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FunMed Random > big boy things > Flashcards

big boy things Flashcards

1
Q

explain how glucose is absorbed from intestinal lumen into portal vein

A

aim: transport glucose from intestinal lumen -> portal vein

1. primary active transport: The sodium-potassium pump maintains the electrochemical gradient of living cells by moving sodium out and potassium in of the cell

2. secondary active transport: SGLT1 symporter brings glucose into the enterocyte / intetinal epithelium cell. this is driven by Na+ and glucose transported (through 2ry AT) from the intestinal lumen into the intestinal epithelium.. (Na+ goes in and glucose goes along with it).

  1. leads to high levels of glucose in intestinal epithelium. faciliated diffusion of glucose via Glut2 facilated diffusion transporter causes gluocse to move from intestinal epithelium into portal vein. (Glut 2 is only expressed on basal lateral membrane)
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2
Q

what is / how does DNA mismatch repair occur?

A

this type of repair, repairs insertion or delation mutations that occurs during DNA replication and recombination:

  1. DNA strand has an error
  2. A nick (break) occurs in strand of DNA that has the error in.
  3. This provides signals that direct mismatch proof reading proteins to DNA strand that has nick.
  4. proteins scan the strand until the nick is found
  5. proteins (MutS and MutL) remove the DNA strand from the error to the nick
  6. DNA repair synthesis occurs to fill in corrected DNA into strand
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3
Q

how does compaction of DNA occur?

A

1. compaction of histomes: (basic proteins that form subunit structures)

  • 8 histomes form a nucleosome bead
  • DNA wraps around histomes: 146 base pairs of DNA wraps around a histome

= v compact !

  1. further compaction of histomes into chromatin
  2. further folding of chromatin into chromosomes
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4
Q

what is PCR used for?

how does PCR work?

A

PCR: amplifies a region of interest within the human genome, using a template DNA and specific primers

  1. denaturation: heats DNA to over 90 degrees - opens DNA up
  2. annealing: 54 degrees. primer is added. DNA binds to primers
  3. extension: 72 degrees. add polymerase enzymes. builds DNA

repeat x lots

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5
Q

what is sanger sequencing?

A

(golden standard for genetic testing)

(Sanger sequencing is the process of selective incorporation of chain-terminating dideoxynucleotides by DNA polymerase during in vitro DNA replication)

uses dideoxyribonucleic acids (ddNTP) to terminate polymerization reaction of DNA.

can find every single base pair in a sequence!

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6
Q

Q what is next generation sequencing? what are the different types?

A

- whole genome sequencing

- whole exome sequencing - sequencing all exons in genome (~2% of genome). no info on mutations outside of exons.

RNA sequencing (RNAseq) - sequencing all expressed RNA and expression analysis. (RNA is direct result of exons to RNA, but also RNAseq gives info about which genes are expressed and if highly / lowly expressed).

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7
Q

why is molecular diagnosis and targeted therapy good?

what can it be used for? (x4)

A

good: offers personalised approach to care. can tailor to specific genetic conditions of patient
- selection of embryos prior to implantation in IVF (carry out genetic testing on embryos and screen for mutations)
- personalised chemotherapy (take a biopsy of cancer and sequence DNA. if have specific changes to target molecules, can target those molecules with chemo. e.g. herceptin)
- gene therapy for genetic conditions (v experimental)

- pharmacogenomics

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8
Q

describe 3 prenatal diagnoses that can be undertaken to test for aneuploidy

A
  1. amniocentesis: genetic testing of amniotic fluid. using needle to extract transabdominal. 15-18 weeks of preg (risk to miscarriage: 1/100). ultrasound guidance used. t

2. chorionic villus sampling: genetic testing of tissue from placenta (choroinic villi), ultrasound guidance used transabdominal or transcervical. 12-14 weeks

3. non invasise technqiues: ultrasound imaging of back of neck of embryo at 11-14 weeks. if depth of fluid at back of neck is 3.5-4.4 mm = 70% chance of delivering baby with no major abnormalities.

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9
Q

what is Xist?

A
  • X-inactivation is assisted / coded by non coding RNA: XIST (X inactivion centre)
  • Xist assocates closely with the X-chr from which it is expressed -> leads to chromatin changes and spatial reorganisation of chr. chr will condense into Bar > results in transcriptional inactivation in that chr.

(X chromosome inactivation (XCI) in females thus leads to similar transcription levels of X-chromosomal genes between males and females, who now both express genes from a single X chromosome. )

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10
Q

what is the Barker hypothesis?

A

thrifty phenotype: if a baby in-utero is subject to poor nutrients (because of bad maternal diet), the epigenome is programmed to expect this environment post-natally. means there are developmental changes in cellular energy metabolism, such as: glucose handling, lipid metabolism and mt biogenesis. if exposed to nutrient poor environment postnally: means pre-disposed to have a survival offspring.

BUT

if born and given a nutrient rich environment -> get increased risk of susceptibility to metabolic disease, such as type 2 diabetes, obesity and CHD

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11
Q

how does DNA methylation of cytosine occur?

A
  • methyl groups can be added / removed from cytosine (the nucleotide base)
  • methylation interferes with binding of transcriptional activators -> causes gene inactivation
  • occurs when you get areas of DNA where cytosine and guanine are adjacent and repeated (CGCG / CpG islands). found in promoter regions.
  • DNA methyltransferase (DNMT) is the enzyme
  • methyl is added to cytosine to make 5-methylcytosine.
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12
Q

describe how chromatin architecture is changed (a factor than influences epigenome mechanism)

A

chromatin architecture modifcations

  • changes shape of histone / DNA complex

- ATP-depending remodelling:

  • complex of proteins sits on the histone nucleosomes. uses ATP. alters:

1. the contact between DNA and histones,

2. the path of DNA wound around histones,

3. the structure of nucleosomes.

normally an immediate effect

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13
Q

explain how histone modifications occurs (a factor than influences epigenome)

where do most modifications occur?

which enzymes used?

A

histone modifications

- post-translational modification of histone proteins: acetylation (acetyl functional group added), methylation M (addition of methyl group) , phosphorylation P, ubiquitylation (U)

  • most of modifications are on lysine (K) and serine a.a. -> can make active genes by doing this. e.g. H3K4me3 (this is 3 methyl groups on K) OR make genes repressed (e.g. H3K27me3- adding 3 methyl groups to K)

can change histone modifcations using enzymes:

a) histone acetylase (HAT): opens DNA to make it accessible

b) Histone deactylase (HDAC) associated with closing DNA to make it inaccessible

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14
Q

explain non-coding RNAs

(a factor than influences epigenome / regulates epigenome):

A
  • non-coding RNA (ncRNA). functional, but not translated into proteins = called interfering RNA.
  • this ncRNA interferes with gene expression at transcriptional and post-transcriptional level. combine to RNA and prevent it from being translated. (involved in splicing, editing and mRNA stability)
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15
Q

how does protein targeting to ER occur?

A
  • polypeptide chain will have an endoplasmic reticulum (ER) signal sequence on it
  • the ER signal sequence interacts with signal recognition particle (SRP)
  • the SRP binds to receptor (on a translocation channel) within the membrane of ER
  • the SRP leaves complex
  • the newly synthesised protein can translocate through the translocation channel.
  • SRP is cleaved
  • leaves the new folded protein in correct place
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16
Q

describe how initiation of transcription works

A
  • DNA unwinds close to a gene, RNA polymerase binds to a promoter sequence: how?:
  • the promoter sequence acts as a template for the assembly of the multi component complex of proteins, called the pre-initiation complex, which brings pol II to gene
  • once bound, the RNA polymerase II can then start trancribing the gene. (get transcription intition, elongation and termination)
  • transcription always starts at ATG ​on Exon 1
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17
Q

what are the two apoptopic pathways?

A

2 pathways:

extrinsic apoptopic pathway

  • enviroment around the cell could cause cell death.

- tumour necrosis factor (TNF) binds to death receptor. activates caspases

intrinsic apoptopic pathway:

  • targets the cell’s mitochondria -> activates caspases
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18
Q

what are caspases? whats mechanism involved?

A

Initiator caspases

  • pro-caspases get activated to active caspases (Caspase 2, 8 and 9)
  • intiator caspases activate the executioner caspases

Executioner caspases

  • again, activated from pro-caspase to activate caspase (Caspase 3, 6 and 9 -> effector caspases)

Cause:

nuclear fragmentation, cytoskeleton disruption, membrane alterations, organelle reduction

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19
Q

what is role of ACh on:

a) skeletal muscle - how?
b) cardiac muscle - how?
c) acinar cells - how?

A
  • *skeletal muscle:**
  • acetylcholine binds to skeletal muscle cell receptors called nicotinic acetylcholine receptors (nAChR)
  • depolarisation occurs (action potential more likely to happen)
  • contraction of skeletal muscle
  • *cardiac muscle:**
  • acetylcholine binds to acetylcholine receptor on heart muscle (called muscarinic receptor M2)
  • muscarinic receptors are G protein coupled receptors that activate ionic channels via a second messenger cascade
  • this causes hyperpolarisation and a decrease in cardiac activity
  • *acinar cells:**
  • acetylcholine binds to mAChr
  • activates the secretion of digestive molecules
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20
Q

whats the mechanism of calcium ions being used as an intracellular messenger?

A
  • calcium ions are stored in the ER
  • calcium enters cytoplasm via transmembrane calcium channels or via channels in the ER
  • calcium ions can bind to proteins and trigger events within the cell
  • after events occurred, calcium signals are deactivated by pumping ions back into ER or out of cell
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21
Q

how are intracellular receptor proteins activated?

A
  • hydrophobic signal molecules diffuse directly across plasma membrane and bind to intracellular receptor proteins
  • e.g signal molecules include: steroid hormones, thyroid hormones, retinoids
  • then, intracellular receptors bind to specific DNA sequences adjacent to the genes the ligand regulates

inactive receptor

  • each receptor will bind to short DNA-binding domain
  • a receptor protein in its inactive state is bound to its inhibitory proteins

active receptor

  • ligand binds to receptor and causes the (ligand-binding domain of the receptor to clamp shut around the ligand) inhibitory protein to dissociate
  • receptor is active
22
Q

what happens with cell signalling when have a stroke?

A
  • dying cells release large amounts of neurotransmitter: glutamate
  • glutamate is toxic at high concs

- excitoxicity -> glumatate spreads outside area of initial damage = braindamage

23
Q

give over view of cell signalling in normal cell - growth factor -> activate gene expression?

A
  • growth factor binds to receptor. two receptors interact (dimerization)
  • intracelllar side: phosphorylation of tyrosine
  • siganlling proteins bind to P-tyrosine
  • causes cascade of phosphorylation events
  • activates two pathways: MAPK pathway and PI3 Kinase Pathway
  • once pathways are activated, activate gene expression and transcription factors occur.
24
Q

explain the ras pathway and how mutation leads to kras cancer

A
  • when ras switched on: (normally ras is switched on by binding to GTP) can switch on ERK and AKT pathways. (ras regulates the pathways by turning on / off the ERK and AKT pathways)

- mutated ras (kras): hydrolysis of bound GTP (first stage in pathway) occurs v slowly. GTP is bound to ras in unhydroloysed form - ras is permenantly switched on. continois proliferation and growth.

25
Q

explain how Bax, p53 and Rb normally work and how they work when mutated?

A

Bax (pro-apoptotic protein)

  • allows cancer cells to survive even when challenged with chemotheropeautic or DNA damaging compounts that normally triger cytotoxic response

p53

normal function

  • transcription factor (activates transcription)
  • causes cells with mutations to undergo cycle arrest, allows DNA repair or entry to apopotic pathway
  • p53 activated by DNA damage, hypoxia or cell injury
  • p53 activation activates p21 -> inhibits cyclin complexes (prevents cell leaving G1 / entering S-phase

mutated function
- cell progresses with cell cycle with cell damage -> cells accumulate mutations -> cancer

mutated pRB (retinoblastoma):

  • pRb prevents cell cycle progression past G1 phase by inhibiting expression of S-phase genes
  • mutation in Rb gene = retinoblastoma
26
Q

where would u find dense irregular connective tissue?

A

in hollow organs -> esp. submucosa (layer beneath epi. lining of organ)

27
Q

explain the cancer stem cell model

A
  1. normal progenitor cell -> can develop into differentiated normal breast cells
  2. within tumours / tissues that will become cancerous: abnormal progenitor cells exist. can self-renew.
  3. abnormal progenitor cells acquire mutations and ability to proliferate become: mutated progenitor cell
  4. mutated progenitor cell self renew and become: cancer stem cell. can also dedifferentiate
  5. further mutations: some will become tumour cells, others remain as stem cells
28
Q

explain clonal evolutionary model

A

(overview: differentiated mammry cells gain mutations and undergo dedifferentiation process. (NOT PROGENITOR CELLS LIKE LAST H)
- start off as differentiated stem cell and mutation occurs
- after 1st mutation: no longer properly functioning mammary epi. cells. acquires characteristics of mutated stem cell
- after 2nd mutation: forms a cancer cell
- undergoes dedifferentiation: forms cancer stem cell
- cancer stem cell becomes cancer cell or cancer stem cell

29
Q

how do u break down origins of tumour?

A

In terms of the origin of the tumour, there are only 2 broad types you need to know:

Epithelial tumours involves stratified squamous, simple cuboidal and simple columnar.

  • Stratified squamous e.g. skin, lining of respiratory tract, upper oesophagus, cervix
  • Cuboidal and columnar e.g. adrenal gland, sweat gland, pancreatic ducts, stomach, etc. – these are cells that secrete things

Mesenchymal is pretty much any other tissue type

E.g. bone, cartilage, nervous tissue, etc.

30
Q

give quick overview of how mestasis occurs

A
  1. vascularisation of tumour occurs
  2. cells detach from primary tumour
  3. BM is degraded :( and invasion into ECM occurs
  4. Intravasation of nearby blood vessels (need to breach membrane of enterocytes to do this)
  5. tumour cells circulate in vascualar system
  6. some cells adhere to walls of blood vessels
  7. Extravasation (leave blood vessels) to local tissues
  8. secondary tumour
31
Q

what happens when change in temperature is activated? (input vs output?)

which areas detect the change of temp from warm and cold?

what does this cause to change?

A

Goes to control centre: brain - specifically the hypothalamus:

Input:

- preoptic area (POA) monitors core temperature: recieves input from warm receptors from skin and and internal receptors

  • paraventricular (PVN) and dorsomedial hypothalamic (DMH) nuclei: recieve input from cold receptors

Integration and Output to Effectors:

  • Preoptic area (POA): regulate blood vessels in skin (vasoconstriction / dilation). stimulates posterior pituitary: conserves water
  • paraventricular (PVN) and dorsomedial hypothalamic (DMH) nuclei: regulates skeletal muscle (shivering). brown fat stimulation (aka:) non-shivering thermogenesis.
32
Q

whats a tautomeric shift

A

tautomeric shift:

  • when a tautomer occurs in DNA replication, the imino or enol pairs with non-complementary base -> base sub
  • BUT: after the first DNAreplication occurs, the BP that was a tautomer reverts back to its stable form. HOWEVER, the the other non-complementary BP stays! (the mutation)
    result: in 3x wild type, 1 mutant. transition mutation. means can go undetected as shape of protein doesnt really change
33
Q

explain the Donnan effect

A

sources of intracellular osmolality:

  1. charged molecules and their counter ions
  2. smaller metabolites and their counter ions
  3. small inorganic ions -> cause Donnan effect

Problem: all of the above attract counter ions, which could create a constant flow of water to counteract ion imbalance into the cell. cause cell repture?

solution: animal and bacteria cells actively pump out inorganic ions (esp K), so that cytoplasm contains a lower total conc of inorganic ions than the ECF.

34
Q

explain where the different exogenic and endogenic reactions occur in the coupled reaction of glucose breakdown and protein synthesis?

A

Coupled reaction of glucose breakdown and protein synthesis

exergonic reaction: glucose breakdown -> Co2 + h20 + heat

endogonic reaction: ATP synthesis

Exergonic reaction: ATP breakdown

Endergonic reaction: protein synthesis

GET NET EXERGENIC REACTION

35
Q
  • where does glycolysis occur?
  • what is high level overview of reaction?
    a) what produced in aerobic
    b) what produced in anaerobic conditions?
A

glycolysis

location: cytoplasm

conditons: with / without oxygen

high level overview of reaction:

glucose (6C) –> 2 molecules pyruvate (3C). uses 2ATP in reaction. BUT produces 4 ATPs overall. also produces 2 NADH2+ molecules.

THEN:

  • if in aerobic conditions: pyruvate used to generate Acetyl CoA for citric cycle
  • if in anaerobic conditions: pyruvate used to generate Acetyl CoA for lactic acid
36
Q

how does krebs cycle occur? where? what does it produce?

A

location: matrix of mitochondria
- Acetyl-CoA (from glycolysis) used, extracts electrons for use in electron transport
- Electrons given off are harnessed by electron carrier molecules
- produces: Co2, 3NADH, 1 FADH2, 1GTP. feeds into oxidative phosphorylation pathway
- role in producing energy even in cells performing fermentation

37
Q

how does ETC occur?

A

- location: mitochondrial membrane

  • 4 protein complexes (I to IV): electrons are passed from one complex to next, causes electrons to be released
  • as electrons are released to acceptors from donors (e.g. NADH), H ions pumped out of the matrix into intramembrane space
  • Proton motive force established and electrons flow down electrochem gradient through ATP synthase channel
38
Q

what is the complement system?
what are the three main functions?

A
39
Q

Q

cholera toxin:

  • produced by?
  • what does it do in the body?
  • does it induce ^?
A

Cholera toxin

produced by: Vibrio cholerae
effect: speeds up normal excreotry process in gut epithelium: massive fluid loss. diarrhoea
induces diarrhoea by:
- A-B toxin
- A part activates cell’s G-protein, modifies G-protein and keeps it in active state
- causes more and more production of adenylate cyclase: causes more cAMP
- this stimulates CFTR channel to have more Cl- leave cell: imbalance of electrolytes
- water follows Cl- and electrolytes
- causes severe diaarhea
- treatment: fluodsa and electroyltes

40
Q

name 3 A-B toxins, what they cause and by which bacteria

A

- Dipertheria: toxin inhibits protein synthesis in heart muscle and and other cells. produced by Corynebacterium diptheriaie

- Tetanus: toxin affects neuromuscular junctions - blocks release of NT (GABA and glycine) in CNS. causes irreversible contraction of muscle and spastic paraylsis. Clostridium tetani

  • Botulism: toxin affects neuromuscular junctions - prevents release of excitatory NM (acetyl choline): lack of stimulus to muscle and flaccid paralysis. Clostridium botulinum
41
Q

which drugs target bacterial cell walls? how work?

explain how pencillin works

explain how glycopeptide antibiotics work

explain how polymyxins work

A
  • *beta-lactam antiobiotics: inhibit cell wall synthesis**
    work: inhibit step in synthesis of peptidoglycan (most contain a B-lactam ring). causes cells to osmotically lyse. e.g:

pencillin:
bacterial cell wall grows: get cross links between cell wall by pentaglycine (using enyzme transpeptidase)
penecillin acts as a mimic: as a substrate for transpeptidase. blocks it working

  • *glycopeptide antibiotics:**
  • too big to get through cell wall
  • block D-ala residues (D-ala form the cell wall cross links) from forming cross links by forming H-bonds between the D-ala
  • used on gram-positive bacteria
  • *polymyxins**:
  • bind to charge structures of cell walls on gram negative bacteria
  • changes the charge
  • this destabilises cell wall
  • rupture
42
Q
A
  • bacterial plasmid makes a toxin and an antidote - antitoxin
  • antitoxin degraded by intracellular enzymes
  • toxin is not degradeed
  • if daughter cell does not inherit the plasmid - cant synthesie the antitoxin = death
  • ensures that daughter cells carry the plasmid

plasmid addiction systems are now on the same plasmids as the resistance genes

43
Q

explain what absolute v relative refractory periods are

A

refractory periods: period time where cell membrane is resetting itself.

  • *absolute refractory period:**
  • the period of time during which a second action potential absolutely cannot be initiated.
  • occurs due to inactivation of Na channels
  • *relative refractory period:**
  • period after firing of nerve when partial repolirasation has occurred a greater than normal stimulis / depolarisation can stimulate a second response
  • peak of AP will be lower (but still goes over threshold)
  • recovering Na channels and open K channels
44
Q

how does chemical synapse work?

A
  • AP passes down axon: depolarisation of presynaptic terminal.

- Ca2+ voltage gated channels open

  • increase in cellular Ca2+ is the trigger to release synaptic vesicles
  • Synaptic vesicle bind to membrane and release neurotransmitter across synaptic cleft
  • NT binds to ionotropic or metabotropic receptors = docking. help from SNARE complex (change from closed to open channels)
  • change in membrane potental (hyper or dep) of post synatpic terminal

ONLY ONE DIRECTION

45
Q

what makes it easier for Ca2+ to diffuse across into presynaptic cleft?

A

calcium concentration outside of cell is 10 000x time higher than inside - large inward concentration and electrical gradient allows free calcium to pass into cell

46
Q

explain ion trapping of aspirin in stomach

A

aspirin: R-COOH. exists in equilibrium of R-COOH (protonated) to R-COO- H+ (un protonated)

  • when take aspirin orally: goes into stomach
  • stomach has low pH, more free H+ ions in solution : pushes aspirin equation to R-COOH (uncharged aspirin, fat soluble, protonated form) = absorbed across stomach mucosa
  • then moves to blood plasma: pH 7.
  • moves to R-COO- + H+ (ionic aspirin, hydrophilic - water soluble) = trapped in blood plasma (where want to be trapped) cant return to stomach.

THEREFORE - NEED TO BE ABSORBED IN THE STOMACH BECAUSE V LITTLE WOULD BE STORED IN AN ALKALI SOLUTION

  • this process = ion trapping
47
Q

what happens in the kidney when you have a tricyclin antidepressant (TCA) overdose?

A
  • pKa = 9.5 (weak base)
  • in the body TCA causes metabolic acidosis
  • in blood: sodium bicarbonate dissociates TCA = charged R-NH2 form: lipid soluble
  • once in acidic urine: reforms R-NH3 form: water soluble
  • excreted
48
Q

how can prodrug use its environment to stop growth of a tumour cell? (e.g. using EGFR)

A

due to different environments:

  • Epidermal Growth Factor Receptor (EGFR) is an oncogene
  • drug is attached to cobolt: in normal o2 conditions = inactive
  • drug moves into hypoxic tissue (the tumour): activated:
  • hypoxic env means cobolt3+ –> cobolt 2+
  • this releases the inhibitor of EGFR to bind to EGFR = switched off / inhbited
49
Q

what are the two types of drug metabolism?

A
  • *phase 1- biotransformation:** drug becomes smaller and more water soluble so the kidney can remove it
  • a polar group is introduced or unmasked (this is the biotransformation) to the drug
  • biotransformation occurs by: oxidation (majority), hydrolysis or reduction
  • some metabolites after this: water soluble enough to be excreted straight away (via kidneys) = metabolite A
  • other drugs may need additional step to make more water soluble / polar -> go to phase 2
  • *phase 2: synthesis** (stick a group onto drug to make it more soluble)
  • conjugation
  • e.g. liverr takes big chem (e.g. glucose) adds it onto drug
  • is able to be excreted
50
Q

describe the differnt pathways of synapses for parasympathetic and sympathetic:

a) general b) adrenal gland c) kidney d) sweat gland

A

parasympathetic:

  • long preganglionic neurons -> synapse = Ach and nicotinic Ach receptor –> short postganglionic neuron: synapse is between Ach and muscarinic receptor at target organ

sympathetic:

most = a

a) short pre ganglionic neuron -> sympathetic ganglion: Ach and nicotinic Ach synapse –> long post-ganglionic neuron to target organ: synpase is between norepinephrine / noadrenaline NT and a or b adrenoreceptor
b) straight to adrenal gland: synapse = Ach N: release of noreinephrine release or epinephrine
c) sweat glands: short preganglionic neurons -> synapse = Ach and nicotinic Ach receptor --> long postganglionic neuron: synapse is between Ach and muscarinic receptor at target organ
d) kidney: short preganglionic neurons -> synapse = Ach and nicotinic Ach receptor --> long post ganglionic neuron -> synapse between dopamine and dopamine receptors

51
Q

how does cell migration in the ECM occur?

A
  1. Polymerization of actin filaments at leading edge gives a protrusive force EXTENSION
  2. New adhesions are rapidly linked to network of actin filaments. ADHESION
  3. Combined activity of retrograde actin movement & contractile forces produced by stress fibers generates tension to pull cell body forward. TRANSLOCATION
  4. Forces produced by contractile network combined with actin filament & disassembly help to retract the trailing cell edge. DE-ADHESION

eat all the dick

52
Q

what is Leukocyte extravasation and what are the five steps of the mechanism?

A

= is the movement of leukocytes out of the circulatory system and towards the site of tissue damage or infection

Five steps: (1) rolling and (2) adhesion to the endothelium, (3) passage through the endothelial layer (4) remaining in the venular wall, and (5) passage through the basement membrane.

FunMed Random (19 decks)

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