USMLE 1 Path and Immuno basics

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Inhibits the Na/K pump: Ouabain
Definition: Chromatin clumping and shrinking: Pyknosis
Definition: Fragmentation of chromatin: Karyorrhexis
Definition: Fading of chromatin material: Karyolysis
(3) stages in order of nuclear damage: Pyknosis -> Karyorrhexis -> Karyolysis
Type of necrosis that forms calcium salts: Fat necrosis

(Saponification)
Definition: Gene product that facilitates apoptosis by decreasing transcription of bcl-2 and increasing transcription of bax: p-53
When cytochrome-c and bcl-2 is released from the mitochondria during apoptosis, what does it cause the activation of to kill the cell?: Caspases
Oncogene that inhibits apoptosis? which gene product promotes apoptosis?: Inhibits: bcl-2

Promotes: bax
Difference b/t local hemosiderosis, systemic and Hemochromatosis: Local Hemosiderosis (no tissue damage):
due to hemorrhage into tissue; breakdown of Hb

Systemic Hemosiderosis (no tissue damage):
from hemorrhage, multiple blood tranfusions, excessive iron or alcohol intake

Hemochromatosis (tissue damage):
usu due to hereditary disorder of increased iron absorption; leads to cirrhosis, DM, inc skin pigment
Dx: micronodular cirrhosis; pancreatic fibrosis; skin pigmentation: Hemochromatosis

("Bronze Diabetes")
what does Hemochromatosis lead to? what does it increase their risk of getting? type of genetic dz?: Leads to: CHF

Inc risk: Hepatocellular CA

Auto Recessive
what do the labs look like for Hemochromatosis: 1. Iron 2. Ferritin 3. TIBC: Iron and Ferritin Increased

TIBC Decreased
(most iron is in the tissue)
Definition: end-product of membrane lipid peroxidation; "wear-and-tear" pigment that accumulates in elderly: Lipofuscin
Lipofuscin + atrophy of organs: Brown Atrophy
difference b/t Metastatic Calcification and Dystrophic Calcification: Metastatic:
due to hypercalcemia (usu hyperPT)

Dystrophic:
from previously damaged tissue (serum calcium is normal)
Toxin associated w/ hepatic fatty change due to impaired apolipoprotein synthesis: Carbon Tetrachloride
(CCl4)
what is the Selectin expressed on PMNs? what do they bind to? Selectin on Endothelial cells? (2) On platelets?: Leukocyte: L-selectin

Endothelial cell: E-selectin and P-selectin

Platelet: P-selectin
where are Intercellular Adhesion Molecules? what do they bind to?: ICAM: Endothelium

bind to: Leukocyte
(5)* steps of Emigration: MP RAT:
Margination
Pavementing
Rolling
Adhesion
Transmigration
(3) Arachidonic Acid metabolite chemotactic factors in Inflammation: HETE;

Kallikrein;

Leukotriene B4
Inflammation causes: 1. fever (2) 2. vasodilation (2) 3. exudation (2) 4. chemotaxis (2) 5. phagocytosis (1) 6. pain (2): Fever: IL-1; prostaglandins

Vasodilation: NO; prostaglandins

Exudation: histamine; bradykinin

Chemotaxis: C5a; IL-8

Phagocytosis: C3b

Pain: bradykinin; prostaglandin
which bacteria has chemotactic factors for PMNs?: E. Coli
(3)* natural Vasoconstrictive mediators: Tightens Large Pipes:

Thromboxane;

Leukotrienes (C, D, E);

Platelet Activating Factor
Main cause of increased capillary permeability by contracting endothelial cells in post-cap venules what (3) cells release it?: Histamine

released by (BMP):
Basophils;
Mast cells;
Platelets
Dx: defect in NADPH oxidase activity causing inc susceptibility to Staph Aureus, E.coli and Aspirgillus what is genetics? what test confirms Dx?: Chronic Granulomatous Dz

X-Recessive

test: Nitroblue
Dx: neutropenia, albinism, cranial and peripheral neuropathy, repeated Staph and Strep infections what is genetics?: Chediak-Higashi

Auto-Recessive
Dx: normal to increased PMNs w/ severe pyogenic and fungal infections and delayed separation of umbilicus: Leukocyte Adhesion Deficiency
(LAD)
Difference in cells (and example): 1. Permanent 2. Stabile 3. Labile: Permanent: can't divide again
(neurons, myocardium)

Stabile: can be taken from Go phase to divide
(hepatocytes)

Labile: divide actively throughout life
(GI mucosa, epidermis)
Definition: promotes proliferative response of fibroblasts and smooth muscle cells and collagen what is it chemotactic for?: Platelet-derived growth factor
(PDGF)

chemotactic: Monocytes
Definition: promotes synthesis of ECM proteins and promotes Angiogenesis: Fibroblast Growth Factor
(FGF)
Produce collagen for scarring: Fibroblasts
What releases it and what does it activate? IL-1: released by: Macrophages

activates: CD4 T-cell
What cytokine stimulates growth of all T-cells and which activates Macros? what cell is responsible for both?: IL-2: stimulates growth of all T-cells

INF-gamma: activates Macrophages

By: Th Cell
What releases it and what does it activate? IL-3: released by: T-cells

activates:
growth / differention of Bone marrow stem cells
Lymph node site of: 1. B-cells 2. T-cells 3. Macrophages 4. Plasma cells: B-cells: Follicle (germinal center)

T-cells: Paracortex

Macros: Medullary sinus

Plamsa cells: Medullary cords
What Dx does not allow for a well developed paracortex in Lymph Nodes?: DiGeorge syndrome

(b/c there are no T-cells to housing in the paracortex)
describe LN drainage (3): Right lymphatic duct - drains Right arm and Right side of head

Thoracic duct - Drains everything else

Efferent lymphatics dump into subclavian
Spleen site of: 1. B-cells 2. T-cells 3. Macrophages: B-cells: Follicles (white pulp)

T-cells: PALS (red pulp)

Macros: Marginal zone
what does it mean if "tdt" is in blood test?: Immature B-cells
(cells exiting marrow too quickly)
Where are the immature and mature T-cells in the thymus? where are Hassall's corpuscles? where does positive and negative selection occur?: Immature: Cortex

Mature: Medulla
(Hassall's corpuscles)

Selection: Corticomedullary junction
(4) steps in synthesis of B-memory cells from immature B-cells: 1. Pre-B = Heavy chain only

2. Immature-B = Heavy and Light IgM

3. Mature = IgM and IgD

4. Memory = Constant region
(w/ class-switch ability b/t IgG, IgE or IgA)
what causes a native helper T-cell (Th0) to become a Th1 or a Th2? what cytokine is needed for each?: Th1: Macrophage w/ IL-12

Th2: unknown w/ IL-4
what are the two major cells that the Th1 cells activate (2) and w/ which cytokines?: Macrophage (INF-gamma)

CD8 T-cell (IL-2)
what turns a B-cell into a Plama cell and w/ which cytokines(2)?: Th2 cells
(IL-4 and IL-5)

(2 = second letter B)
Major function of B-cells (3): Defense against bacteria (opsonize)

Allergy - Type 1 hypersensitivity

Autoimmunity
Major function of T-cells (cell-mediated immunity) (4): Defense against TB, virus, fungi

Allergy - Type 4 hypersensitivity

Graft and tumor rejection

regulates Ab response
What are the MHC class 1 genes? how many are there?: A, B, C

2 from each parent (six total)
What are the MHC class 2 genes? how many are there?: DP, DQ, DR

2 from each parent (six total)
Between class 1 and 2 MHC, which uses: 1. Endogenous peptides 2. Exogenous peptides 3. one polypeptide 4. two polypeptides 5. alpha and beta chain 6. B2-microglobulin 7. loading occurs in acidified endosome 8. load: MHC-1:
Endogenous;
one polypeptide;
B2-microglobulin;
RER loading

MHC-2:
Exogenous;
two polypeptides;
alpha and beta chains;
Acidified endosome loading
what cells have MHC-1 and 2?: Antigen-presenting cells
(macros, B-cells, dendritic cells, etc)
what is the co-stimulatory signal b/t a MHC-2 and a Th-cell?: MHC-2 has B7, which combines to Th-cell's CD28
Definition: Localized increase in the volume of blood in capillaries and small vessels: Hyperemia
Definition: Occurs from obstructed venous return or increased back pressure from shock, acute inflammation or sudden right heart failure: Acute passive congestion
What can cause chronic passive congestion of the lungs? (2): Left heart failure

Mitral stenosis

(congestion and distention of capillaries can lead to rupture and RBCs in alveoli)
Pathologic name for chronic passive congestion of the liver causing dilated and congested veins w/ brownish, fattly liver cells what is the cause?: Nutmeg liver

Cause: Right Heart failure
(2) causes of decreased oncotic pressure: Nephrotic syndromes

Cirrhosis
(leading to Dec Albumin production)
(2) basic causes of shock: Decreased Cardiac output

Widespread peripheral Vasodilation
(sepsis, severe trauma; hypotension is main feature)
class of bacteria that is most likely to cause Septic shock: Gram-negatives
what acid-base disorder is a result of the progressive stages of shock?: Metabolic Acidosis
what affect does shock have on the kidneys?: Acute Tubular Necrosis
(2) organs that have Hemorrhagic infarcts versus Anemic infarcts?: Lung

GI tract

(will show red instead of white)
what part of the Ab structure recognizes antigens?: Variable of L and H chains
what part of the Ab structure fixes complement?: Constant part of the Heavy chain
(in IgG and IgM)
what part of the Ab does the heavy chain contribute to? light chain?: Heavy chain: Fab and Fc

Light chain: Fab only
Portion of the Ab w/ Carboxy terminal and Carbohydrate side-chains: FC
what are the light chain and heavy-chain genes that undergo random "Recombination" for Ab diversity?: Light: VJ

Heavy: VDJ
Ab that crosses placenta: IgG
Ab that prevents attachment of viruses and bacteria to mucous membranes: IgA
what joins IgM together?: J-chain

(J = Join)
Ab that mediates immunity to worms: IgE
Definition: Ig epitope that differs among members of the same species; on light or heavy chain: Allotype

(polymophism)
Definition: Ig epitope common to a single class of Ig: Isotype
(IgG, IgA, IgE, etc)

Iso = same (class)
Definition: Ig epitope determined by antigen-binding site: Idiotype

Idio = unique

(Hypervariable region is unique)
source of the following chemotactic factors: 1. f-met 2. C5a 3. IL-8 4. LTB4: f-met = bacteria

C5a = serum

IL-8 = Macro

LTB4 = PMNs
cytokine: supports growth and differentiation of bone marrow stem cells (myeloid cells): IL-3
cytokine: growth of B-cells; enhances class-switching of IgE and IgG: IL-4
cytokines: differentiation of B-cells (to make Ab); enhances class-switching of IgA: IL-5
cytokine: attracts and activates PMNs; stimulates dendritic cell migration to LN: TNF-alpha
what is the only human cell without a MHC-1?: RBC
(2) unique CD markers for Th cells that are not on Cytotoxic T-cells describe use of each: CD28:
binds to the B7 on Macros and B-cells

CD40L:
binds to CD40 on B-cells to switch isotypes of B-cell
CD markers on: 1. Macro (2) 2. NK cell (2): Macro = CD14, B7

NK cell = CD16, CD56
what are the cell surface proteins on the B-cell? (7): IgM
B7
MHC-1 and 2
CD19
CD20
CD21 (for EBV)
CD40
what activates the classic complementary pathway? Alternative pathway?: Classic = IgG and IgM
(GM os a classic car)

Alternative = Microbes
(esp. endotoxin)
Complement: Deficiency causes hereditary angioedema: C1 esterase inhibitor
Complement: Deficiency causes severe, pyogenic sinus and respiratory infections: C3
Complement: Deficiency leads to Neisseria infections: C6 - C8
Complement: Deficiency leads to paroxysmal noctournal hemoglobinuria (PNH): Decay-Accelerating Factor
(DAF)

(DAFfy Pees red Near bugs Home) PNH
Definition: proteins that place uninfected cells in an antiviral state; induce the production of 2nd protein that inhibits viral synthesis what does it degrade?: Interferons
(alpha, beta and gamma)

degrades Viral mRNA
what does each specific interferon do? (2) what cells do they activate?: Alpha and Beta:
Inhibit viral protein synthesis

Gamma:
Increases MHC-1 and MHC-2 in
all cells

All:
Activate NK cells to kill virus-infected cells
Difference b/t Active versus Passive immunity: Active:
Created by self;
Long-lasting protection

Passive:
created by mother or outside source;
rapid onset, short life span of Ab
(4)* toxins that require the rapid onset of Preformed Ab (Passive immunity): To Be Healed Rapidly:

Tetanus toxin;

Botulinum toxin;

HBV;

Rabies
Definition: the ability of a T-cell (more then B) to become non-reactive without costimulation: Anergy
Antigen variation technique in: 1. Salmonella 2. Borrelia 3. Neisseria: Salmonella = two flagellar variants

Borrelia = relapsing fever

Neisseria = pilus protein
Antigen variation of Influenza major and minor: Major = Shift
(ex. DNA rearrangement)

Minor = Drift
Which parasite has Antigen variation by programmed rearrangement?: Trypanosomes
how do NK cells lyse the bad guys?: Ab-Dependent Cell-mediated Cytotoxicity
(ADCC)
which hypersensitivity rxns are Ab-mediated?: 1, 2, 3
which hypersensitivity rxn deals w/ histamine?: type 1

(anaphylactic, atopic, alergic)
which hypersensitivity rxn deals w/ Urticaria (hives)?: type 1
which hypersensitivity rxn deals w/ antigens localized to tissue BM or RBCs?: type 2

(though antigen is not intrinsic component of target cells, as in type 3)
how do the bad cells get killed in hypersensitivity 2 rxns? (2): Antibody and complement lead to MAC

ADC Cytotoxicity
(w/ NK cells, macros, PMNs, etc)
MC type of hypersensitivity rxn (if unsure about question, guess this one): type 2
which hypersensitivity rxn deals w/ antigen-Ab complexes that can bind complement? what other factors are involved? (2): type 3

also involved:
Hageman factor (XII) -> vasodilation and edema

Platelet aggregation
which hypersensitivity rxn deals w/ SLE, RA, PAN?: type 3
which hypersensitivity rxn deals w/ serum sickness and arthrus rxn?: type 3
which hypersensitivity rxn deals w/ post-strep GN, hypersensitivity pneumonitis (farmer's lung)?: type 3
what does the word "ACID" represent in hypersensitivity rxns?: four types:

1 - A: Anaphylactic, Allery

2 - C: Cytotoxic (Ab-mediated)

3 - I: Immune complex deposits

4 - D: Delayed (cell-mediated)
which hypersensitivity rxn deals w/ Goodpastures syndrome?: type 2

(Ab to basement membrane)
which hypersensitivity rxn deals w/ myasthinia gravis?: type 2

(Ab to Ach receptor)
which hypersensitivity rxn deals w/ ITP?: type 2

(Ab to platelets)
which hypersensitivity rxn deals w/ T-cells encountering antigens and then releasing lymphokines, leading to Macro activation?: type 4

(Delayed, Cell-mediated)
what are the (4) "T's" of the Delayed hypersensitivity type?: type 4:

T-cells mediated;

Transplant reactions;

TB skin tests;

Touching (contact dermatitis)
which unique (2) hypersensitivity 4 Dx deals w/ Antibodies?: DM-1;

Hashimoto's thyroiditis
Transplant Rejection type: Ab-mediated, occurs in minutes, a localized Arthus rxn: Hyperacute rejection
Transplant Rejection type: T-cell mediated, days to months after transplant: Acute rejection
Transplant Rejection type: Ab-mediated vascular damage, months to years after transplant, usu accompany scarred kidneys: Chronic rejection
Transplant Rejection type: due to graft's T and B-cells that affect host give (2) examples: Graft-vs-Host Dz

examples:
whole blood transfusion in SCIDs pt,
bone marrow transplants
Dx: maculopapular rash, jaundice, hepatosplenomegaly, diarrhea, recent bone marrow transplant: Graft-vs-host Dz
what is the most potent APC?: Dendritic-Langerhan's cells
if newborn (or fetus) has an infection, what Ab is made?: IgM
what are the structures that Ab are made against (usu proteins) on an infectious agent?: Epitopes
what is the immune response w/ Toxic Shock Syndrome from S. Aureus?: Activates T-cells in an antigen-nonspecific manner
what test is used to assess the level of CD-4 lymphocytes in HIV patient?: Flow cytometry
what test is used to detect a group A strep infection on a throat swab?: Latex Agglutination

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