Cell Physiology Flashcards
1
Q
Cytoskeleton
- what is it
- function
- microtubules
- intermediate filaments
- microfilaments
- kartegeners
A
- scaffolding of cell
- size and shape of cell, transportation
- alpha and beta tubulin, cilia and flagella, mitotic spindles, cell structure; 2 in center with central bridge then 9 pairs of microtubules around it, connected by nexia; have dynein arms allowng for cilia and flagella to move
- IF proteins; allow for cell to undergo stress because they are springy
- actin subunits; flexible, used for cytokinesis
- problem with dynein
2
Q
Glycolipid
- what is it
- main role
A
- lipid with card attached
- cell membrane, serve as markers for cell recognition
3
Q
Cell channels
- what are they
- transporter vs channel
- GAP junction
A
- proteins embedded into cell membrane
- T: use ATP and C: do not use ATP
- connections between cells allowing for cytoplasm from two cells to touch; allows for free passage of molecules
4
Q
Extra cellular matrix
- what is it
- ground substance
- fibers
- cells
A
- now considered largest organ in body
- ordinary: water, glycosaminoglycans (complex carbs -> attracts Na and pulls in fluid to ECM), proteoglycans and glycoproteins; bone: minerals, blood: plasma
- collagen and elastin
- fibroblast, adipocyte, mast cells
5
Q
GAGs
- heparin sulfate: what is it, function
- chondroitin sulfate: function
- keratan sulfate: function
- hyaluronic acid: functoin
A
- one of the glycosaminoglycans that helps with angiogenesis, blood coagulation, tumor mets and developemntal processes
- part of cartilage, provides tensile strength to tendon, ligaments and aorta; role in neuroplasticity by stabilizing normal brain synapses
- huge part of developing cornea and keeping tranperancy of cornea; also part of cartilage and bone; secreted by glial cells and helps with gliosis
- part of articular cartilage. It absorbs water and resists compressive force (shock absorber)
6
Q
Fibers: Collagen
- function
- formation
A
- most abundant protein in ECM, makes 9/10 of bony matrix, and provides structural support for surrounding cells
- pre-procollagen -> pro- collagen (3 form alpha helix) -> cleaved on both sides to make
7
Q
Connecting Proteins
Fibronectin
A
- connect cells to collagen fibers in ECM allowing cells to move through ECM
8
Q
Basement membrane
- where
A
- thin fibrouc structure under epi and endothelium; lines cavities and surface of organs and skin
- epi -> basement membrane -> CT
- anchor epi to underlying CT
- stimulates angoigensis
9
Q
Epidermolysis Bullosa
- caused by
- causes
- sequelae
- prognosis
A
- loss of anchoring proteins of epi to BM
- skin detaches from BM
- high risk infection
- 1 to 5 yrs old
10
Q
Good Pastures Syndrome
- what is it
- sxs
- epi
- tx
A
- AI dx that attacks BM in lung and kidney bc they have type IV collagen
- hemoptysis and hematuria
- young males
- heavy immunosuppression
11
Q
Cytokeratin
- what is it
- used for
A
- keratin containing intermediate filaments that make up cytoskeleton of all epi cells
- IH marker for epi derived cancers
12
Q
Roles of Epi
6
A
- protection
- diffusion: alveoli allow for diffusion of O2 and CO2
- secretion
- excretion: kidney and skin
- absorption: GI tract
- stretch: bladder (dome when unstretched and squamous when stretched out), uterus, GI, blood vessels
13
Q
The most common cause of irreversible cell injury
- what is injured
A
- ischemia
- nuclear, lysosomal, mito
14
Q
Apoptosis steps
- how
- intrinsic
- extrinsic
A
- apoptotic bodies are formed and then those bodies are phagocytosed by macrophage
- ROS or Hypoxia activate p53 -> cytochrome c release from mito into cytoplasm -> capase 9 activated -> caspase 3,6,7 -> apoptosis
- IL-1, TNF, LPS binds to death receptor -> activated caspase 8, 10 -> activates capase 3,6,7 -> apoptosis
15
Q
2 tyoes cell death
A
- apoptosis (programed) and necrosis (non-programed)
16
Q
Nucelar side
- karyolysis
- pyknosis
- karyorrhesis
A
- dissolving of nucleus
- nuclear fading
- nuclear shrinkage
- nuclear fragmentation -> nuc membrane has to rupture
17
Q
Necrosis
- caused by
- similar to apoptosis
- coagulative: caused by; characteristics
- fibrinoid
- caseous: caused by, characteristics
- noncaseating (granulomas)
- Fat: location, caused by, saponification
- Liquefaactive
A
- external factors
- only the nucleoside part
- blebb formation but as one giant bubble that then bursts and all cell stuff is released
- ischemia, spider bites, MI; tissue architecture stays same but with pink cytoplasm
- rheumatoid, vasculitis, and auto immune disorders; accumulation of protein material
- TB; cheesy consistency
- Fungal infection (histoplasmosis), sarcoidosis, chronic granulomatous dx, chrons dx, leprosy, cat scratch
- In fatty organ; breast - trauma to breast, pancreas is from pancreatitis; saponification is when FA combine with Ca
- brain ischemia; complete digestion and removal of necrotic tissue with formation of cystic cavity (no remainder of architecture) -> cannot be treated with abx, must cut and drain
18
Q
Concentration gradient
- electrolytes that want n cell
- electrolytes that want out of cell
A
- Na, Cl, HCO3, Mg
- K
19
Q
Electrolyte movement
- depolarization
- repolarization
- hyperpolarization
- reopening of Na/ K atpase
A
M gate opens -> Na influx -> upstroke -> H gate gloses -> terminate up stroke
- Voltage gated K channels open
- Too much K released, both m gate and h gate closed
- H gate opens back up ready for another AP
20
Q
Electrocution
- worried about
- plan
- platelets
A
- arrythmias and seizures
- will admit and watch 24 hrs
- electrical current runs through blood giving platelets negative charge and repellng them from BM inhibiting them from making platelet clots
21
Q
Diffusion
- fat soluble
- water soluble
- most important factor
- reflection co-efficient
A
- all steroid are fat soluble and able to freely pass through membranes and bind to nuclear receptor to affect transcription; cortisol is steroid that binds to cytoplasmic receptor; regulated by intracellular concentration
- has to bind to membrane bound receptor in order to get into cell
- concentration
- permeability of membrane to particular solute
22
Q
Transport Proteins
- primary
- seconday
- symport
- antiport
- carrier
A
- Na/K ATPase
- Na/ Ca exchanger -> uses energy from one of ion moving down its concentration gradient
- moves in same direction as Na ,Na/ glucose
- moves in opp direction of Na, Na/ Ca
- uses carrier proteins and can only transport a certain amount (Na/ gluc in PCT)
23
Q
Acute Inflammation
- pathway
- next step
A
- PRR on macro recognizes PAMP -> releases cytokines
- activates fibrinolysis, complement, kinin and coagulation cascade
24
Q
Fibrinolytic Pathway
- function
A
- produces inflamm mediators, counterbalances clotting cascade,
- plasminogen uses TPA to make plasmin -> plasmin acts on fibrin clot and degrades it
25
Complement Cascade
- function
- pathway
- other function of C3b
- creates MAC and other proteins to helps with degradation and infected cell destruction
- c1 converts C2 into C2b and C4 into C4 b -> C2b and C4b combine to form C3 convertase -> converts C3 into C3a (vasodilation, chemotaxis) and C3b -> C2b, C3b, C4b combine to make C5 convertase -> converts C5 into C5a (vasodilation, capillary leak, chemtaxis) and C5b -> C5b + C6, C7, C8, C9 form MAC and punch holes in bacteria to kill them
- C3b can also be used for opsinozation
26
Kinin system
- pathway
- othery function of kallikrien
- pre-kallikrein to kallikrein w/ factor XII -> kallikrein converts High Molecular Weight Kininogen to bradykinin -> activates pain receptors, chemotaxis, vasodilation, etx
- kallikrien can also convet plasminogen into plasmin
27
Vascular respone to injury
- vasodilation
- exudation
- margination and emigration
- allows for fibrin, Ig, PMNs to get to site of injury
- the extra fluid in area funneled through lymph whoch can activate that immune system if it hasnt been activated yet
- when PMN makes it outside of vessel and into ECS so that it can digest debris and bugs
28
Extravasation
- p selectin
- chemoattraction,
- rolling adhesion
- tight adhesion,
- transmigration
- from cytokines (IL1, TNF alpha) and various pathways (complement and kinin)
- cytokines cause for endothelial cells to express p selectin allowing PMN to attach; p selectin forms transient bond with PMN causing it to slow down
- P selectin and ICAM1 expressed at place where it needs to stop and PMN binds with VCAM-1 causing the PMN to come to stop
- PMN spreads out, extens psuefopods and pass through gaps between endo cells using PECAMS and then binds to ECM via integrins and CD44 then phagocytoses
29
Types of CAMS
- intergrins
- cadherin
- selectins
- allow cell to connect with collagen, fibrinogen, fibrinoctin alowing for links between extracellular environment and cell
- calcium dependent adherance molecule; runs between actin filaments
- bind fucosylated carbs like mucin and also known as CD62; specific p selectin will bind to inflamm cell through psgl1
30
Cytokines
- TNF alpha
- IFN- gamma
- IL-1
- fever, cytokines, chemotaxis, leukocyte, fibroblast
- tumor suppressor
- causes fever, produces cytokines, chemotaxis
31
Wound healing
- bleeding
- inflamm
- proliferative
- remodeling
- making clot
- inflammation comes in and makes sure no infection
- creating collagen
- strenghtening collagen
32
Time frame
- 1-5 min
- 10-30 min
- 1hr- 1 month
- 1 day - 1 month
- 1 wk - 2 yrs
- vasoconstriction (thrombaxane and prostaglandin cause vasospasm until hemostasis (clotting) is achieved)
- vasodilation
- inflammation -> produces granulation tissue and new epi
- wound contraction w/ matrix metalloproteinase and myofibroblast accumulation-> contract wound edges to heal faster but can produce deformities if in a bad area
- remodeling
33
Coagulation Cascade
- Intrinsic: pathway, test w
- extrinsic, test w
- 12 +11 -> 11a -> 11a+ 9-> 9a -> 9a+8 +10 -> 10a -> 10a+5 +2 -> 2a -> 2a + fibrinogen -> fibrin; PTT
- 3 + 7 -> 7a -> 7a +10 -> 10a -> then common pathway; PT
34
Regulators of thrombosis
- protein C: function, activation
- anti-thrombin: function, increased work
- Tissue factor pathway inhibitor
- plasmin: function, activated by
- prostacyclin: function; created by
- main anticoagulant that binds to factor 5a and 8a; activated by vit K
- inactivates thrombin, 9a, 10a, 11a, 12a; constantly active but heparin makes it work better
- inhibits factor 3a
- breaks down fibrin into d-dimers; activated by tPA
- binds to platelets Gs protein -> increases AC in cell -> increase in cAMP -> decreases Ca -> inhibits release of granules that would activate surrounding platelets; made by endothelium
35
Angiogenesis
| - what happens
- fibroblasts enter injury site, release fibronectin which attracts endothelial cells, then pericytes are attracted to area and begin to reconstruct the vessel including a new BM
36
Function of fibroblasts in wound healing
| - it is same?
- use fibrin from clot to create scaffolding and recoop the ECM then secretes collagen (type 3) to help harden it up
- no is made up of fibronectin and hyaluronic acid to keep moist to aid in wound healing -> but later replaced by normal ECM (type 1 collagen)
37
Contraction
- how does it occur?
- which way
- some fibroblasts are turned into myofibroblasts because of tension in matrix which will help to pull wound together
- will only pull in one direction
38
Epithelialization
- what is it
- secrete plasminogen activator
- collagenases and matrix metalloproteinases
- keratinocyte on top of granulation tissue but under scab
- to dissolve scab
- dissolved parts of damaged ECM
39
Maturation
- what is it
- tensile strength
- type 3 collagen replaced by Type 1 collagen
| - 50% after 3 months and 80% after 6 months
40
Chronic Inflammation
- what is it
- characteristics
- fibrosis
- granuloma: what is it
- persistent reaction to injury -> unable to get out of inflammatory phase to allow for healing
- will have macrophages and lymphocytes, plasma cells, destruction of tissue, and diff stages of repair
- scar tissue
- macrophages surrounded by CD8 cells and some firoblasts walling off foreign entity
