Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

49 Cards in this Set

  • Front
  • Back
Accumulation of phospholipids (due to lack of what ?, 3 diseases, def. in each, what is stored)
Lack of lysosomal enzymes. Tay sachs - Hexoaminidase -> GM2 storage. Neimann pick - Sphingomyelinase -> Sphingomyelin. Gaucher -> Glucocerbrosidase,
Proteins in plasma cells ?
Russel bodies
Glycogen storage diseases - glycogenoses (where usually stored, where in pompe, forms)
Usually in cytoplasm, in Pompe in lysosomes. Hepatic form - Von Gierke, Type I - G6P def. Myopathic - Mcardle - Type V - glyocgen phosphrolyase. Pompe - Type II - lyososmal acid maltase (heart). Brancher's - Type IV - abnormal glycogen
MPS accumulation : name of materials, clinical, Variants
Keratin sulfate, Heparin sulfate, Chondrotin sulfate. Clouding of cornea, joint stiffness, mental retard. MPS - Hurler (AR, 6-10y, L-Iduronidase def). Hunter - X linked, milder.
How do calcium salts look like in dystrophic Ca ?
Fine white granules or clumps
Endocrine amyloidosis ?
C-cells --> Calcitonin associated amyloid (calcitonin is betasheet). IAPP from islet cells in DM
In amyloidosis in the liver : where is the amyloid deposited first ?
Space of disse then to sinousids
Fate of thrombus ?
Propagation, emboli, dissolution, organization&recanalization
Causes of DIC
Placenta rupture (TF), Granules release from leukemic cells, Gram-negative spesis (TNF, IL1 decrease thrombomodulin, initate & endothelial injury in burns, SLE etc)
define infarct
area of ischemic coagulation necrosis
shape of infarct
wedge, occluded vessel at apex
Types of shock. Stages of shcok.
Cardiogenic, hypovolemic, Septic, neurogenic, Anaphylactic. Stages - Nonprogressive, Progressive, Irreversible (lysosomal leakage)
What are the two components of inflammation ? What are the forms of increased vascular permeablity ?
Vascular changes and cellular events.
Increased vascular perm. :
Endothelial venules contraction. Endothelial retraction. Direct endothliela injury and leukocyt mediated injury.
Signs of inflammation ?
Heat - Calor. Redness - Rubor. Swelling - Tumor. PAin - Dolor. Functio laeasa.
Steps of leukocyte cellular reaction to inflammation?
Margination/rolling, Adhesion and transmigration, Chemotaxis and activation, Phagocytosis and degranulation
chronic inflammation occurs when ?
-Pesistant infection, -Prolonged exposure to non-degradable, -Autoimmune
Regulation of cyclins, also 3 types of cells
Cyclins - transcriptional regulation and proteolytic. Cells - continously dividing, quiescent, permanent
4 components to repair by CT
Angiogenesis, Fibrosis, ECM deposition, remodeling
Morphology in Type III HS (specificly in serum sickness). Also, name a local type III HS reaction ?
Fibrinoid necrosis (acute necrotizing vasculitis), microthrombi, GN. Arthus reaction.
Transplant rejection: Direct presentation, Indirect presentation
Direct - Self T cells recognize donor APCs + foreign MHC I/II and peptides. Response is CD4/CD8.
Indirect : Self APCs take up foreign peptides and present on MHC2 --> Only CD4 response
Self tolerance :
Central. Peripheral -- Anergy (no Costiumulatr), AICD (Fas), Regulatory T cells
Etiology of SLE (genetic, non-genetic, immunologica)
Genetic - HLA-DQ. Non genetic - Drugs (procainamide), Hormones, UV. Immunologic - B/T cell hyperactivity or an intrinsic B cell defect
SLE morphology - Vessels, Kidney
Vessels- Small arteries mostly, Fibrinoid necrosis with DNA/C3/Immunecomplexes, lumen narrowing. Kidney - Class I - normal. Class II - Mesengial Lupus (IC in mesengium). Class III - Focal proliferative GN (less than 50% of glomeruli, hematuria). Diffuse proliferative GN (severe, nephritic/nephrotic, crescents). Class V - Membranous GN
SLE morphology - Skin, Heart, Spleen, Heart
Skin - Butterfly rash, Heart - Liebmann-sacks endocarditis, Spleen - capsule thickening, onion skin vessel lesions. Heart - Interstitial fibrosis
Morphology of RA
Small joints, blah. Chronic synovitis, Pannus (synovial space, granulation tissue). Ankylosis. Acute necrotizing vasculitis.
ANAs in SS ?
Anti-DNA topoisomerase in diffuse. Anti-centromere in CREST
Two factors that contribute to SS ?
Acitvation of Th cells (autoimmune) and Endothelial injury
Marker for inflammatory myopathies (DM, PM, MCD). Injury in DM is mediated by ? Injury in PM is mediated by ?
Anti-tRNA (Jo-1). In DM - Antibodies (also note periorbital edema). In PM - CTL damage
Bruton disease is ? give 3 SCID examples
Bruton - X-linked agammablobulinemaia. Btk mutation - B cells maturation stops at Pre-B. SCID : X-scid (IL7), ADA/PNP, Autosomal SCID (Jak3 kinase)
Problems in DiGeorge
Thymic hypoplasia (3rd-4th pharyngeal pouches). Lips, ear, aortic arch, PTH. HypoPTH, Deficient T cells
HIV virus is ..? Has 2 glycoproteins..? each of these binds ?
Retrovirus from the Lentivirus family. gp120 - binds CD4R, gp41 - binds CCR5/CXCR4 COr
Phases of HIV infection ? Clinical features of full-blown AIDS ?
Early acute, Middle chronic, Final crisis. AIDS --> Oppourtunitis infections, diarrhea, neuorlogical, neoplasms, hairy leukoplakia
AD diseases ?
ADPKD, Neuroblastomas, Ehler-Danlos, NF, MEN
Marfan syndrome (gene), EDS(definition, features, Type VI, Type VII, Type IV)
Marfan - Fibrillin gene on Chr 15. EDS - Defects in collagen with skin-hyper, hype-mobile joints, c0lon rupture. Type VI - Lysyl hydroxylase, retinal detach. Type VII - Procollagen I to collagen I. Type IV - Type III collagen mutations - colon rupture
NF1 - gene, criteria
Neurofibromin on chr. 17 - TSG, negative regulator of ras. Criteria - multiple cafe-au-lait spots with multiple skin tumors.
NF2 - gene, freq, difference from NF1
Merlin, a TSG on chr.22. RARE 1:40,000. No lisch nodules.
AR syndromes ?
Hurler, ARPKD, Hemochromatosis
CF is the...? also - freq, gene
CF is the most common lethal genetic disease. Freq - 1:25 carriers, 1:2500 express. Gene - CFTR on chr. 7
Polygenic inheritance is involved in ?
DM, HT, Gout, schizo, height, weight..etc
Morphology of Gout
Acute arthritis, Chronic tophaceous arthritis, Gouty nephropathy
Chronic tophaceous arthritis (What is deposited, where, results in, leads to). What are tophi composed of ?
Large, irregular depositis of sodium-urate TOPHI deposited in articular cartilage. This results in a granulmatous inflammation and leads to fibrosis and ankylosis. Tophi are composed of crystalline urate surrouned by mac's, lympho, fibro
What is karyotype ?
Photographic presentation of a stained metaphase spread with the chromosome arranged in decreasing length (1-->22+XY), stained by Giemsa
Cytogenic disordes --> talk about ?
General, karyotype, numerical abnormalities, structural abnormalities
Cytogenic disorders compatible with life are ? Kleinfelter ? Turner ?
45,X to 49,XXXXY (or more Y's). Kleinfelter - Males, 2 or more X's --> Hypogonad, long, low testo-sterlity, no mental. Turner - 45X females --> hypogonad, lymphedema of neck, short, horse-shoe kidney, mental, streak ovaries
Teratomas are ? Choristomas are ? Hamartomas are ?
Teratoma - From totipotent cells, more than one cell layer, usually all 3. Choristomas - ectopic, Mature cells located in wrong place. Hamartoma - Immature tissue at right place
Biology of tumor cell growth - talk about ?
History of a tumor, Influences on growth, kinetics of growth (Ki67), Angiogenesis, Tumor progression&clonal expansion
Mechanisms of metastatic spread - mention ? Sarcomas spread by ? Cc spread by ?
Detachement of tumor cells, Attachement to ECM, Degradation of ECM and migartion, Vascular dissemination, extravasation and homing. Sarcomas = hematogenous, Cc = lymph
Heredity in cancer - mention ?
Inherited cancer syndromes (TSG's, AD), Familial cancers clustering, AR syndromes of defective DNA repair
Products of TSGs
Regulation of cell cycle (Rb, P53), Regulation of signal trans (ras), Regulation of cell adhesion (DCC), Growth inhibitory factors (BRCA1/2)