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P215 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Major functions of the circulatory system

A
  1. transportation of O2, nutrients, hormones, waste 2. temp regulation 3. immune function 4. wound care
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2
Q

Atria

A

left and right, small higher pressure than the ventricles

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3
Q

Ventricles

A

left and right, very strong higher pressure generated

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4
Q

AV Valves

A

one way valves, only PRESSURE opens valves -tricuspid: RA and RV -mitral: LA and LV

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5
Q

Chordae TEndinae

A

at bottom of AV valves structural support to help stay sealed, prevent AV valves from being pushed in atria

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6
Q

Papillary Muscles

A

continuous with ventricular muscle

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7
Q

Semilunar Valves

A

pulmonary: out to the blood (R) aortic: out to the body (L) much thicker, no extra support

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8
Q

Septum

A

divides L from R APs can go L -> R with no inhibition

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9
Q

Fibrous Skeleton

A

non conductive, includes all 4 valves doesn’t share AP’s directly

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10
Q

Differences of Endocrine and Nervous System

A

-signal accuracy -signal speed -signal duration -cortical control

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11
Q

Endocrine Glands

A

-ductless, by need basis

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12
Q

3 Functions of Endocrine Glands

A
  1. produce hormone 2. store 3. secrete
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13
Q

Hormones

A

messengers, link to SPECIFIC receptor -initiate action in target tissue

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14
Q

Hypothalamus and Posterior Pituitary

A

-PP is extension of hypothalamus -no direct contact -releases hormones into bloodstream (oxytocin and ADH) **produces final ACTION

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15
Q

Hypothalamus and Anterior Pituitary

A
  1. hypothalamus releases hormones to bloodstream via “releasing hormones” 2. hormones reach gland cells in anterior pituitary 3. gland cells send “stimulating” hormones to distant targets
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16
Q

Hypothalamus-Endocrine Roles

A
  1. produces PP hormones 2. controls Ant. Pit hormone release
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17
Q

Antidiuretic Hormone

A

kidney: increase water absorption

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18
Q

Oxytocin

A

increase uterus contraction in labor, stimulates lactation -key in socialization and trust -increases wound healing rate

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19
Q

Corticotropin-Releasing Hormone (CRH)

A

-increases release of ACTH by the ant. pit.

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20
Q

Thyrotropin-Releasing Hormone (TRH)

A

-increases release of TSH by the ant. pit

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21
Q

Gonadotropin-Releasing Hormone (GnRH)

A

-increases release of FSH and LH by ant. pit.

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22
Q

ACTH Target

A

adrenal cortex to produce cortisol

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23
Q

TSH Target

A

thyroid gland to produce “active” thyroxine (T4)

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24
Q

FSH Target

A

testes/ovaries to produce egg and sperm

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25
Q

LH Target

A

testes/ovaries to produce estrogen and testosterone

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26
Q

Control of Anterior Pit. Function

A

neg. feedback

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27
Q

What happens if hormone levels are too low?

A

sensed by hypothalamus, stimulate MORE hormone

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28
Q

What happens if hormone levels are too high?

A

inhibit hypothalamus and ant. pit.

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29
Q

CRH and Function of Cortisol

A

“stress hormone”: increase blood sugar, BP, pain threshold, and immune response ^normal to acute amounts of stress

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30
Q

Chronic Stress

A

“breaks” negative feedback, chronically high cortisol levels -low cognitive function, immune function -increase BP and blood sugar –> hypertension and type 2 diabetes

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31
Q

Function of Thyroxine

A

helps regulate metabolism **requires iodine to activate hormones

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32
Q

Iodine Deficiency

A

-goiter -inactive thyroxine triggers hypothalamus and ant. pit. to send more hormones, and they send more INACTIVE forms -hypothyroid=gain weight

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33
Q

Function of TEstosterone

A

-stimulate “male” characteristics increase of muscle mass

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34
Q

Anabolic Steroids

A

-mimics testosterone (agonists) hypothalamus and ant. pit. levels increase, but testosterone levels are still low -> problem in testes -gland size becomes smaller (testes shrink)

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35
Q

Endocardium

A

transition smoothly and resistance free

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36
Q

Pericardium

A

attached to the heart, for protection

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37
Q

Epicardium

A

outside layer of the heart, more connective tissue and a layer of fat; protective layer

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38
Q

Myocardium

A

muscular layer, made of cardiac muscle thickness=how much strength

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39
Q

Max HR Equation

A

=220-age ^age = decrease in HR = AP increasing in duration

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40
Q

Electrical Activity of the Heart

A

when one muscle fiber is activated, the entire atria becomes activated very rapidly

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41
Q

Cardiac Muscle Structure

A

striated, sarcomeres, branching = more structural support **use GAP junctions

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42
Q

Cardiac Muscle Function

A

generate pressure to move more blood

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43
Q

Cardiac Muscle Contractile Properties

A

actin and myosin, Ca causing a crossbridge cycle SLOW OXIDATIVE

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44
Q

Cardiac Muscle APs

A

4 APs/sec, resting more than acting, **CANNOT summate

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45
Q

SA node depolarization mechanism

A

once it is depolarized enough with Na, cause Ca channels to open to continue to depolarize Ca causes long plateu and long AP

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46
Q

SA node (Pacemaker Potential)

A

**initiate here “pacemaker”, spontaneously depolarize @ a specific rate, does NOT need help to depolarize travels from RA -> LA very rapidly (via gap junctions) b/c of septum

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47
Q

AV Node

A

acts as antenna to pick up electrical activity (AP), carries AP down to the ventricles

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48
Q

AV Bundle (Bundle of His)

A

insulated wire

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49
Q

L and R bundle branches

A

AP is divided out, does NOT decrease AP into the ventricular muscle!

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50
Q

Purkinje Fibers

A

raw nerve endings, allows the AP out into cardiac muscle (starts @ apex of the heart) **starts bottom -> top to push blood up towards the semilunar valves and closes AV valves so atria has time to do job

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51
Q

____ innervation of the SA node if the primary modifier of HR

A

Autonomic

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52
Q

Sympathetic/ Parasympathetic effect of the SA node

A

sym- increase HR para- decrease HR by decreasing “funny” channel leakage

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53
Q

Sympathetic/Parasympathetic effect of AV node

A

sym- increase conduction rate para- decrease conduction rate

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54
Q

Sympathetic/Parsympathetic effect of Ventricular Muscle

A

sym- increase contraction strength para- none

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55
Q

Bradycardia

A

slow HR at rest (below 60) **endurance athlete -potential contractility contraction of heart muscle?

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56
Q

Norepinephrine

A

open more “funny” channels, muscles contract stronger, and AV node contraction increases

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57
Q

Tachycardia

A

fast HR @ rest (over 100)

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58
Q

Fibrilation

A

heart is contracting and fails to contract in the right order (not generating any pressure), less force output blood flow stops **ventricular is WORST **atria could be fibrilated and ventricles keep working

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59
Q

P-Wave

A

atrial depolarization (contraction)

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60
Q

QRS Complex

A

ventricular depolarization (contraction)

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61
Q

T-Wave

A

repolarization of ventricles (relaxation phase AKA diastole)

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62
Q

Depolarization of Atria and Ventricles

A
  1. SA node generates impulse -> atrial excitation 2. impulse delayed @ AV node 3. impulse passes to apex -> ventricular excitation starts 4. ventricular excitation complete
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63
Q

Cardiac Cycle

A

events in heart during ONE heartbeat

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64
Q

Cardic Cycle Order (1-3)

A
  1. atria begins filling (not due to local pressure) due to a CLOSED CIRCUIT 2. ventricles begin filling due to pressure gradient opening AV valves up to 85-90% full 3. atria contracts b/c SA node depolarizes & fills last 10-15% of ventricle w/ blood from atria
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65
Q

Cardiac Cycle Order (4-6)

A
  1. ventricles contract of AV node 5. atria repolarization (relaxes) 6. ventricles relax **4 & 5 happen at the same time
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66
Q

End Systolic Volume (ESV)

A

min. volume within left ventricle

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67
Q

End Diastolic Volume (EDV)

A

max volume within left ventricle

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68
Q

Stroke Volume (SV)

A

amount of blood that successfully leaves the ventricle in one beat =EDV-ESV

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69
Q

Why is the local BP in and around the heart important?

A

need pressure gradients to open valves

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70
Q

What would happen if cardiac VP was constant? Does it ever happen?

A

blood would stay passively in one place, happens during fibrilation

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71
Q

What is the pressure of blood entering the atria? Why?

A

almost zero, sometimes a neg. pressure due to veins (not pressurizing blood)

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72
Q

What is the pressure of blood in the aorta?

A

120/80

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73
Q

P-V Loop: Point A

A

ESV

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74
Q

P-V Loop: A–>B

A

increase volume, barely increase pressure NOT related ventricles filling

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75
Q

P-V Loop: Point B

A

EDV; AV valves close

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76
Q

P-V Loop: Point B–>C

A

isovolumetric contraction - ventricles contract sarcomeres are contracting; build up pressure must be > than atria

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77
Q

P-V Loop: Point C

A

semilunar valves open ventricular pressure > aortic pressure

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78
Q

P-V Loop: C-> D

A

moving blood to the aorta through semilunar valves ventricles keep contracting -> ejection of blood

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79
Q

P-V Loop: Point D

A

aorta has higher pressure, semilunar valve shuts

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80
Q

P-V Loop: Point D->A

A

ventricle goes into relaxation, keeping AV valves shut “isometric relaxation” phase

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81
Q

Where is ventricular filling on P-V loop?

A

A-B

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82
Q

Where is Atria contracting on P-V loop?

A

Last 10% of A->B

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83
Q

Where is the ventricle contracting on P-V loop?

A

B->C->D

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84
Q

Where is the ventricle relaxation of P-V loop?

A

D->A & A->B

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85
Q

Ventricular “ejection fraction”

A

= SV /EDV **important clinical measure of cardiac efficiency (normal = 50-60% at rest)

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86
Q

The RA receives blood from ____ and sends it to ___, then the RV sends blood to the ____

A

vena cavae, RV, lungs

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87
Q

The LA receives blood from ____, and sends it to ____, then the left ventricle sends to blood to the ____

A

pulmonary vein, LV, aorta->body

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88
Q

Cardiac Output

A

amount of blood that leaves a single ventricle in a minute =SV*HR

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89
Q

Average CArdiac Output

A

5.5 L/min

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90
Q

How long does it take a RBC to travel through the body

A

1 minute

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91
Q

How does EDV affect SV

A

“preload”, increase EDV increases SV

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92
Q

How does total peripheral resistance (TPR) affect SV?

A

impedance to blood flow out of the arteries arterioles and capillaries create the resistance from artery -> vein nutrient exchange, waste exchange increase of pressures on arteriole side = kinking blood vessels ** increase of TPR = decrease SV = increase BP

93
Q

Contractility

A

how much pressure the ventricle generates over cardiac cycle

94
Q

How does contracility affect SV?

A

autonomic activity (extrinsic)- outside of heart, sympathetic increases contractibility Frank-Starling law of the heart (intrisic)- related to length/tension relationship, filling of heart increase contractility = increase SV

95
Q

Cardiac Muscle Length-Tension relationship

A

preload- “stretch” on muscle fibers increase of EDV = increase SV

96
Q

TPR and Point C on P-V Loop

A

increase of TPR = increase preload = decrease of SV

97
Q

COntractility / EDV and point B on P-V Loop

A

increase EDV = increase preload = increase SV

98
Q

How would the loop initially change after someone had a mild heart attack

A

-does not change venous pressure increase TPR = increase afterload = decrease SV **higher point C, smaller C->D length

99
Q

How would loop initially change if someone had mitral valve stenosis

A

mitral valve stenosis- hardening and wearing of the valve increase internal resistance b/w atria and ventricle decrease contractility & max volume C-D length decreases due to less % of contractility

100
Q

Vasculature

A

heart -> arteries -> arterioles -> capillaries -> venules -> veins -> heart

101
Q

Systemic Circulation

A

path from the LV to the body and back to the heart

102
Q

Pulmonary (Thoracic) Circulation

A

path from the RV thru the lungs and back to the heart

103
Q

The rate (velocity) that blood flows through the systemic circulation is ___ the flow rate through the pulmonary circulation

A

equal b/c need entire blood flow to be consistent blood cell takes longer through the systemic

104
Q

Peripheral resistance in the systemic circulation is ___ the pulmonary circulation

A

greater 5-7X more tubing = resistance (more friction)

105
Q

The amount of work done by the LV is ___ times ___ greater than the RV

A

battle against resistance LV has thicker myocardial layer (3-4X thicker) **athletes have > amount of heart thickness

106
Q

3 layers of large arteries and veins

A

Externa Tunica Tunica Media Tunica Interna

107
Q

Major characteristic of artieres

A

thick layer of tunica media, small luminal space, can snap back and recoil

108
Q

Major characteristic of arterioles

A

narrow, resistance vessles entrance point to capillary beds decrease pressure

109
Q

Major characteristics of capillaries

A

exchange of materials, increase surface area decrease velocity of blood b/c it is VERY narrow

110
Q

Continuous Capillaries

A

most common tightly joined together b/w endothelial cells & therefore impermeable (only small particles can pass)

111
Q

Fenetra Capillaries

A

in kidney for filtering RBC, WBC, and big proteins CANNOT pass have pores that increase permeability (300X) tight junctions, still only small particles can pass at a HIGHER rate

112
Q

Discontinuous Capillaries

A

gaps b/w endothelial cells, large particles can cross located in liver and bone marrow

113
Q

Venous Return

A

rate of blood returned to the atrium from a low pressure environment due to a closed circuit and pressure gradient

114
Q

Veins

A

barely any pressure, only one-way valves capacitence vessels decreased muscle layer, increased lumineal space very flexible

115
Q

Blood Flow

A

continuous movement of blood though the circulatory system (LV -> RA)

116
Q

Continuous blood flow requires a ___

A

pressure gradient **if gradient increases, total venous return increases

117
Q

Blood Flow Equation

A

pressure difference / resistance **relatively independent

118
Q

Change in Pressure (Unknown)

A

Around 92 mmHg

119
Q

Dam Analogy

A

reservoir is the arterial side w/ LOTS of pressure arterioles and capillaries are the dam w/ VERY high resistance that keeps the water from flowing downstream result- very low water pressure on the other side of the dam

120
Q

Externa Tunica

A

elastic, thickness depends on artery or vein

121
Q

Tunica Media (Smooth)

A
  • constrict vessel = decrease luminal space, relaxation = dilation and decrease resistance
122
Q

Tunica Interna

A

elastic layer, endothelial layer

123
Q

Increase BP

A

increase arteriole pressure and increase pressure gradient

124
Q

Vasodilation

A

increase diameter of vessel, more easy blood flow decrease resistance **sympathetic response uses precapillary sphincters

125
Q

How do the skeletal muscles actively change resistance

A

uses B-2 to increase blood flow

126
Q

Vasoconstriction

A

narrowing of vessel due to the contraction of SMOOTH muscle increase resistance

127
Q

**Resistance will also change if the volume and/or viscosity of the blood changes, and can occur as a result of dehydration, blood doping, hemorrhage, etc.

A

NOT the capillaries b/c they have no muscle

128
Q

Blood Pressure (BP)

A

force blood exerts against inner walls of blood vessels

129
Q

Systolic Pressure

A

highest pressure when aorta is stretched (120) ventricle contracting

130
Q

DIsastolic PRessure

A

pressure after relaxation, prior to next contraction (80)

131
Q

Pulse Pressure (PP)

A

systolic - diastolic shows range of arterial pressures narrowing ranges = result of failure

132
Q

Mean Arterial Pressure (MAP)

A

1/3(pulse pressure) + diastolic BP must be > 60 mmHg or organs can die

133
Q

3 Factors to determine arterial BP

A
  1. cardiac output 2. total peripheral resistance 3. total blood volume
134
Q

Baroreceptors

A

BP sensors, communicate w/ CNS responds faster than hormones b/c it runs through CNS increase BP = vasodiaation decrease BP = vasoconstriction

135
Q

Hormones

A

regulate blood volume via ADH and aldosterone **for CHRONIC changes increase ADH/ aldosterone= more water stays in body and not excreted

136
Q

Carotic Body

A

blood only to the brain

137
Q

Extrinic Control of BP

A

stress- increase BP b/c of cortisol smoking- arteries harden = increase TPR ; short term is nicotene = vasoconstriction = increase BP diet- increase sodium = increase BP; increase glucose (diabetes) = increase BP ; increase fat/cholesterol = increase BP exercise- lifting weights = increase BP

138
Q

*** Look @ “big picture” of factors that effect BP

A

Look up

139
Q

Hypertension

A

hardening arteries is a result, stroke work load on heart is increased (always) try to build cardiac muscle 24/7 -> LV hypertrophy and decrease in ventricular volume muscle is not being build well = no increase in contractility of heart **BP needs to be below 120/80 (like 110/70) to be healthy

140
Q

If you stand up fast, what happens to the blood in your upper body?

A

fluid stays still, gravity pulls blood toward feet

141
Q

What happens to the BP in your upper body when you stand up?

A

drops

142
Q

Why does standing up make some people faint?

A

depriving brain of blood, oxygen, and glucose -> neurons don’t function as well

143
Q

Why do only some people and only some of the time faint when standing up too fast?

A

dehydration = decrease blood volume, decrease BP stress = increase resistance = increase pressure = less likely to faint

144
Q

What changes do baroreceptors initiate to regulate blood pressure when standing up too fast?

A

change TPR, vasoconstrict in legs and force blood up acts quickly

145
Q

What process do baroreceptors use?

A

in orthostatic hypotenstion - neg feedback

146
Q

Plasma

A

90% H2O with electrolytes (lots of Na), hormones, waste products, nutrients, proteins

147
Q

Erythrocytes

A

RBCs, biconcave discs, carry oxygen and CO2 in body, NO mitochondria

148
Q

Hematocrit

A

% of RBCs in whole blood (45%)

149
Q

Platelets

A

smallest “formed” elements, from the bone barrow for wound care and clot formation (not essential) cause vasoconstriction to prevent more blood from leaving, increase rate of healing

150
Q

What makes up “Whole Blood”

A

formed elements and plasma

151
Q

Anemia Hematocrit

A

30% decrease in RBCs = not delivering oxygen as fast = fatigue faster increase in plasma to maintain total blood volume (for BP) = decrease viscosity increase plasma = increase BP

152
Q

Polycythemia Hematocrit

A

70%, decrease plasma = more fatigue resistance = increase blood viscosity **blood doping

153
Q

Dehydration Hematocrit

A

70%, but a decrease in blood volume

154
Q

Hematopoiesis

A

formation of blood cells from stem cells in bone marrow and lymph nodes

155
Q

Erythropoiesis

A

formation of RBCs stimulated by erythropoietin (EPO) in response to oxygen level changes production in bone marrow via DISCONTINUOUS capillaries

156
Q

Leukopoiesis

A

formation of WBCs, stimulated by immune system

157
Q

Hemostasis

A

cessation of bleeding, needs fibrin to “web” RBCs

158
Q

Reactions initiated by vessel injury

A
  1. vasoconstriction 2. formation of “platelet plug” - become sticky and clump together 3. fibrin web completes the clot, “internal bandaid” **protein synthesis is stimulated
159
Q

How much water is inside cells (ICF) and outside cells (ECF)

A

2/3 inside, 1/3 outside ECF is 75% ISF and 25% blood plasma

160
Q

What causes the movement of water between the ICF and ECF (ISF and Plasma)

A

pressure gradients (oncotic or hydrostatic) **movement of water is DYNAMIC EQUILIBRIUM

161
Q

Sweating and dynamic Equilibrium

A
  1. take water from ISF = increase in ISF molarity = water moved from plasma -> ISF = increase plasma osmolarity = water movement from ICF -> plasma = increase ICF osmolarity
162
Q

Filtration

A

movement of water from the inside of the capillary to the ISF

163
Q

Absorption

A

movement of water from ISF to the capillary

164
Q

Net Fluid Movement

A

difference between the sum of the filtration pressures and the sum of the absorption pressures = (P cap + Pi if) - (P if + Pi cap)

165
Q

Hydrostatic Pressure (P)

A

force of water against a capillary wall to cross a membrane; “PUSH”

166
Q

Capillary Hydrostatic Pressure (P Cap)

A

38 mmHg @ arteriole end 16 mmHg @ venule end water pushing out into the capillary **Filtration

167
Q

Instersitial Fluid Hydrostatic Pressure (P if)

A

= 1 mmHg water trying to push INTO the capillaries **absorption important in BP

168
Q

Oncotic (Colloid Osmotic) Pressure (Pi)

A

plasma protein drawing water “Pull”

169
Q

Capillary Oncotic Pressure (Pi cap)

A

=25 mmHg **filtration **a change in conc. of plasma proteins could change it

170
Q

Interstitial Fluid Oncotic Pressure (Pi if)

A

=0 mmHg if broken capillary, this number increases **absorption

171
Q

Net fluid movement at beginning of capillary

A

= (38 + 0) - (1 + 25) = 12 mmHg outward forces > = net filtration

172
Q

Net fluid movement at end of capillary

A

=(16 + 0) - (1 + 25) = -10 mmHg inward forces > = net absorption

173
Q

Is absorption or filtration stronger and what does it mean to the body?

A

filtration (arteriole) end blood entering venule is more dehydrated than arteriole means an increase in ISF

174
Q

What happens is the filtration/absorption goes unchecked?

A

edema (swelling)

175
Q

Lymphatic System

A

takes excess ISF to check for pathogens - lymphatic vessels -lymph nodes -tonsils, spleen, and thymus

176
Q

3 Functions of Lymphatic System

A
  1. picks up excess fluid filtered out in capilary beds and returns it to veins 2. helps produce immunological defense 3. transports absorbed fat from the SI to the liver
177
Q

Immune System Function

A
  1. defense- prevent infection and protection 2. offense- actively fight off invasion
178
Q

Pathogens

A

things that cause disease

179
Q

Antigen

A

unique pattern on cells when a foreign antigen is found, the immune system responds to it

180
Q

Bacteria

A

most common life form on earth, only 3% are pathogenic **can be detected by their waste products

181
Q

Virus

A

nonliving, uses other organisms to reproduce flu, cold, HIV

182
Q

Cell Damage

A

“roughness” of uneven cell membrane can trigger an immune response via chemical signals

183
Q

Genetic Mutation

A

“internal” cell damage if DNA is damaged, the cell may not function and die on its own OR it can become cancerous

184
Q

Autoimmunity

A

WBC attacks a healthy cell ex: type 1 diabetes, multiple sclerosis, myasthenia gravis immuno-suppresents can treat autoimmunity

185
Q

Granulocytes

A

4-72 hours lifespan 1. neutrophils- most common WBC 2. eosinophils- fight parasites 3. basophils- inflammation **2 & 3 make up 3% of WBC

186
Q

Agranulocytes

A

take time to activate 100-300 day lifespan 1. monocytes / macrophages- 5% of WBC 2. lymphocytes- 30% of WBC

187
Q

What does lymphatic system do?

A

early warning stations throughout the body

188
Q

Bone Marrow (Central Tissue)

A

WBC production

189
Q

Thymus Gland (Central Tissue)

A

specializing the WBC

190
Q

Peripheral Tissues

A

-adenoids and tonsils - spleen 3. lymph nodes

191
Q

Skin

A

physical barrier symbiotic relationship w/ bacteria on skin

192
Q

GI Tract

A

acidic environment to destroy pathogens digestive enzymes and bacteria

193
Q

Importance of Microbiome

A

all bacteria inside and outside the body nonpathogenic as long as they are balanced symbiotic relationship 90% of cells in body are bacteria

194
Q

Respiratory

A

mucus traps pathogens and cilia brings pathogens up to be sneezed/coughed out

195
Q

Tears and Sweat

A

contain lysozymes - antimicrobial enzyme that destroys bacteria and virus

196
Q

Lymph nodes

A

in lymphatics WBCs with lymphocytes, monocytes, etc filters lymph and searches for pathogens

197
Q

Interferons

A

chemical that is released by infected (viral) cells leads to temporary resistance in neighboring cells & makes a chemical gradient to attract WBCs

198
Q

Cytokinesis

A

chemical signals ex: interferons, metabolic waste products (bacteria), ISF from damaged cell, signals sent from neighboring cells

199
Q

Chemotaxis

A

movement toward a cytokine

200
Q

Diapedesis/Extra Vasation (Neutrophils)

A

getting the WBC out of the blood, then to the lymph nodes

201
Q

ENdogenous Pyrogens

A

cytokine, released when WBC attacks a pathogen -raises set point in hypothalamus to raise body temp - fever slows down reproduction rate of pathogen -WBC works better in a fever

202
Q

Immune System point of view during infection

A

large increase in WBC production (leukopolesis) must occur -needs lots of numbers, an increase in nuetrophils and replacements

203
Q

Antigen Presenting Cells (APC)

A

neutrophil picks up and brings antigen to lymphocyte ^ACP b/c it physically presents an antigen in lymph node

204
Q

Cell-Mediated Immunity

A

non-specific immunity 1. APC 2. APC sensitize T lymphocytes 3. T cells divide and differentiate

205
Q

Cytotoxic/Killer T

A

-cell is physically killing a specific antigen -attacks pathogen membrane and DNA **Cell mediated

206
Q

Helper T

A

-works like APC -activate T cells and B cells -target of AIDS **cell mediated

207
Q

Suppresor T

A

-inhibit killer T and B cells -loss can lead to autoimmunity **cell mediated

208
Q

Memory T

A

-recognize a return of the pathogen -APCs are NOT needed when these are present **cell-mediated

209
Q

WHy isn’t cell-mediated immunity enough to fight off most infections?

A

low in numbers

210
Q

Humoral Immunity

A

indirect attack

211
Q

Memory B

A

similar to memory T cells **humoral immunity

212
Q

Plasma (Active) B

A

-secrete specific antibodies -secrete 2000/sec **humoral immunity

213
Q

Antibody (Immunoglobulin)

A

-have specific antigen binding site -“mark” pathogens by binding to them

214
Q

How do antibodies contribute to fighting off infection?

A
  1. neutralization- can no longer interact w/ cells 2. enhanced phagocytosis- easier to gulp together 3. activation of complement system- pinches pathogens and creates holes for the cell to burst
215
Q

How do antibodies provide an advantage in fighting an infection?

A

-kill pathogens directly (membrane attack complex) -more numbers -can’t phagositize (clean up)

216
Q

Pharmaceutical Interventions for Disease

A
  1. destroy the pathogen 2. prepare the immune system 3. stop pathogen replication (buying time) 4. prevent cell infection
217
Q

External Disease Prevention

A

antimicrobials- destroy living and nonliving material ex: bleach, alcohol, soap

218
Q

Vaccination/Immunization

A
  1. earlier lymphocyte activation 2. faster lymphocyte replication 3. larger number of active lymphocytes 4. more antibodies
219
Q

Active Immunization

A

inject weak/destroyed pathogen -still has antigens -initiates a primary response and creates memory B and T cells -long lasting effects

220
Q

Passive Immunization

A

ex: going to a foreign country, needed for emergencies -antibodies from a donor -donor was actively immunized -short term effect (liver filters them out) artificial- giving shot of antibodies natural- breast feeding

221
Q

BActericide

A

kills bacteria -destroy plasma membrane -prevent vital protein synthesis

222
Q

Bacteriostatic

A

-prevent bacteria from replicating (prevent replication related protein synthesis) -prevent folic acid formation

223
Q

Precapillary Sphincters

A

in arterioles, either dilate/constrict and determine where blood flow goes and how much

224
Q

PReload

A

“stretch” on muscle fibers

225
Q

Antiviral

A
  1. prevent cell infection -disable docking mechanism of virus -interferon temporary immunity 2. prevent viral replication -down regulation of protein synthesis of cell 3. prevent viral escape -contain virus in cell
226
Q

Why do you need to get a flu shot every year?

A

flu is constantly changing

227
Q

WHy isn’t there a vaccine for the common cold ?

A

too many viruses to cause the common cold

228
Q

Why is it a problem giving an antibiotic to a common cold?

A

kill good bacteria (microbiome)

P215 (3 decks)

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