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84 Cards in this Set

  • Front
  • Back

non specific defense

1 barriers to entry


2 activation of innate immunity


3 phagocytosis


4 fever


5 interferon


6 inflammatory responce

activation of innate immunity

PAMPs (surface proteins)


Toll like receptors ( on immune cells)


recognize foreign objects



phagocytosis

cell eating



steps of phagocytosis

rolling-capture-activation-spreading-extravasation

fever

due to a chemical called pyrogen ( increases body heat)



why are fevers good short term

-increases phagocytosis (work good under higher temperatures)


-iron sequester in spleen and liver (pathogens are unable to multiply)

interferon

chemical released from affected viral or cancer cell, it has antiviral or anticancer properties



inflammatory response

complement triggers mast cell to release histamine which causes vasodilatation then extravasation

specific defense

t-cells and b-cells

t-cells

-cell mediated immunity


-mature in the Thymus


-killer T-cells release perfurin ( which makes holes in the cell membrane)



b-cells

-antibody mediated immunity


-mature in the bone marrow


-plasma cells (secrete antibodies)


-memory cells( hangout in lymphatic cells until needed)



actions of antibodies

-agglutination (clumping/dying)


-neutralize bacterial toxins


-opsonizations (stimulates phagocytosis)


-complement activation (protein cascade system puts holes in membrane)

primary response

first time a pathogen enters the body, typically takes 3 to 5 weeks

secondary response

after the first time a pathogen enters the body, typically takes a day to recognize because of memory cells

types of acquired immunity

active-antiges


passive- antibodies


natural- not injected


artificial- vaccinations

sever immunodeficiency disorder

born without a thymus, there for no T-cells and no cell mediated immunity

allergies



immune response to nonpathogenic substances ( a lot of inflammation occurs)

immediate hypersensitivity

B-cells


antihistamines and adrenergic drugs


ex: epi pen

delayed hypersensitivity

T-cells


corticosteroids

lymphatic system function

-transport water


-transport and absorb lipids


-defense/immunity

arteries

-carry blood away from the heart (oxygenated).


-pressure system


-tunica media is much thicker because it deals with high levels of pressure



vasoconstriction

blood vessel diameter decreases ( pressure increases)

vasodilatation

blood vessel diameter increases (pressure decreases)

veins

-carries blood to the heart (deoxygenated)


-volume resivor


-contain valves


-tunica media is thinner because it does not handle high levels of pressure

how does blood return to the heart?

-gravity


-respiratory pump


-skeletal muscle pump

capillaries

-site of material exchange


-1 cell membrane thick (endothelium)


-material exchanges by filtration and diffusion

systolic pressure

arterial pressure during ventricular contraction

diastolic pressure

arterial pressure during ventricular relaxation

normal blood pressure range

120/80

prehypertension

120-139/80-89


are likely to develop hypertension if you do not make major life changes

hypertension

140+/90+


high blood pressure



why is hypertension bad?

if you have an increase in blood pressure this means you have an increase in in pressure filtration and long term this causes tissue edema. could also cause stroke

hypotension

below normal range in blood pressure

why is hypotension bad?

because to low of blood pressure could shut off pressure filtration completely and cause tissue to die

formula for net pressure

net pressure=BP-PCOP




BP-blood pressure


PCOP- plasma colloidal osmotic pressure


(dissolved albumin)

positive number in pressure filtration

filtration

negative number in pressure filtration

reabsorption

Mean arterial pressure (MAP) function and formula

MAP= CO xPR




helps regulate pressure filtration

factors that affect MAP

-blood volume


-blood viscosity


-vessel diameter/nervous system


-barcoreceptors and vasomotor center

erythrocytes

-RBC


-lack a nucleus so have 120 day life span


-main function is to transport oxygen and carbon dioxide via hemoglobin

hemoglobin

respiratory pigment in RBC. they are divided into four subunits and each unit contains a HEME group. Within the heme group is an iron and each iron can bind to one oxygen for transport. GLOBIN binds to carbon dioxide for transport.

erythrocytosis

increased RBC count. could be to high elevations or blood dopping.

erythropoietin

hormone released by the kidneys to stimulate RBC production.

erythrocytopenia

decreased RBC count. could be because of anemia

anemia

lack of hemoglobin


(low iron and vitamin B12)

RBC destruction

RBCs are destroyed in the spleen by macrophages (monocytes) via phagocytosis. When RBCs are broken down they recycle iron and bilirubin (makes bile) is released.

Physiological Jaundice

increased level of bilirubin in babies who's livers are properly not functioning yet. Yellow skin color

plasma and plasma proteins


albumin

regulates blood pressure, released by the liver

plasma and plasma proteins

antibodies/components

immune response

plasma and plasma proteins

fibrinogen

important factor in blood clotting (hemostasis)

platelet function

involved in hemostasis (stoppage of bleeding)

steps of clot formation

1- vasoconstriction


2-platelet plug formation


3-coagulation

Step 1 of clot formation

vasoconstriction, blood vessel diameter decreases which reduces the blood flow to site

step 2 of clot formations

platelet plug formation


platelets are not active when they reach site so ADP activates platelets and VWF makes everything stick together

step 3 of clot formation

Coagulation


fibrinogen is converted to fibrin by: Ca, protein factos, and prothrombin is converted to thrombin

blood clotting disorder

hemophilia- blood does not clot (inherited)


vitamin K deficiency (acquired)



systemic circulation

blood is being pumped throughout the body, left ventricle, heart wall is much thicker because it handles high pressures pumping the blood throughout the entire body

pulmonary circulation

pumps blood to the lungs, right ventricle, heart wall is thinner because it is not dealing with high pressures and only has to pump to the lungs

systole

phase of ventricular contractions

diastole

phase of ventricular relaxation

equation for pulse pressure

pulse pressure= systolic pressure-diastolic pressure

lub

first sound of the heart, it is the A-V valve closing

dub

second sound of the heart, the semilunar valve closing

heart murmur

due to leaky valves, less blood being pumped out of the heart because of backflow

equation for cardiac output

CO= HR x SV




if increase in PP than increase in SV, if decrease in PP than decrease in SV

Regulation of cardiac output


pace maker

SA node in the right atrium sets the rhythm of heart

Regulation of cardiac output

nervous system

sympathetic- fight or flight (increases HR and SV)

parasympathetic- rest and digest (decrease HR)


Regulation of cardiac output

hormones

epinephrine

Regulation of cardiac output

auto regulation

Frank-Starling law= an increase stretch on the heart will increase the force of contraction to a limit

congestive heart failure

when the heart passes the level of stretch

arteriosclerosis

hardening of the arteries, a build up of lipids and cholesterol thus decreasing the blood vessel diameter and blood flow

HDL

high density lipoprotein


increase in proteins and a decrease in lipid


LOW CHOLESTEROL "good"

LDL

low density lipoprotein


decrease in protein and increase in lipid


HIGH CHOLESTEROL "bad"

stain drugs

can decrease LDL and increase HDL (reverse the affects)

Ischemic heart disease

Heart attack, low blood flow into the heart muscles thus low levels of oxygen in muscle which causes the muscle to die




fixing it by angioplasty and coronary bypass surgery

ventilation

breathing

inspiration

moving air into the lungs from the environment, the diaphragm and external intercostals are involved. NEGATIVE PRESSURE SYSTEM, when diaphragm contracts(moves down) it increases the volume and decreases the pressure

expirations

air moving from the lungs to the environment, POSITIVE PRESSURE SYSTEM, diaphragm relaxes (moves up) it decreases the volume and increases pressure

equation for minute volume

minute volume= tidal volume x breathing rate

Chronic bronchitis

inflammation of the bronchi and bronchioles


emphysema

alveolar wall destruction, it decreases the surface area for gas exchanges and CO2 gets trapped making it hard to expire

asthema

increased amount of bronchiole construction which reduces air flow to lungs

pulmonary surfactant

lipoprotein secreted by type 2 alveolar cells which decreases surface tension and prevents alveolar wall collapse

respiratory distress syndrome

surfactant is produced 24-27 weeks




premature babies are placed in hyperberic oxygen chambers so they can have gas exchange occur until surfactant is produced.