Wk1-3 MSE questions Flashcards
Cell injury:
What are the 6 basic pathological mechanisms of cell injury?
- ATP depletion*
- mitochondrial damage*
- loss of calcium homeostasis.*
- oxidative stress (free radicals)*
- defects in membrane permeability*
- DNA damage*
What are the 3 responses to cell stress of injury:
- Adaptations: new steady state, cell surviving and continuing to function
- Reversible cell injury: or degeneration
-
Cell death/irreversible injury
- Apoptosis: cell is activating cell death and can be pathological or physiological
- Necrosis: acquired pathological cell death
Reversible and irreversible changes: give examples of each
- Reversible cell injury: hydropic degeneration
- Irreversible: necrosis or apoptosis:
Necrosis and nuclear changes:
What are the 3 patterns of nuclear changes are:
- Pyknosis = nuclear condensation with shrinkage and intense basophilia (tiny nucleus with darker cell)
- Karyorrhexis = nuclear fragmentation (fragmented nucleus)
- Karyolysis nuclear dissolution or complete loss (nothing there)
NECROSIS AND APOPTOSIS: WEEK 1:
What are the 4 types of necrosis:
-
Coagulative
- Most common type, usually what we see in the kidney, heart etc.
- Liquefactive
-
Caseous
- ‘cheese like’ necrosis, tissue replaced by crumbled, yellow-like exudate
-
Gangrenous
- Common in frost bite, due to loss of blood supply. E.g. Arterial thrombosis, frostbite.
Cell aging:
3 most important mechanisms of cellular aging:
- DNA damage
- Decreased cellular replication
- Decreased proteins and damaged proteins
Conjugated and unconjugated bilirubin:
- unconjugated = body can’t get rid of it*
- conjugated = can get rid of in the liver*
the 3 pathogenesis of jaundice are: (think liver)
- Prehepatic –> BEFORE liver –> destruction of RBC (anaemia test) = increased unconjugated bilirubin (unconjugated = body can’t get rid of it, conjugated = can get rid of in the liver)
- Hepatic –> IN the liver –> hepatocellular injury = reduced uptake and conjugation or secretion of biliruin in liver
- Post hepatic –> AFTER liver in bile system –> obstruction of bile causing decreased outflow of bile from the liver
Cell aging:
3 most important mechanisms of cellular aging:
- DNA damage
- Decreased cellular replication
- Decreased proteins and damaged proteins
What pigment is referred to as the aging pigment?
- Lipofuscin = aging pigment = lysosomal waste in aged cells
- Granules = cytoplasmic, round, small, pale/brown colour and are uniform in size, whereas hemosiderin is brown but large and irregular
What is melanin?
skin pigment, normal skin pigment. Reduced production = albinism, and increased production = chronic dermatitis
Hemosiderin
-
= too much breakdown of blood = excess iron (thus hemosiderin only found in cells that can remove iron = macrophages)
- big and dark brown granules, only in macrophages (only cells that can remove iron)
Bilirubin =
jaundice, yellow colour in fat, caused by increased level of bilirubin in the plasma (unconjugated)
Anthracosis =
= accumulation of carbon particles in the lung (exposure to polluted air) –> look like dark brown/black granules in the airways
acute inflammation:
What are the leukocyte recruitment stages in order/4 movements of leukocytes?
- Rolling
- leukocytes temporarily bind to the endothelium and then release
- Adhesion
- binding of B2 integrin expressed on stimulated leukocytes
- Transmigration
- Across the endothelium (diapedesis)
- Migration
- Into interstitial tissue
MCQ: What adhesion molecule is involved in leukocyte recruitment during inflammation?
- histamine
- interferons
- immunoglobin
- selectin
- Selectin
- selectin families which are initial contact between leukocytes and endothelial cell
- E selectin = endothelial
- P selectin = platelets and endothelial
- L selectin = leukocytes
Selectin is for contact between ____ and ____ cells.
What are the 3 types of selectin for: E selectin, P selectin and L selectin?
- selectin families which are initial contact between leukocytes and endothelial cell
- E selectin = endothelial
- P selectin = platelets and endothelial
- L selectin = leukocytes
-
Lipidosis:
- Hepatic lipidosis: what are 3 mechanisms that lead to hepatic lipidosis?
- Too many FA’s from diet
- Abnormal hepatic metabolism
- Impaired lipoproteins –> can’t metabolise them
Describe classical activation of macrophages*
What is the importance of this pathway for M1 macrophages?
M1 macrophages
- microbe with LPS binds to TLR receptor
- causes reactive oxygen species or nitric oxide
- cause microbicidal action
this is important for host defenses against microbes
describe the alternative activation of macrophages*
what is the main this this activation of M2 macrophages releases?
- less microbicidal; involved in tissue repair
- TH2 cell with IL4 and IL13 → bind → release growth factors → result in fibroblast activation, increased collagen synthesis or increased angiogenesis (new BVessels)
What are the ‘death receptors’ of apoptosis?
TNFR and Fas
What protein binds the Fas molecules together in apoptosis?
FADD
What enzyme mediates final step of apoptosis?
Caspases
What can cause haemorrhage (know 2 factors)
- Loss of endothelial integrity or damage to blood vessels
- Platelet pathology - genetic defect in platelet function
- Defects in coagulation factors –> can be inherited or congenital
- Platelet dysfunction = reduced coagulation
- Vitamin K deficiency, liver failure etc.
Life cycle of thrombi: 4 stages:
- Lysis (dissolution)
-
Organisation and recanalisation:
- Recanalisation: new small blood vessels can penetrate/grow within the organising thrombus, due to additional platelets, fibrin and RBCs
- Propagation: an increase in size of the thrombus > may eventually occlude the vessel
- Embolisation: can occur if pieces break off the thrombus and travel downstream
outcome of thromboses wherein the thrombi tend to grow due to reposition of additional platelets, fibrin and RBCs is:
- recanalisation
- resolution
- propagation
- organisation
- recanalization: this is where the new BVs can penetrate/grow within the organising thrombus
What would best describe a granuloma? (what cell is most present)
an accumulation of macrophages that fight persistent bacterial infections
Leukocyte migration to the site of infection or injury is mediated by what cell?
chemokines
Can neutrophils fuse to form multinucleate giant cell?
negative
major effects of histamine are?
- mediator of inflammation
- vasodilation
- increased vascular permeability
- pain and itching
- neural reflexes
during acute inflammation, why is the burst of oxygen consumption (respiratory burst) in neutrophils essential?
essential for generation of microbicidal activity
Multistep theory of neoplasia / carcinogenesis: (4 main things*)
- Initiation = irreversible DNA damage in a cell initiates first cancer cell development
- Promotion = tumour formation is stimulated in the tissue with DNA damage by increased or continued cell division
- Conversion = benign tumour forms
- Progression = progressive mutations lead to nastier forms of cancer
What are the 2 main things a tumour needs to have to be considered malignant?
- Able to infiltrate or invade the surrounding tissue
- Able to metastasise-
- spread to distant sites often via blood or lymphatics through some tumours will ‘seed’ within a cavity.
multistep theory of neoplasia
- initiation
- promotion
- conversion
- progression
provide the 3 types of shock
- cardiogenic
- hypovolaemic
- blood maldistribution
list the 3 systemic effects of acute inflammation: the 3 main ones:
- fever
- leukocytosis
- alterations to acute phase proteins
describe the systemic effects of acute inflammation: the 3 main ones:
- fever: exogenous and endogenous pyrogens, increase prostaglandin synthesis and production of neurotransmitters
- leukocytosis: increased release of cells from bone marrow postmitotic reserve pool. release of less mature neutrophils
- acute phase proteins: C-reactive protein, serum amyloid A (AA), increase during inflammation
briefly outline the reactions of blood vessels in acute inflammation:
injury → activation of resident inflammator cells → proinflammatory chemical mediators ( 2 pathways: vasodilation or increased vascular permeability)
this can then lead to:
- vasodilation: → slowing of blood flow → leukocyte margination
- increased vascular permeability: → fluid leakage into extracellular space
