Clinical Medicine II
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| Three functions of the immune system | protection from foreign substances, tumor surveillances, self recognition
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| What are tissue components to immune system | bone marrow, thymus, lymph nodes, spleen
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| Cellular components to immune system | leukocytes, marcrophages, antigen presenting cells
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| Proteins involved in the immune system | immunoglobulins , complement proteins
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| Two types of immunity | humoral and cellular
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| Parts of humoral immunity | B cells→ plasma cells→ abs
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| Types of celluar immunity | T cells: cytotoxic, activate phagocytes, direct humoral immune response
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| Types of congenital defects | B,T or combined defects
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| Types of acquired immune def | Human immunodeficiency, malignancy(Cll, lymphoma, myeloma), chemo, radiation
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| 3 functions of the spleen | Hematopoiesis, filtering, immune defense
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| Do we need the spleen | important organ but can live w/o it
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| Major site of hematopoiesis during fetal life | spleen, mostly during the second trimester
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| How does the cell “kill” foreign cells as blood trickles through it | Very acidic, ↓glucose, ↓ o2
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| What are howell-jolly bodies | w/ removal of spleen, RBC have reminents of its nucleus that the spleen normally removes
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| What are Heinz bodies | insoluble globin proteins within RBC’s d/t no spleen
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| Functions for immune defense of the spleen | 25% lymphoid mass, 50% total ab producing B cells-clear bacteria from circulation
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| What is the spleen especially good at | removing encapsulated bacteria like S. peumo, H.flu, and N. meningitides
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| What type of organ is the spleen | lymphoid organ, largest one being 25% lymphoid material
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| What is a spleen enlarged | when you can feel it
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| What causes splenomegaly | liver dz, hematolgic malignancy, infx, congestion/inflammation, 1 splenic dz
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| Causes massive splenomegaly | CML myelofibrosis, gaucher dz, lymphoma, parasitic infx, thalassemia
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| Indications for splenectomy | clinical infxs, diagnostic, therapeutic
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| Can we biopsy the spleen | not usually good candidate, leaky jelly like supstance, will leak post biopsy
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| Consequences of splenectomy | leukocytosis: 10-15, thrombocytosis, Howell-jolly bodies, infx risk
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| Nuclear remnants in RBC | howell-jolly bodies
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| Huge complication of a splenectomy | splenectomy sepsis w/I 3 years of splenectomy ~5% lifetime risk
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| What is PSS commonly caused by | Strep pneumo, H. flu, N. meningitides
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| How do we prevent PSS | those 3 vaccines for those bugs 2 weeks before, prior to splenectomy, but can get vaccines at any time and an annual influenza vaccine
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| Who do we prophalactically treat to prevent PSS | kids until age 5 (pen or amoxicillin) or 3 years after, highly immunocomprimised adults, adult survivers of pneumococcal PSS
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| When do we give empiric abx | if no spleen, give abx for febrile illnesses 7-10days
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| 5 types of WBCs | neutrophils, lymphocytes, monocytes, eosinophils, basophils
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| Polymorphoncuclear cells (PMNs) | Neutrophils, 45-75% all WBC
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| Fxns of Neutrophils | find, ingest, kill invading microganisms (creates pus)
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| What ↑ neutrophil count | bacterial infx, physiologic stress, corticosteroids
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| What ↓ neutrophil count | viral infx, drugs/toxins, some bacterial infxns: brucella
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| When do we compaire ↑ vs ↓ neutrophil count | CBC w/ diff, look at the percentage
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| ANC, levels that create risk | absolute neutrophil count nl >1500, sig risk 100-500, great risk <100
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| What cells are primary for generating the immune response | lymphocytes: B, T and NK cells 20-45% all white cells
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| What are signs for most viral infections | lymphocytosis
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| Where are lymphocytes | circulating in blood and in lymphoid tissue: lymph nodes, spleen
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| Where does differentiation of B lymphocytes occur and maturation | D: in bone marrow, M: in llymphoid tissues
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| Functions of B lymphocytes | synthesize immunoglobulins (abs)
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| MC lymphocyte and location of them and types | T lymphocytes, Helper T (CD4) Cytotoxic suppressor (CD8) 60-85%
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| Fxn of Helper T cells | regulators of immune sys, influence production of abs by B cells
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| Fxn of cytotoxic suppressor T cesll | recognize kill virus, ↓ regulate ab production by B cells
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| What are natural killer cells (NK) | large lymphocytes w/ small number of granules important in preventing growth and spread of tumors
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| When do we see monocytosis | chronic infx: TB, lymphomas, granulomatous dz like sarcoid
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| Fxns of monocytes | phagocytize and kill microorganisms
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| What is significant when monocytes are highly fxns | secrete cytokines that induce fever and inflammation
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| What are 4 things that cause ↑ eosinophilic | invasive parasitic dz, chronic inflammatory skin d/o, hypersensitivity states (allergies, vasculitis), certain malignancies (Hodgkins lymphoma)
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| Problem w/ eosinophils | chronic infiltatrion can cause organ damage by release of granular contents
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| When do basophils come into action | in allergic d/o’s and myeloproliferative dz (CML, Polycythemia vera)
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| What do basophils differentiate into | mast cells
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| What signals for basophils | IgE causes histamine release
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| Causes for leukopenia and leukocytosis | know it pg 7
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| When would we call a hematologist or just recheck it | call 0-2,000 2,000-4,000 usually recheck it
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| What does lymphocytosis signify | viral infx (usually ↓ neutorphils)
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| What is leukemia | cancer of the blood and bone marrow
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| What are the two types of leukemia | acute: block in differentiation of immature WBC: rapid, dead days-wks, Chronic: excess proliferation of more mature WBCm insidious,survive yrs even if untreated
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| Initial presentation of non | specific
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| Abno CBC examples | pancytopenia, marked leukocytosis
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| Leukemia classifications | acute vs. chronic, myeloid vs. lymphoid
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| Excess proliferation of a nl WBC | chornic leukemia, still fxns nl but way more than there should be, ex CLL or CML
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| Block in differenctiation of immature WBC’s | Acute leukemia, can’t make nl RBCs death fast
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| 4 types of leukemia and MC | ALL CLL AML CML MC is CLL hight dealths AML
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| MC types is young kids, and Old ppl | Y: ALL, Old: AML, CML
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| How to tell b/w acute and chronic | acute: sxs fast, chronic slow and often diagnosis is mistaken CBC
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| Tx for leukemia | Chemo, stem cell trx, prognosis varies widely
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| 3 phases of Acute leukemia | chemo, induction, consolidation, maintenance
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| Highly curable in kids w/ chemo | ALL
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| Not curable ~10% in adults need bone marrow trx cure | ALL
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| Seen rarely in kids, mostly young/middle aged adults, tx | CML tx:
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| What is Gleevec | in CML Philidelphia chromosome croses: 9 and 22→BCR protein→rapid proliferation, gleevec stops this BCR protein
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| Common lymph nodes you can feel and nl size | cervical, supraclavicular, axillary, inguinal nl: 1cm
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| Soft, tender mobile lymph node | often infx/inflammation
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| Firm, rubbery, mobile lymph node | lymphoma
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| Hard, fixed, non-tender | carcinoma
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| Cancer of the lymphoid tissues | lymphoma
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| Which is more common HL or NHL | NHL
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| Dx of lymphoma | CBC renal and LFTs, coags, LDH, peripheral blood immunophenotyping, CT< MRI, PET, biopsy
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| Nodes on both sides of diaphragm | stage iii
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| 1 node group | stage I
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| Marrow or other extranodal site | Stabe IV
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| >1node gropu, same side of diaphragm | stage II
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| What does A or B staging of lymphoma | B + for fever, night, sweats, wt loss
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| CT scans for internal lymph nodes | eyes to thighs
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| Tx for lymphoma | chemo, radioation, stem cell tx
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| Excess production of gamma globulin protein by a single clone of B cells/plasma cells | monoclonal gammopathy
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| MGUS | monoclonal gammopathy of underteerminded significance
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| Why is MGUS so important! | 10-20% develop myeloma but can take more than 10 years
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| How dx MGUS | monoclonal paraprotein band less than 30 g/L (< 3g/dL);
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| Malignant proliferation of plasma cells | multiple myeloma
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| Where is MM seen more often | AF’s and rare in Asians
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| What are clinical manifestations of MM | monoclonal protein (causein renal failure, hyperviscosity,amyloidosis, lytic bone lesions causing bone pain, pathologic frx, hypercalcemia, anemia and infections
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| Major criteria for MM | plasmacytoma, >30% plasma cells in bone marrow, serum M-smike, Urine M-smike
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| Minor criteria for MM | 10-29% plasma cells, smaller M-smike, lytic bone lesions, ↓ immunoglobulin levels
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| How do we dx MM | 1 major + 1 minor or 3 minor
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| Tx MM | chemo effective, not dcurative, survival 2.5-3 yrs w/ chemo
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