Structure

Microfilaments- provide movement

Microtubules- Contron size and shape

Starts with Glycolgenic pathway

Little energy in cytoplasm

Pyruic acid builds up and creats lactic acid that damages the cell

Aerobic metabolism stops> Less ATP is produced> NA/K pump can't run and causes cell to swell

Lots of energy in Mitchocondria

Molecules diffuse accross membrane with help

Pinocytosis- form a vacuole= no chem bond

Carrier Protien- helps drap= Chemical bond

G-protien

Enzme linked

Ion Channel

Open when ion gradiant changes according to voltage

*Concentration on ions in and out of cell. cells depend on electrical single

cell firing occurs in response to

chemical, Electricle, physical- Activity

Stimulus

Cell is neg

stimulus causes some NA+ channels to open

NA+ rushes in making cell +

At threshold more NA Channels open

After threshold NA rushes in making cell very += Depol

AP cells respond by contracting

K+ channels open

K diffuses out making cell neg Repol

Na/K pump remove NA and pump K back in

When ever our cells adapt their is gonna be change

 Name 5 ways and what is wrst?

Atrophy- wasting away

Hypertrophy- enlarge

Hyperplasia- more cells created

Metaplasia- Cells change in type

Dysplasia-WORST- Abnormal cells

Direct

Free radicals

Calcium homostasis

Hypoxia

Free Radicals- cell damage

Unpaired electrons in outter shell

Veryunstable and damage cell

removed by antioxidants

inhibit action of reactive 02

*MUST HAVE GOOD BF TO HAVE GOOD 02*

Aerobic- metabolism>Less ATP> Na/K can't run fast enough cell swells

Anarobis met>pyruic>Lactic>acid damages cell mem, intracellular structures and DNA

Calcium homeostasis is important...excess damage could be caused by ishemia or toxins

Act as 2nd messenger in cell

Excess opening= more calcium gates in cell mem causing calcium causcade... This causes denaturing of protien, atp depletion and eventually shut cell down

Cortisol- Alter glucose, fat and protien met

Epi/norepi- SNS activation, ^BP & HR, Decrease urine output

Renis- Angio 2 vasoconstriction

ADH- vasoconstrict, decrease urine

1. Heart>^HR & strenght=^BP

2. Blood vessels> vasonconstrict in skin, gut and kidneys- ^ BP

*ALL ABOUT PERIPHERIAL CONSTRICTION

Cortisol.. Reulates in 2 ways

1. Alters glucose fat and protien met

2. Suppresses immun and inflam response

Decrease urine in kidney

Kidney release renin

A1-weak

Ace- lungs

A2- strong vasoconstriction

adrenal cortex

aldosterone

Vasoconstricts

Kidneys reabsorb water from urine to blood

1. Mutastion of protoncogene
2. Mutation of tumor suppressor gene

Const reproduce

Spred/ metastise

imortal

can act like normal tissue

take up resources

Malignant- poor differentiated

benign- look like normal tissue

Present @ birth

does not distinguish among diff types

Mech include:Epithelial barriers, phag cells, killer cells, plasma protiens

Nutrophils- 1st respnders, phagocytic, release protease and cytokines- break protien

Macrophages- fixed or magratory, phag, enhance inplamm resonce to active in healing

Dendrite- APC show to T&B cells lyphocyte

NK- undiff lymphocyte, special to cancer

What is acquired immunity

Something that you have ben exsposed to

Humoral- antibody in blood that attack specific antigen

Cell mediated- phagocystic attack specific antigen, T lymph

serious 20 plasma protiens that promote and enhance immune inlamation function- activated by antigen or metabolic function

Opsonization- coats bacteria

chemotaxis- cytokines to attact

Cell mem attack complex- final event

Start with platelet plug over injury

coagulation cascade begines forms a mesh

Fibrin makes clot

Plasmin breaks the clot

4 types of Hyp sence Reaction

1- Allergic/anaphalactic

2. Antibody mediated

3. Immune- complex mediated

4- Tcell mediated

Antibodies block @ receptor sight

* antibodies against our specific cell

Inappropriate responce that causes our tissues to get injured

Immunce complex mediated- deposited in tissues and activate complement... causes tissue damage d/t inflammation responce, plaque formed. inappropriate responce

Abnormal t cells attack tissue antigen

Delayed- type hypersensitivity

Direct killing of all viral infections

*For unknown cause t cells can't get activated

ateries vein dilate to increase bf to injury= redness &warmth

Cap become per to allow exudate to exscape to tissue= swelling &pain

Inflamm mediators released

Destroy infective organism

Remove damage cells

Release more inflamm mediators to control further inflammation and healing

Thrombopoeting:stimulate production

Made in liver kidney smooth m, bone marrow

Megakarocytes:formed in bone marrown break apart to form platelets

Stored in spleen live 8-9days

Monocytes/macrophages

APC

Phagocyte

Create inflam mediators

healiong

Aquired/lymphoid

T Lymphocytes

Tcells

control immune response

cell mediated immunity

Poor Perfusion as a result of vessel incomp

* all the fluid leaves vasc space to tissue

Increase BP pulls fluid from vasc space..Brain will create osmoles that will hold onto water there fore increase salt levels will not effect brain

Give fluid slow isotonic

exchange H+ for buffer change in PH

increase K increase membrain potential

HRT can be affected

*Controls resting mem potential

Cofact in enzyme reaction

reg ca+ levels by binding to receptors

Interdependant with k+- alters hrt rhythem life threatening

*causes hrt dysrythmias

Hypercalemia- blocks na+ gates- muscle cell control excessive firing= nerve mess able to fire

Hypocalemia. block rewer na+ nerve fire more easy

Alkalosis= not enough H+. block k> hypokalemia

Acidosis= too manh h+> blood k increaes hyperkalemia

Blood gas levels

Ph

Paco2

Hc03

7.34- 7.45

35- 45

22- 26

How tight Hgb to bond with 02

High hgb= bind easy= acidotic

low hgb= release 02 more= alkolotic

periphery= carotid

central= medulla oblongota

Stimulus- hypoxic 02

if paco2- this will kick in to make you breath can depend on

Depend on pheripheral

this is only pt you want to be hypoxic

chronic increase PC02

Pt will want 02 up but you cant d/t it wil short out pheripheral and your central system won't kick in

Air in plura cavity

air takes up space restricts lung

partial or complete collapse

increase pressure can move trak and mediastinum to opp side of chest

Chronic infection d/t hypersecretion

increase globlet cells

airway plugging, inflammation

lung chroncally inflammed as result leads to cor pulm

Barrel chest

Increase air space & destruction alveoli ts chronically sob

Start= lung exspode to hypoxia causes damage tissue starts inflammation process causes= scar tissue

Hypoxia that does not respond to ^02

d/t lung injury or inflam mediators this leads to scar tissue= 02

large lipid core

thin fibrous cap

fissured cap

inflam w/i cap

superficual endothelial erosion

chest pain

Sob

diaphoresis

ecg change

Where it starts

cardiac starts at hrt- causes decrease C/o

distribuative starts with bad perfussion at tissue level, causes excessive relase inflamm mediator

Hrt Failure L vs R

R= congestion peripherial tissue= fluid in body

L= decrease c/0 pulm congestion= fluid in lungs

Emema

Hyperlipidemia

Hypercoagibility

decrease immune comp

Chonic infect= inflam

repeat kidney infection

prevent healing

can lead to kidney failure

damage to glomerlus 2 ways to get

1. membrane antibodies

2. complex decomposition

Prerenal= decrease bs to kidney

Intrarenal= intrinsic tubule funct

Post renal= urine flow is blocked cause a build up and lead to compartment syndrome

colitis= parital mucosa linning

Chrons transmural more likey to dies w/ infection

Fibrotic scar tissue

gallbladder problem

viral hep

bile duct problem

idiopathic

fatty liver

alcoholic hep- can turn around

cirrhpis= cant help

lots of extra fluid

under high pressure

0 colloud pressure

moves out in to peritoneal space

decrease colloid

increase hydro

aldosterone and adh remain in blood