Pathology Flashcards
(27 cards)
Nucleolus
Site where rRNA are transcribed and ribosomal subunits are assembled
Use rRNA is diagnostics to determine bacterial and fungal identification!
LARGER nucleolus means more protein synthesis !!!
Ribosomes
Synthesize mRNA (translation)
Can either be free within cytosol (these proteins stay here, nucleus, or mitochondria) or proteins can be attached to ribosome (get secreted, membrane, ER, Golgi, or lysosomes)
Rough ER
Processes and sorts proteins that are sectioned for secretion, plasma membrane, ER, golgi, or lysosomes
All this processin is NECESSARY for protein to be functional!
(Folding, polypeptide assembly, disulfide bond formation, glycosylation, addition of glycolipid anchors)
Smooth ER
Lipid metabolism and membrane lipid synthesis
Major production site of molecules composed of iPods like steroid hormones rom cholesterol
Major role in metabolizing lipid soluble compounds, home of cytochrome p450s in hepatocytes!
Able to inactivate numerous drugs by converting them to water soluble compounds that are then eliminated in urine
Acetaminophen Toxicity
Cats do NOT have glucoronyl transferase to break down drugs via GLUCURONIDATION
Alternative routes of detoxifying processes then get overwhelmed (sulfation, depletion of glutathione stores)
THUS increased amount of drug in bloodstream that is metabolized by p450 (in smooth ER of hepatocytes) leads to toxic metabolite NAPQI production and this leads to HEPATOCELLULAR NECROSIS
Golgi apparatus
“Post office”
Receives proteins from ER
Processes and sorts them for transport to final destination, lysosome, plasma membrane, secretion
Peri-nuclear clear zone
In plasma cells, can see Golgi apparatus because of this zone (antibody secretion)
Mott Cells
PLASMA CELLS that are “constipated” and can’t secrete antibody
Dilated ER cistern are full of antibody==Russel bodies
Lysosomes
Waste and recycling
Membrane bound
Has many enzymes
Degrades material from endocytosis !!!!
Engulfed material from outside the cell by pinching of the plasma membrane——form vesicle
Vesicle merges with endoscope and transport material to golgi for recyclingg and lysosomal functions to degrade the rest
Mycobacteria
Normally, phagocytosis allows phagosome to fuse with lysosome to form phagolysosome
BUT, mycobacteria prevent this step !! So they persist and digestion of the microbe cannot occur by enzymes
Mitochondria
Power plant
Generate ATP via citric acid cycle and oxidative phosphorylation
Cytoskeleton
- Intermediate filaments, IF proteins
- Microtubuls, tubulin protein
- Microfilaments, actin protein
What can undergo passive diffusion?
Gases, hydrophobic molecules, small polar molecules
Groups of CAMs (cell adhesion molecules)
- Selections
- Integrins
- IgSF
- Cadherins
Pemphigus
Cell-adhesion proteins in disease
Immune mediated destruction of desmoglein 1 and 3 (Catherine proteins)
Secreted signaling molecules
- Autocrine
- Paracrine
- Synaptic/neural
- Endocrine
Pattern-recognition receptors (membrane proteins)
toll-like receptors
NLRs nucleotide-binding
CLRs C-type lectin
RLRs RIG1
Etiology
The CAUSE(s)
Can be intrinsic or extrinsic
Intrinsic: genetic mutations (primary) or secondary (age, gender, coat color,etc)
Extrinsic: weather, trauma, toxins, bacteria, viruses, etc
Pathogenesis
how the disease DEVELOPS
Etiology….sequence of events….lesion
Lesions
Structural/morphological alterations in cells or tissues
Macro or microscopic
Visual representations of tissue injury and response
Lesions secondary to euthanasia
- Barbiurate salts
- Splenomegaly
- Cranial hemorrhage (captive bolt)
Common post-Mortem changes
Gas-dissensions (emphysema, prolapses, gastric rupture), Staining (bile imbibition, Melanosis), rigidity, live Mortis (blood pooling)
Clinical SIGNS vs SYMPTOMS
Signs: manifestation of disease that physician perceives, OBJECTIVE and mostly can be measured
Symptoms: apparent to the patient/owner, can be misleading, vague, and SUBJECTIVE “anxiety, fatigue, nausea”
Diagnosis
Interpretation of the nature of disease taking into context the lesions and clinical signs