Patophysiology lecture qs

alapaj's version from 2017-03-22 23:13

Cell injury

Question Answer
hallmarks of reversible cell injuryreduced oxidative phopshorylation, ATP depletion, cellular swelling
cellular swelling is caused bychanges in ion concentration and water influx
hallmarks of irreversible cell injurylarge densities in mitochondria, loss of selective membrane permeability
cell injury results from failure ofaerobic respiration, integrity of cell membranes, protein synthesis, cytoskeleton, genetic apparatus
ATP is produced inoxidative phosphorylation, glycolytic pathway
anaerobic glycolysis leads toacumulation of lactic acid and reduction pf pH → diminished activity of enzymes
low ATP leads to (Ca)influx of calcium and damage of cellular components
high calcium leads todecreased cellular and mitochondrial membrane permeability
increased intracellular calcium activatesATPase, phospholipase, proteases, endonucleases
oxidative stress effectslipid peroxidation of membranes, oxidative modification of proteins, lesions in DNA
mitochondria are damaged byincreased in calcium, oxidative stress, phospholipids breakdown, lipids reakdown
mitochondrial damage resluts inMPT formation (mitochondrial permeability transition)
cytochrome cleakeage out of mitochondria triggers apoptosis
physiological apoptosiselimination of unwanted or harmful cells
pathological apoptosisdamaged affecting cells DNA
apoptosis stepscell shrinkage, chromatin condensation, formation of blebs and apoptotic bodies, phagocytosis by Mø
features of apoptosisprotein cleavage(caspases→DNAses), DNA breakdown - endonucleases, phagocytic recognition - trombospondin
death receptorsFas-FasL CD95, TNF member 6
FADDFas Associated Death Domain
extrinsic pathway of deathFADD + caspase 8
executonerscaspase 3 and 6
executoners functioncytoskeleton & nuclear matrix cleavage
caspase 3 functionactivates DNAase
protein FLIP functionbinds to pro-caspase 8 and inhibits extrinsic pathway of death
TRADD and FADD functionfavour apoptosis
TRAFsfavour cell survival
CTL secreteperforin
perforin functionallows entry of GRANZYME B
Granzyme B functioncleavage of protein, activation of caspases
anti-apoptotic proteinsBcl-2, Bcl-x
pro-apoptotic proteinBax, Bak, Bim
cytochrome c functionbinds to Apaf-1
Apaf-1apoptosis activating factor 1
Apaf-1 functiontogether with cytochrom c activates caspase 8
p53 functiontriggers apoptosis by activation of Bax, Bak, Apaf-1


Question Answer
blood vessels responseaccumulation of fluid and leukocytes in extravascular space
acute inflammation components↑blood flow (vasodilation), ↑permeability for proteins and leukocytes, emigration of leukocytes
vasodilation is mediated byhistamine, nitric oxide
exudate containsfluid, proteins, RBC
pus containsleukocytes (neu), dead cell debris, microbes
transudate containslow protein, ultrafiltrate of blood plasma
vasoactive amineshistamine (mc), serotoni, (pt)
mast cell dengrnulation is triggered byC3a, C5a, substance P, IL-1, IL-8
inflamatory mediating cytokinesTNF, IL-1 (produced by Mø)
chemokinse functionwork as chemoatractants for leukocytes
α chemokines attractneutrophills
β chemokines attractmonocytes, eos, bas, lymph,
γ chemokines attractlymphocytes
G protein receptors familyCXCR, CCR
G protein receptors functionare found on neu, Mo, they recognize bacteria
important prostaglandins during inflammationPGD2, PGE2, PGF2α, prostacyclin, thromboxane
Thromboxane (TxA2) functionpotent platelet aggregating agent, vasoconstrictor
Prostacyclinvasodilator, inhibitor of platelet aggregation
COX-1 functionin charge of production of prostaglandins involved in inflammation
COX-2 functionstimulates the production of the prostaglandins that are involved in inflammatory reactions
leukotrienes familyC4, D4, E4
leukotrienes causevasoconstriction, bronchospasm, increased vascular permeability
lipoxins functioninhibition of leukocyte recruitment
VasoconstrictionThromboxane A2, Leukotrines C4, D4, E4
VasodilationPGI2, PGE1, PGE2,PGD2, NO, prostaglandins, histamine
Increased vascular permeabilityLeukotrienes C4, D4,E4
Chemotaxis↑Leukotriene B4, HETE,
leukocyte adhesion↓lipoxins
resolvins functioninhibit leukocyte recruitment and activation, inhibit cytokines production
PAF functionplatelet stimulation, vasoconstriction, bronchoconstriction, chemotaxis, degranulation
PAF extremely low concentration functionvasodilation, increased permeability
complement functionincreased permeability, chemotaxis, opsonization
classical pathwayC1 + IgM/IgG + antigen
alternative pathwaytrigger by microbial surface (no antibody)
lectin pathwaymannose binding lectin + microbial carbohydrates → C1 activation
MAC is composed ofC5 + C6-C9
C5a functionchemotactic agent for neu mono eos bas
C3b functionopsonin
bradykinin functionsimmilar to histamine
VEGF functionincreased vascular permeability
factors increasing vascular permeabilityC3a, C5a, bradykinin, PAF, leukotrienes

Alzheimer's disease

Question Answer
Alzheimer disease definitiondementia - progressive loss of cognitive function
Alzheimer disease is common inindividuals with 21st chromosome trisomy
Alzheimer disease featuressenile plaques, neurofiblary tangles, amyloid angiopathy (vascular)
plaques contain proteins such ascomplement, proinflamatory cytokines, apolipoproteins, antichymotripsin
Neuritic plaques containAβ-40 and Aβ-42
Diffuse plaque containsAβ-42
neurofibrillary tangles are composed ofpaired helical filaments
paired helical filaments are composed ofprotein TAU
vascular amyloid is composed ofAβ-40
hirano bodies are characteristic forAlzheimers diasease
hirano bodies synonymeosinophilic bodies
genes loci linked to alzheimerAPP, PS1, PS2, ApoE

Parkinson's disease

Question Answer
Parkinson' disease affectsnigrostriatal dopaminergic system
Parkinson' disease symptomsslowness, pill rolling tremor, diminished facial expression
Parkinson' disease may be induced byneuroleptics, toxins (MPTP), pesticides
typical macroscopic findingspallor of substantia nigra, locus ceruleus, Lewy bodies
typical miroscopic findingsloss of pigmented catecholaminergic neurons in regions associated with gliosis
Lewy bodies are composed ofα-synuclein,parkin, ubiquitin
Lewy bodies can be found insubstantia nigra, nucleus of Meynert


Question Answer
Schizophrenia mechanismexcess of dopaminergic transmission at D2 receptors, deficit of glutamate transmission at NMDA receptors
positive symptomsillogical thoughts, odd behaviour, delusions
positive symptoms are associated withD2 receptors
negative symptomssocial withdrawal, poverty of speech, autism
negative symptoms are associated withD1 receptors
MRI findingslarger lateral and 3rd ventricles, reduced temporal grey matter, decrease in frontal lobe activity and metabolism


Question Answer
most common inherrited cancerretinoblastoma
inherrited cancer causepoint mutation in single allele
ovarian cancer genesBRCA1, BRCA2
factors predisposing to malignancycytokines (chronic inflammation), stem cells, ROS
factor increasing risk of colon cancerCOX-2
COX-2 functionconverts arachidonic acid into prostacyclines
E-cadherin functionkeeps epithelial cells together and relay signals between cells
steps of invasionlossning up tumor cells from each other, attachment to matrix components, degradtion of ECM, migration of tumor cells
E-cadherins are linked to cytoskeleton bycatenins
neoplastic epithelial cells expressintegrins
proteases function in generalprotein cleavage
3 classes of proteasesserine, cysteine, matrix metalloproteinase
MMP9 and MMP2 functioncleave type 4 collagen of epithelial and vascular basemwnt membranes
growth factors released by active proteasesPDGF, TGFbeta, b-FGF
tumors that don't metastizegliomas, BCC of skin
DDRDNA damage response
DDR functionthey monitor genome integrity
targets of genetic damageproto-oncogenes, tumor supressor genes, apoptosis genes, DNA repair
protooncogenesphysiologic regulators of cell proliferation and difrentiation
oncogenesmutated protooncogenes - promote growth in cancer cells
oncoproteinsproducts of oncogenes, devoided of important regulatory elements


Question Answer
types of painnociceptive, neuropatic
niciceptive painnociceptors (pain receptors) activatd due to injury
neuropatic painarises from direct injury of nerves (DM, alcohol, renall insufficiency)
hyperalgesiaextreme sensitivity to pain
allodynianon painful stimuli initiate the pain
hypoalgesiaabsence of pain that normally would be painful
stages of nociceptiontransduction, transmission, perception, modulation
transductionconverting of painful stimuli to neuronal action
NSAIDs functioninhibits cyclooxygenase
cyclooxygenase functionconverts arachidonic acid to prostaglandins
modulationtransmission of pain is stopped
inhibitory modulatorsenkephalins, NE, serotonin
gate control theorynon painful input closes the gates to painful input
cutaneous painsharp, bright with burning wuality
deep somatic paindiffuse, originates in deep body structures (sprained ankle)
visceral paindiffuse poorly localized, distension of organ
chronic daily headachedisease process, >6 months, depression
migraine headachegenetic influence is stronger for migraine with aura.
auraodczucie zapowiadające
migraine characteristics without aurapulsative, throubbing, uniateral, 1-2 days
migraine characteristics with aurasame as without + visual and neurologic symptoms proceeding the headache, nausea and vomiting
migraine mechanismhyperexcitability > dilation of blood vessels > pain
cluster headacheunilateral pain located in retroorbital, temporal, supraorbital, infraorbital. rapid onset, last up to 180 min
tension headachedull, aching, diffuse, no nausea nor vomiting
trigeminal neuralgia causepresence of anomalous artery or vein
gene of painSCN9A, crippling (okaleczający), sodium channels open to easily
Primary erythromelalgiahands and feet, severe episodic erythema, pain and flushing
Paroxysmal extreme pain disorderchronic episodic pain, rectum and lower extremities involved

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