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106 Cards in this Set
- Front
- Back
- 3rd side (hint)
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3 characteristics of carrier-mediated transport
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Stereospecificity
Saturation Competition |
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What type of transport are each of the following?
- Na-glucose - Na-Ca - SERCA |
Na-glucose - cotransport
Na-Ca - countertransport SERCA (sarcoplasmic and endoplasmic reticulum) - primary active transport |
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How do tetrodotoxin (TTX) and lidocaine work?
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Block voltage-sensitive Na channels and abolish action potentials.
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How does hyprekalemia affect action potentials?
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Accommodation occurs in which depolarization closes inactivation gates on the Na channels and the threshold can be reached without firing of an AP.
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What catalyzes the formation of ACh? From what?
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Choline acetyltransferase catalyzes the formation of ACh from acetyl coenzyme A and choline.
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How does neostigmine affect action potentials?
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Neostigmine - blocks degradation of ACh to prolong action at muscle end plate
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How does hemicholinium affect neuron - muscle end plate interaction?
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Hemicholinium - blocks choline reuptake and depletes presynatptic endings of ACh stores
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How does curare affect neuron - muscle end plate interaction?
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Curare competes with ACh for receptors on motor end plate.
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How does botulinus toxin affect neuron - muscle end plate interaction?
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Botulinus toxin blocks release of ACh from presynaptic terminal,
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How do inhibitory postsynaptic potentials work? What are they?
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Open Cl- channels to hyperpolarize cells
- GABA and glycine |
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What are the chief cells that release norepi? Onto what does norepi bind?
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Post-synaptic sympathetic ganglia
- alpha and beta receptors |
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How is norepi cleared from synaptic cleft?
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1. Reuptake
2. MAO 3. COMT |
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What norepi metabolite is increased in urine of a person with pheochromocytoma?
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Pheo --> increased VMA (vanillylmandelic acid)
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In which neurons is dopamine prominent? What does it do?
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Midbrain neurons - inhibits prolactin secretion
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What do the different dopamine receptors do? Which is affected by Parkinson's? Schizophrenia?
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D1 - activate adenylate cyclase via Gs protein
D2 - activate adenylate cyclase via Gi protein Parkinson's - degeneration of D2 Schizophrenia - increased levels of D2 |
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Where is serotonin found and from what is it formed? What is it converted to?
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Serotonin - found in brain stem, formed from tryptophan and converted to malatonin by pyneal gland
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In which neurons is histamine found?
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Histamine - neurons of Hypothalamus
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What is the most prevalent excitatory neurotransmitter in the brain? What are the different receptor types?
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Glutamate - 3 ionotropic receptors (ligand-gated) including the NMDA receptor
- one metabotropic receptor coupled to ion channels via a G protein |
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What are the different receptors of GABA? On which do benzo's and barbiturates work?
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GABA - inh neurotransmitter
GABAa - increases Cl- conductance GABAb - increases K+ conductance Benzo's and barbs act on GABAa |
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What type of neurotransmitter is NO (nitric oxide)? Where is it found and how is it formed?
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Nitric oxide - inh neurotransmitter found in the intestines and formed from arginine --> citrulline --> NO via NO synthase
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What receptor is present at the ends of T-tubules? How is it regulated?
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Dihydropyridine receptor - changes conformation based on depolarization
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To what is Ca bound in the sarcoplasmic reticulum? Through what channel is this calcium released?
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Ca-ATPase pump keeps Ca in sarcoplasmic reticulum (from cytoplasm) where it's bound to calsequestrin. It exits via ryanodine receptors.
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How does tetanus come about?
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Repeated stimulation --> increased Ca release from SR extending the time for cross-bridge cycling.
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Describe muscle contraction in smooth muscle.
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No troponin. Instead, depolarization of cell membrane -->opening of voltage gated Ca channels --> Ca enters cell and Ca is released from SR via IP3-gated Ca channels. Intracellular [Ca] increases and binds calmodulin. This complex activates myosin light-chain kinase --> phosphorylates myosin which can then bind actin.
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By what method does H+ leave parietal cells?
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H-K-ATP pump - primary active transport
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What are the important selectins and where are the expressed?
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L-selectins - neutrophils
P-selectins - endothelial cells (stimulated by histamine and thrombin) E-selectins - endothelial cells |
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Generally, what induces selectins?
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IL-1 and TNF induce selectins
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What are the three types of adhesion molecules?
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Selectins, Ig-family adhesion proteins (ICAM-1 and 2), Integrins
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Infarction will lead to influx of mainly what type of inflammatory cell?
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PMNs (early) and monocytes/macrophages (2-3 days)
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What are causes of eosinophilia?
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Asthma and other allergic rxns
Polyarteritis nodosa Hodgkin lymphoma |
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What are causes of basophilia?
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Chronic myelogenous leukemia
Other myeloproliferative dz's |
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What are the main chemotactic factors for PMN's?
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Complement (C5a)
Arachidonic acid metabolites (LTB4, HETE, kallikrein) IL-8 |
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What are the most important opsonins?
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IgG and C3b
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What is the most important intracellular microcidal process?
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O2-dependent killing, via initiation of the hexose monophosphate shunt to create O2-, H2O2 or OH radical.
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What is myeloperoxidase-halid system of bacterial killing?
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H2O2 + myeloperoxidase and halide ion oxidizes microbial proteins and disrupts cell walls
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How is histamine released and what does it do relative to inflammation?
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Histamine is released from basophils and mast cells when
(1) antigen binds to membrane bound IgE (2) C3a or C5a binding (anaphylotoxins) (3) heat or cold, other ---> increase capillary permeability |
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Where does platelet activating factor come from and what does it do?
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granules of basophils/mast cells, endothelial cells, macros, PMNs and eosinophils all --->
PAF --> activates and aggregates platelets which release histamine and serotonin |
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TxA2 vs. PGI2
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Thromboxane from platelets causes vasoconstriction and platelet aggregation
Prostacyclin from endothelial cells causes vasodilation and inhibits platelet activation Both are derived from the cyclo-oxygenase pathway |
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What comes from the lipoxygenase pathway?
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Leukotrienes (LTC4, LTD4, etc.) that are potent vasoconstrictors, bronchoconstrictors and are sometimes referred to as "slow-reacting substance of anaphylaxis"
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What pathways are set off by complement factor XIIa?
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XIIa -->
1. Kinin system (bradykinin) 2. Intrinsic pathway of coag 3. Plasminogen (fibrinolytic) pathway 4. Complement pathway |
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What role does C3b play?
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Opsonin
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How does complement component deficiency affect a person and which deficiencies are worth remembering?
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Increased susceptibility to infection
- C2, C3, C5 |
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Dz in which phagocytic cells ingest but do not kill some microorganisms?
Which org's are killed, which aren't? |
Chronic granulomatosis dz (CGD)
- X-linked - Deficient activity of enzyme involved in NADPH oxidase - Catalase positive org's (s. aureus) cannot be killed, cat negative can |
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How does myeloperoxidase deficiency manifest clinically?
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Often of little significance, but some increased susceptibility to candida albicans
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How does Chediak-Higashi syndrome present? Inheritance and pathophys?
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Neutropenia, albinism, cranial and peripheral neuropathy and repeat infections.
- AR disorder - Abn microtubule formation --> decreased chemotaxis and migration - Lar cytoplasmic granules in lymphs and mono's due to impaired membrane fusion |
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Leukocyte adhesion deficiency
- ass. w/ what type of infections - what is the cause? What is the most telling sign? What function is impaired? |
Ass. w/ recurrent bacterial infections
- deficiency of B2 integrins (type 1) - mut in gene for fucosyltransferase (type 2) The most telling early sign is delayed falling off of the umbilical stump. PMNs cannot migrate to areas of infection and instead collect to high levels in the BVs. |
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How are granulomas formed?
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Macrophages present antigen to CD4+ T cell --> triggers cytokine release (interferon-gamma) --> transforms monocytes and macrophages into epithelioid cells and giant cells
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What etiologic agents most often induce granuloma formation?
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1. Mycobacterium tuberculosis and M. leprea
2. Blastomyces, histoplasma, coccidioides and many fungi 3. Treponema pallidum 4. Bacteria of cat-scratch dz 5. Foreign bodies 6. Sarcoid |
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What is the key role of fibronectin?
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Fibronectin - chemotactic factor for fibroblasts and endothelial cells
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What type of hypersensitivity rxn is each of the following?
- Tuberculin rxn - Serum sickness - Goodpasture syndrome - Graves Dz - Contact dermatitis - Asthma |
Tuberculin rxn - type IV
Serum sickness - type III Goodpasture syndrome - type II Graves Dz - type II Contact dermatitis - type IV Asthma - type I |
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Type I hypersensitivity rxns
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Antigen reacts with IgE bound to surface of basophils or tissue mast cells--> degranulation --> histamine release --> vasodilation and SMC spasm
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Type II hypersensitivity
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Antibodies react to antigens that are intrinsic parts of cell membranes --> complement fixation and cell lysis
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Type III hypersensitivity
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Antigen-antibody complexes are deposited in vessel walls or on serosal surfaces--> PMNs attracted and release lysozomal enzymes and other chemotactic agents
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Type IV hypersensitivity
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"delayed;" proliferation of CD4+ memory T cells, with secretion of IL-2 and other cytokines which recruit and stimulate phagocytic macros
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Hyperacute transplant rejection
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Antibody mediated rxn due to the presence of preformed antidonor antibodies in the transplant recipient (type II)
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Acute transplant rejection
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T-cell mediated reaction that occurs days to weeks after transplantation and is characterized by infiltration of lymphs and macro's.
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Chronic transplant rejection
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Antibody mediated vascular damage that occurs months to years after an otherwise successful transplantation.
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What causes graft vs. host dz?
What are the chief organs affected by graft vs. host dz? |
Bone marrow or whole blood transplant (in SCID patients)
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liver, skin and GI mucosa (jaundice, papulomacular rash, diarrhea)
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What is X-linked agammaglobulinemia of Bruton?
What types of infections do these patients get? |
Failure of pre-B cells to mature into B-cells resulting in absence of plasma cells in tissue and absence of serum Ig's. Also, absent germinal centers in lymphoid tissue
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X-linked agammaglobulinemia of Bruton - recurrent bacterial infections
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What is the most common inherited B cell defect?
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Isolated IgA deficiency which is most often asymptomatic but can be related to recurrent URI and frequent diarrhea.
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How does DiGeorge syndrome cause an immunodeficiency?
What infections are common in DiGeorge? |
Congenital T-cell deficiency due to abberant development of 3rd and 4th branchial arches
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DiGeorge - recurrent viral and fungal infections and tetany from hypoPTH with hypocalcemia.
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CATCH-22
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DiGeorge acronym
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Cardiac defects, abn facies, thymic hypoplasia, cleft palate, hypocalcemia, microdeletion on chr 22
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What is Wiskott-Aldrich syndrome? What is the classic triad?
What labs do you see with this disorder? |
Wiskott-Aldrich syndrome is an X-linked disorder characterized by progressive deletion of B and T cells. The classic triad is
TIE: T - Thrombocytopenia, I - Infections E - Eczema |
Wiskott-Aldrich labs:
- Increased IgE and IgA - Decreased IgM |
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What cell does HIV recognize and how?
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HIV expresses surface protein gp120 with recognition sites CXCR4 and CCR5 that recognize CD4+ T cells.
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What tests are used to diagnose AIDS?
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1st: ELISA
Definitive: Western blot and direct assessment of viral RNA |
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What hypersensitivity rxn will be decreased in a patient with HIV/AIDS? Why?
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type IV bc he has less CD4+ T helper cells
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What paradoxical immunological state do AIDS patients exhibit?
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hypergammaglobulinemia due to polyclonal B cell activation
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What malignancies are increased in AIDS patients?
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Kaposi sarcoma
Non-Hodgkins lymphoma |
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Anti-smith antibody
What test will be a false-positive in patients with this dz? |
SLE
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SLE --> false-positive syphilis test
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CREST syndrome
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Scleroderma (progressive systemic sclerosis)
ANTICENTROMERE antibodies |
Calcinosis
Raynaud Esophogeal dysfunction Sclerodactyly Telangiectasia |
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Xerostomia
Keratoconjuctivitis Arthralgias What glands are often involved? |
Sjogren syndrome
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Parotid glands, lacrimal glands are infiltrated by lymphocytes
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Anti-SS-B
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Sjogren syndrome
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How is dermatomyositis / polymyositis dx?
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muscle biopsy
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What autoimmune disorder occurs more commonly in men? What is it's pathophys?
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Polyarteritis nodosa
and Bruton's agammaglobulinemia |
Polyarteritis nodosa - Immune complex vasculitis --> fibrinoid necrosis of small and medium arteries with antigen as Hep B or drugs.
Bruton's agammaglobulinemia - defect in B cell tyrosine kinase --> failure of pro-B cells to mature --> recurrent bacterial infections after 6 months |
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T helper 1 cells secrete?
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IL-2 and INF-gamma
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Antibodies to centromeric proteins?
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Scleroderma (PSS)
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Where are MHC I and II expressed?
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MHC I - all nucleated cells
MHC II - only on APC |
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With what is HLA B27 associated?
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PAIR
psoriasis ankylosing spondylitis IBD Reiter's syndrome |
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Which antibody is involved in opsonizing bacteria and neutralizing viruses?
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IgG
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What signals natural killer cells to activate?
How do they then kill? |
Lack of class I MHC on target surface
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use perforin and granzymes to induce apoptosis
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Link CD 4/8+ with their respective MHC class
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CD4+ - MHC II on APCs
CD8+ - MHC I on virus-infected cells |
CD x MHC always = 8
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CD3 complex
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Cluster of polypeptides associated with a T-cell receptor. Important in signal transduction.
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How does the body respond to endotoxins/ lipopolysaccharides (gram-negative bacteria)?
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Endotoxins directly stimulate macrophages by binding to endotoxin receptor CD14; Th cells are not involved.
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What is released during the macrophage (APC) - CD4 cell interaction?
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CD4+ Th1 cell releases IFN-gamma to stimulate macros
Macros release IL-1 and TNF-alpha to stimulate CD4+ Th1 cells |
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What two signals are required for activation of a Th cell?
How then is a Tc cell activated? |
1. MHC II presents antigen
2. Costimulation by B7-CD28 interaction |
1. Endogenously synthesized proteins presented on MHC I and recognized by TCR.
2. IL-2 from Th cell activates to kill |
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How do B cells switch classes?
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1. IL4, 5 or 6 from Th2 cell.
2. CD40 on B cell binds CD40 ligand on Th cell. |
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What do the Fab and Fc portions of the antibody do?
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Fab - antigen binding fragment, specific
Fc - constant, complement binding portion (carboxy terminal) |
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Which antibody is found in secretions? What is its role?
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Secretions - IgA - prevent bacterial / viral attachment to membranes
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Which antibody is the most abundant? What is its role?
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Most abundant - IgG - delayed response to an antigen, crosses placenta, fixes complement
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Which antibody is produced in the immediate response to an antigen?
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Immediate response to antigen - IgM
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Which antigen mediates immunity to worms? How?
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Worms - IgE - activates eosinophils
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What antibody isotypes are on the surface of mature B lymphocytes? What determines isotype
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IgM and IgD - determined by heavy chain
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Hot T-Bone stEAk and other cytokines
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IL-1 - fever
IL-2 - T-cell stimulation IL-3 - Bone marrow stimulation IL-4 - IgE stimulation IL-5 - IgA stimulation |
IL-8 - PMN chemotaxis
IL-12 - activate NK and Th1 cells |
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Which cell expresses the following markers?
CD 19 CD 3 CD 40 CD 21 CD 14 CD 16 |
CD 19 - B cell
CD 3 - T cell CD 40 - Macrophage CD 21 - B cell CD 14 - Macrophage CD 16 - Natural killer cell |
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The membrane attack complex defends against ____ and is activated by ____ in the ____ pathway and activated by ___ in the ___ pathway
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The membrane attack complex defends against gram-negatives and is activated by IgG or IgM in the classic pathway and activated by endotoxins in the alternative pathway.
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Which complement components are responsible for (1) opsonization and (2) anaphylaxis (3) the membrane attack complex?
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Opsonization - C3b and IgG
Anaphylaxis - C3a and C5a MAC - C5b, 6,7,8,9 |
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Deficiency of C5-8 --->
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Neisseria bacteremia
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To Be Healed Rapidly
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Tetanus, botulism, HBV and rabies
- give antibodies for passive immunity |
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What type of hypersensitivity is tested for by Coombs (direct and indirect)?
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Type II
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Highly increased IgE
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Job's syndrome - FATED
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FATED
course Facies cold, staph Abscesses retained primary Teeth increased IgE Dermatologic problems (eczema) |
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Negative nitroblue tetrazolium dye reduction test
--> what condition? --> what result? |
Negative nitroblue tetrazolium dye reduction test --> CGD (lack of NADPH oxidase)
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CGD - Increased susceptibility to catalase positive org's (S aureus, E coli, aspergillus)
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How does cyclosporin work?
What is its toxicity? |
Cyclosporin inhibits calcineurin thus blocking formation of IL-2 so that T cells cannot activate or differentiate.
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Cyclosporin toxicity
- increased viral infections, lymphoma - nephrotoxic |
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How does tacrolimus work?
What is its toxicity? |
Tacrolimus binds FK-binding protein, again inhibiting IL-2 and other cytokines necessary for T cell diff and activation.
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Tacrolimus toxicity
- nephrotoxic, peripheral neuropathy, hypertension, pleural effusion and hyperglycemia |
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How does azathioprine work?
What is its toxicity? |
Azathioprine is an antimetabolite of 6-mercaptopurine and interferes with production of nucleic acids. Toxic to proliferating lymphocytes,
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Azathioprine toxicity
- bone marrow suppression - toxic effects increased by allopurinol (metabolized by XO) |
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How does Muromonab-CD3 (OKT3) work?
What is its toxicity? |
Muromonab-CD3 (OKT3) is a monoclonal antibody that binds to CD3 to block T-cell signal transduction.
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Muromonab-CD3 (OKT3) toxicity
- Cytokine release syndrome, hypersensitivity reaction |
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How does sirolimus (rapamycin) work?
What is its toxicity? |
Sirolimus binds to mTOR to inhibit proliferation of T cells in response to IL-2.
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Sirolimus toxicity
- hyperlipidemia, thrombocytopenia and leukopenia |
