the 3 types of anaphylactic reactions?

A

Immunologic IgE mediate
Immunologic non-IgE
Non-immunologic

64
Q

Examples of immunologic IgE mediated

A

insect bites, venom, food, medications

65
Q

Ex of immunologic non-IgE mediated

A

IvIG, transfusion, complement activation, coagulation system activation, autoimmune mechanisms

66
Q

Ex of non-immunologic?

A

physical factors (cold, water, heat, exercise), medications, chemotherapeutics

67
Q

What is the high affinity IgE receptor involved in immunologic anaphylaxis?

A

FcERI - on mast cells and basophils

68
Q

The IgE independed pathway is mediated by

A

IgG, FcyRIII receptors, macrophages

69
Q

What two ILs important in initial generation of anaphylaxis?

A

IL-4 and IL-13

70
Q

What anti-inflammatory effects limit anaphylaxis?

A

heparin

chymase

71
Q

Where are H3 receptors?

A

presynaptic terminals of sympathetic effector nerves that innervate the heart and systemic vasculature - inhibit endogenous NE release

72
Q

Criteria to diagnose anaphylaxis?

A

One of the 3
1. Acute onset with involvement of skin, mucosal, or both and EITHER resp involvement OR hypotension

  1. 2 of the 4 that occur rapidly after exposure to likely allergen: skin/mucosal, respiratory, hypotension, GI signs
  2. Hypotension after exposure to known antigen
73
Q

What are 2nd generation antihistamines?

A

loratidine, fexofenadine, cetirizine

74
Q

Aminophylline MOA

A

PDE inhibitor bronchodilator, competitively inhibits PDE, inc cAMP, increases epi, relaxes SM in bronchi

75
Q

What is the Bezold-Jarisch cardiac reflex?

A

bradycardia in response to fluid bolus during anaphylaxis due to sudden, dramatic hypovolemia d/t fluid extravasation; protective response

76
Q

AVP benefits in anaphylaxis?

A

blocks KATP channels in vascular SM, blocks guanylate cyclase and decreases NO signaling

77
Q

How is glucagon potentially helpful with anaphylaxis?

A

Patients with anaphylaxis previously on beta blockers; reverses refractory bronchospasm and hypotension by activating adenyl cyclase directly and bypassing beta receptor

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