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Boards II > Cell Physiology > Flashcards

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
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2
Q

Glycolipid

  • what is it
  • main role
A
  • lipid with card attached

- cell membrane, serve as markers for cell recognition

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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
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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
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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)
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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
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7
Q

Connecting Proteins

Fibronectin

A
  • connect cells to collagen fibers in ECM allowing cells to move through ECM
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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
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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
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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
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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
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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
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13
Q

The most common cause of irreversible cell injury

- what is injured

A
  • ischemia

- nuclear, lysosomal, mito

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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
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15
Q

2 tyoes cell death

A
  • apoptosis (programed) and necrosis (non-programed)
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16
Q

Nucelar side

  • karyolysis
  • pyknosis
  • karyorrhesis
A
  • dissolving of nucleus
  • nuclear fading
  • nuclear shrinkage
  • nuclear fragmentation -> nuc membrane has to rupture
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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
Q

Complement Cascade

  • function
  • pathway
  • other function of C3b
A
  • 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
Q

Kinin system

  • pathway
  • othery function of kallikrien
A
  • 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
Q

Vascular respone to injury

  • vasodilation
  • exudation
  • margination and emigration
A
  • 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
Q

Extravasation

  • p selectin
  • chemoattraction,
  • rolling adhesion
  • tight adhesion,
  • transmigration
A
  • 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
Q

Types of CAMS

  • intergrins
  • cadherin
  • selectins
A
  • 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
Q

Cytokines

  • TNF alpha
  • IFN- gamma
  • IL-1
A
  • fever, cytokines, chemotaxis, leukocyte, fibroblast
  • tumor suppressor
  • causes fever, produces cytokines, chemotaxis
31
Q

Wound healing

  • bleeding
  • inflamm
  • proliferative
  • remodeling
A
  • making clot
  • inflammation comes in and makes sure no infection
  • creating collagen
  • strenghtening collagen
32
Q

Time frame

  • 1-5 min
  • 10-30 min
  • 1hr- 1 month
  • 1 day - 1 month
  • 1 wk - 2 yrs
A
  • 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
Q

Coagulation Cascade

  • Intrinsic: pathway, test w
  • extrinsic, test w
A
  • 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
Q

Regulators of thrombosis

  • protein C: function, activation
  • anti-thrombin: function, increased work
  • Tissue factor pathway inhibitor
  • plasmin: function, activated by
  • prostacyclin: function; created by
A
  • 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
Q

Angiogenesis

- what happens

A
  • 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
Q

Function of fibroblasts in wound healing

- it is same?

A
  • 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
Q

Contraction

  • how does it occur?
  • which way
A
  • 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
Q

Epithelialization

  • what is it
  • secrete plasminogen activator
  • collagenases and matrix metalloproteinases
A
  • keratinocyte on top of granulation tissue but under scab
  • to dissolve scab
  • dissolved parts of damaged ECM
39
Q

Maturation

  • what is it
  • tensile strength
A
  • type 3 collagen replaced by Type 1 collagen

- 50% after 3 months and 80% after 6 months

40
Q

Chronic Inflammation

  • what is it
  • characteristics
  • fibrosis
  • granuloma: what is it
A
  • 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

Boards II (20 decks)

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