General Path Flashcards
What is aplasia vs hypoplasia?
Aplasia is a lack of cell production in embryogenesis. (absent organs)
Hypoplasia is decreased cell production in embryogenesis (smaller organs)
3 general causes of hypoxia
Ischemia
Hypoxemia
Decreased O2 carrying capacity
What is Methemoglobinemia?
When iron in the Hb is oxidized to Fe3+ which cannot bind oxygen
(treatment is methylene blue to get Iron back to Fe2+)
Hallmark of reversible cell injury
Cell Swelling
Hallmark of irreversible cell injury
Membrane Damage
How does irreversible cell injury result in apoptosis
Membrane damage occurs to the mitochondria in the cell which leads to leakage of Cytochrome c and activation of apoptotic enzymes
List the 3 nuclear changes that occur in cell death.
Pyknosis: condensation (shrinks)
Karyorrhexis: Fragmentation
Karylolysis: dissolution (fading)
Necrosis where the tissue is firm and architecture is maintained. Usually due to infarction, pale area.
Coagulative necrosis
Type of necrosis in brain infarction
Liquefactive
Coagulative necrosis that resembles mummified tissue.
Gangrenous Necrosis
Cottage-cheese like appearance necrosis
Caseous Necrosis
Combination of coagulative and liquifactive necrosis.
Caseous necrosis
Necrotic damage to blood vessel walls
Fibrinoid Necrosis
3 enzymes that reduce the amount of free radicals in the body.
Superoxide dismutase
Glutathione Peroxidase
Catalase
Mechanism of Reperfusion Injury.
Ishcemia to a region of tissue causes cell injury. Immediate return of blood to the area brings accumulated oxygen free radicals in high concentration which further damage the tissue.
Congo Red Staining with Apple Green birefringence.
Amyloidosis: misfolded proteins (from Ig light chains) that deposit in extracellular space
Most common organ involved in amyloidosis
Kidney: nephrotic syndrome
can also have restrictive cardiomyopathy, or tongue enlargement
Arachidonic acid metabolite that mediates pain.
PGE2
- produced from arachidonic acid by COX enzymes
- primary thing ASA tries to prevent from forming
Arachidonic Acid metabolite that is chemotactic
LTB4
-made from lipoxygenase enzymes
Major mediator from mast cells and what it does.
Histamine: increased vascular permeability, vasodilation of arterioles
Activators of classical complement pathway
IgG and IgM
Activators of the alternative complement pathway
Microbial products
2 complement anaphylatoxins
C3a
C5a
Complement that is chemotactic for neutrophils
C5a
Complement that opsonizes bacteria
C3b
2 inflammatory mediators that induce pain
Bradykinin and PGE2
2 pyrogen mediators
IL-1
TNF
Lymphocyte receptor on all T cells for antigen surveillance.
CD3
Lymphocyte receptor on helper T cells
CD4 (recognizes MHCII)
Lymphocyte receptor on cytotoxic T cells
CD8 (recognizes MHC I)
Cells that have MHCII
Any antigen presenting cells (APCs)
-usually macrophages, monocytes, dendritic cells, Langerhans cells
Cells that have MHCI
Any nucleated cells
Describe the two types of T helper cells and what each does.
Th1: secretes IL-2 for T cells growth Th2: secretes IL-4 for Ab class switching, IL-5 for eosinophil chemotaxis and class switching to IgA
Mechanism of granulomatous inflammation. (3 steps)
- Antigen detected by macrophages and is presented to helper T cells on MHCII
- Macrophages also secrete IL-12 which makes CD4 cells turn into Th1 cells
- Th1 cells secrete INF-gamma converted macrophages into epitheliod histiocytes and giant cells
Patient presents with severe susceptibility to fungal, viral,bacterial, protozoan, and opportunistic infections. Treatment is isolation. Describe the problem.
SCID
- cytokine receptor defect
- adenosine deaminase deficiency
- MHC II deficiency
6 month old baby presents with recurrent bacterial, viral, and Giardia infection. Describe the pathogenesis.
X-linked agammaglobulinemia
-mutated Bruton Tyrosine Kinase
Patient presents with recurrent viral pharyngitis, nasal infections, conjunctivitis.
IgA deficiency
-many mucosal infections
Patient develops no Long-term immunity to previously acquired diseases, is able to fight them off in acute states however. What is the pathogenesis.
Hyper IgM syndrome
- Either CD40L mutation on CD4 cells or CD40 mutation on B cells
- inability to class switch
Patient has Thrombocytopenia, eczema, and recurrent infections.
Wiskott Aldrich Syndrome
-WASP gene mutation
Patient keeps getting N. meningitides infections.
Complement deficiency in C5-C9 preventing MAC formation
Complement deficiency that results in hereditary angioedema.
C1 inhibitor deficiency
-C1 is overactive and creates increased vascular permeability most noticeably at mucosal areas leading to swelling
Patient presents with arthritis, rash across the nose and cheeks, and hematuria. What tests would be positive?
SLE
-ANA, anti-dsDNA
Patient is positive for Antihistone Abs causing SLE symptoms. What is most likely the cause?
Drug-Induced: procainamide, hydralazine, isoniazid
Patient presents with keratoconunctivitis, zerostomia and recurrent dental carries. What type of Hypersensitivity is this?
Sjogren Syndrome
-Type IV: lymphocyte mediated, delayed
Patient presents with trouble swallowing, little white nodules on the fingers, and stiff fingers.
Scleroderma
-CREST syndrome: calcinosis, raynauds, esophageal dismotility, sclerodactyly, telangiectasia
When does repair occur vs. regeneration?
Regeneration is mainly in labile cells. However, whenever the regenerative stem cells are damaged, replacement of fibrotic scar tissue occurs.
Hallmark of tissue repair and its composition
Granulation Tissue
-type III collagen
Main two tumor suppressor genes and how they regulate the cell cycle.
p53: regulates G1 to S phase
Rb: regulates G1 to S phase (E2F transcription factor)
Function of the Bcl gene in apoptosis.
Stabilizes the mitochondrial membrane. If Bcl2 is damaged, the apoptotic pathway progresses. In certain cancers, Bcl2 is over-expressed and even if a cell is cancerous it doesn’t undergo apoptosis because the Bcl2 doesn’t let it.
How do tumors invade and spread? (4 steps)
- Downregulation of E-cadherin allows dissolution of cells to one another
- Attachment to laminin destroys the basement membrane so the cells can invade.
- Cells attach to fibronectin in the ECM
- Cells enter lymph or blood and spread
