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Anatomy > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

2 major components of blood

A

1) Formed elements: cells and parts of cells
2) Matrix (binding element): Plasma

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2
Q

During clotting, what becomes visible?

A

No fibers present normally, dissolved strands of fibrin become visible during clotting

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3
Q

Function of blood: Transporter

A

Of important substance within body
Substances delivered to organ system
Oxygen - from lungs to tissue
Metabolic waste - urea delivered to kidneys to be excreted
Various hormones - from thyroid or adrenals to target tissue

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4
Q

Function of blood: Body temperature

A

Blood acts as large sink - absorbs and distributes heat
Working in combination with the heart and blood vessels system

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5
Q

Function of blood: Body pH

A

Blood contains proteins and solutes which prevent abrupt changes in acidity
Blood acts as buffer (anything that lessens changes in pH)

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6
Q

Function of blood: volume

A

Blood proteins can osmotically “pull” fluid from tissue space into circulation

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7
Q

Function of blood: protection

A

Protein from environmental factors which can disrupt homeostasis

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8
Q

Function of blood: hemorrhage

A

Hemorrhage: formed elements (platelets) initiate blood clot formation
Prevents blood loss in damaged vessels

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9
Q

Function of blood: infection

A

Blood plasma contains antibodies and immune cells (leukocytes)
Work together to defend against foreign substances

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10
Q

mixed blood is considered a…

A

suspension: large solute particles (formed elements) which fall to the bottom of plasma when not mixed
To rapidly separate the formed elements from plasma - centrifuge blood sample

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11
Q

Normal levels of components of blood

A

55 % plasma - fluid portion/less dense
45% red blood cells - hematocrit/most dense
<1% WBCs and platelets - buffy coat

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12
Q

Total blood volume

A

5-6 L in males
4-5 L in females
Account for 8 % of total body weight

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13
Q

What is in the highest quantity in the blood?

A

Electrolytes are the most abundant dissolved component in the blood, followed by proteins

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14
Q

Mixture type of plasma

A

colloid - scatters light but dissolved components stay dissolved
92 % water

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15
Q

Electrolytes in the blood

A

other electrolytes such as chloride, calcium, magnesium, phosphate, and bicarbonate
Help to maintain plasma pH - slightly alkaline (7.35-7.45)

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16
Q

Other plasma components: proteins

A

carrier molecules made by the liver to transport substances through blood,
such as glucose, fatty acids, etc.
osmotically maintain fluid balance

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17
Q

Most abundant plasma protein

A

Albumin (60%)
large: not permeable through capillary wall
Causes water to stay in blood vessel via osmotic pressure
counter-balance blood pressure pushing water out of vessel

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18
Q

What happens when plasma protein is too low?

A

Low plasma protein results in edema
Fluid accumulation in interstitial space, joint cavities, lungs
Healthy liver will make more if needed

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19
Q

Other plasma proteins are…

A

Globulins (36%) and Fibrinogen (4%)

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20
Q

Globulins

A

maintain fluid balance
- transport lipid soluble nutrients (Vitamins D, E, K)
- contribute to immune response (antibodies)

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21
Q

Fibrinogen

A

Largest protein in blood
contributes to blood coagulation (clotting) - strands of fibrin

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22
Q

major plasma components: Non-protein Nitrogenous Substances (NPNs)

A

Molecules that contain nitrogen, but are not proteins
Urea: product of protein catabolism; about 50 % of NPNs
Amino acids: product of protein digestion
creatinine: product of creatine metabolism in muscle

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23
Q

Creatinine in blood

A

Kidney should almost completely remove from blood to be excreted in urine
Creatine supplement causes strain on kidneys

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24
Q

What contributes to BUN level?

A

NPNs, particularly urea contribute to blood urea nitrogen (BUN) level

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25
Q

BUN levels and what they indicate

A

Indicator of kidney health: Normal 7-21 mg/dl
High BUN: kidney is not excreting urea in normal quantity causing urea to accumulate in blood
Low BUN: impaired liver function - not breaking down proteins

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26
Q

Other factors that can effect BUN

A

burns, dehydration, malnutrition
other tests usually needed to investigate kidney/liver function

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27
Q

major plasma components: gases and nutrients

A

Blood gases: oxygen, carbon dioxide - small amount dissolved in plasma (most is bound to hemoglobin in RBCs)
Plasma nutrients: amino acids, sugars (glucose), nucleotides, lipids: fats (triglycerides), phospholipids, cholesterol

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28
Q

Why are platelets and erythrocytes not considered true cells?

A

Platelets: cell fragments
Erythrocytes have no nuclei or organelles - without mitochondria, they can only produce ATP via glycolysis
Most blood cells do not divide - blood stem cells in red bone marrow divide to replace them

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29
Q

Erythrocytes structure

A

Small doughnut shaped cells (bi-concave disk) - most abundant of all formed elements in blood
Very simple structure but highly functional

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30
Q

Erythrocytes function in relation to Hb

A

carry oxygen bound to hemoglobin
Hb: RBC protein that binds to oxygen - greatly increases amount of O2 that can be carried by non-Hb containing cells
Discounting water, RBC is 97% Hb

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31
Q

Why are RBCs efficient?

A

they do not have organelles - only use anaerobic metabolism for ATP - glycolysis, can never consume the O2 it is carrying
Doughnut shape = 30 % more surface area for absorbing dissolved O2 from plasma - cytoplasm within RBC is never far from cell surface
Good for O2 delivery to tissues

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32
Q

What gives RBCs its doughnut shape?

A

RBCs contain a structural protein called spectrin - attached to the inner surface of plasma membrane
Forms of network of structural proteins just under cell surface which maintains its irregular shape

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33
Q

Spectrin

A

highly flexible
Allows RBCs to bend and contort to squeeze through capillaries smaller than diameter of cell

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34
Q

what do changes in RBC count indicate?

A

changes in blood’s oxygen-carrying capacity

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35
Q

Anemia

A

O2 carrying capacity of blood is reduced, due to low RBCs or hemoglobin
- Bone marrow deficiency damaged by radiation
- iron/B12 deficiency

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36
Q

Sickle cell disease

A

Oddly shaped RBCs occlude small vessels
rupture very easily - releases iron which clogs kidneys

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37
Q

Carbon Monoxide Poisoning

A

CO binds strongly to hemoglobin
Less room for O2 to bind
Less willing to release O2 to tissues
RBCs and Hb levels remain normal - O2 content of blood is reduced

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38
Q

Polycythemia (and causes)

A

Too many RBCs which causes the blood to be thick and viscous
Increased strain on the heart
Causes: dehydration, blood doping (artificial erythropoietin)

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39
Q

Erythropoiesis (the process)

A

Occurs in red bone marrow - axial skeleton in adults
Begin as blood stem cells = hematopoietic stem cell
- aka hemocytoblast
- does have a nucleus
Matures over a 15 day period
- commit to becoming RBC
- produce ribosomes and Hb
- eject nucleus

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40
Q

Stimulus for erythropoiesis

A

Low blood O2 causes kidney and liver to release EPO (erythropoietin), which stimulates RBC production
Negative feedback loop

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41
Q

Dietary factors related to RBCs

A

Vitamin B12 and folic acid: required for DNA synthesis; necessary for the growth and division of all cells
Iron: required for hemoglobin synthesis

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42
Q

Destruction of RBC

A

RBC cells live 120 days, circulate 75,000 times, become fragile with age
Damaged cells rupture when passing through liver or spleen
White blood cells phagocytize damaged RBCs
Some iron from hemoglobin recycled to make new heme and RBCs
remaining iron is turned into bilirubin - yellow pigment - picked up by liver for concentration (liver damage- jaundice)

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43
Q

General Functions of White Blood cells

A

least numerous of formed elements
Protect against disease - can leave bloodstream to fight infection
Chemical signal released by damaged or infected tissue

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44
Q

Diapedesis

A

(WBCs) cross through capillary wall by squeezing between endothelial cells and can leave blood vessel; can migrate toward infection site

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45
Q

Chemotaxis

A

Attract WBC to area of infection by chemicals released by damaged cells
Stimulate production of more WBCs

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46
Q

5 types of WBCs

A

Granulocytes (granular cytoplasm):
Neutrophils, Eosinophils, Basophils
Agranulocytes (no noticeable granules):
Lymphocytes, Monocytes

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47
Q

Neutrophil apperance

A

More numerous of WBC: 50 - 70% of all WBCs - 2x size of RBCs
Small, light purple granules in acid-base strain type
Lobed nucleus; 3-6 sections

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48
Q

Neutrophils function

A

Bacteria slayers - first to arrive at infection site
- strong phagocytes - engulf bacteria, fungus
After phagocytosis, kill bacteria in 2 ways
- produce oxygen free radicals - “respiratory burst”
- granules in cytoplasm make protein “spears” to puncture cell wall

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49
Q

Eosinophils appearance

A

2 - 4% of WBCs
Coarse granules - color varies by strain type
Bi - lobed nucleus connected by wide bridge

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50
Q

Eosinophils function

A

Defend against parasite infestations
- Flatworms/roundworms from food/contact
- Burrow into intestinal or respiratory mucosae along with eosinophils
Most parasite too large to phagocytize
- eosinophil granules release digestive enzymes directly onto parasite

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51
Q

Basophils function

A

Increased during allergic reaction
granules release histamine and heparin
- histamine - attracts more WBCs, increases vessel permeability
- Heparin - vasodilator, increases blood flow

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52
Q

Basophils appearance

A

rarest of all WBCs, less than 1% of WBCs
Large granules with obscure view of multi-lobed nucleus

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53
Q

Monocytes appearance

A

Largest of WBCs (3 - 8% of WBCs)
No granules in cytoplasm
Single nucleus in kidney or U-shaped with some cytoplasm visible

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54
Q

Monocytes function

A

Main function: defense against viral infection
Also attack some bacterial parasites and chronic infections - leave bloodstream and enter tissue to become macrophages
HIGHLY proficient phagocyte
Also activate lymphocytes to mount a stronger immune response

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55
Q

Lymphocytes appearance

A

Most are only slightly larger than RBCs; smallest WBC (25-33 % of all WBCs)
Large spherical nucleus surrounded by thin rim of cytoplasm

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56
Q

Lymphocytes function

A

2 major types of lymphocytes:
- T cells: attack virus infected cells and tumor cells
- B cells: produce antibodies - tag foreign cells or molecules

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57
Q

Where are lymphocytes found?

A

Do not reside in blood, mainly found in lymphoid tissue (spleen, lymph node)

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58
Q

Leukocytosis

A

High WBC count (> 10,800 / microliter)
Acute infections, vigorous exercise, great loss of bodily fluids

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59
Q

Leukopenia

A

Low WBC count (< 4,800 / microliter)
Measles, mumps, chicken pox, AIDS, polio, anemia

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60
Q

Most mobile and active phagocytes

A

Neutrophils and Monocytes

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61
Q

Inflammatory response by WBCs

A

Reaction that restricts spread of infection; promoted by basophils, by secretion of heparin and histamine; involves swelling and increased capillary permeability

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62
Q

Thrombocytes

A

Fragments of megakaryocytes: a type of stem cell in red bone marrow

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63
Q

What regulates formation of platelets?

A

Thrombopoietin regulates formation of platelets
Megakaryocytes send extensions out of bone marrow into blood vessel within bone
- extension breaks off to form a platelet

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64
Q

Platelets (and what they contain)

A

Has membrane, lacks a nucleus - less than half of a RBC in size
Platelet count: 150,000 - 350,000 / microliter of blood
Contain granules that release Ca2+, serotonin (5-HT), and factors which assist in clot formation - all contribute to hemostasis

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65
Q

What is hemostasis and what the 3 steps?

A

Hemostasis refers to the stoppage of bleeding - limit blood loss
3 steps that limit or prevent blood loss include:
- Blood vessel spasm - decrease blood flow
- Platelet plug formation - plug hole in injured vessel
- Blood coagulation - thicken blood near clot

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66
Q

Hemostasis: Vascular Spasm

A

When blood vessel is ruptured, smooth muscle in blood vessel contracts rapidly
- slows blood loss very quickly
- end of vessel may close completely

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67
Q

What is the vascular spasm triggered by?

A

Triggered by:
- stimulation of the blood vessel wall
- Local pain receptor reflexes
- Chemical released by damaged endothelial cells
Effect continues for 20 - 30 minutes
- allows time for other 2 homeostasis mechanisms to take effect

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68
Q

Hemostasis: Platelet plug formation

A

triggered by exposure of platelets to collagen
- activates platelets causing them to become sticky
— activated platelets also release 5-HT, Ca2+, and thromboxane A2
- increases platelet clumping and vascular spasm
- acts as positive feedback loop

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69
Q

Hemostasis: Blood coagulation

A
  • most effective mechanism of chemostasis: happens very fast
  • form blood clot in a complex series of reactions which reinforce platelet plug with fibrin threads
    — acts as a molecular glue to trap blood cells
  • effective in sealing larger openings
  • involves numerous clotting factors (several require Vitamin K for production)
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70
Q

What are blood clotting mechanisms caused by overall?

A

By release of chemical from damaged cells
By contact with foreign surface without tissue damage

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71
Q

What happens to blood clots? (Fate of Blood Clots)

A

After a blood clot forms, it contracts and pulls the edges of a broken blood vessel together
- Platelets contain actin and myosin
Platelet-derived growth factor (PDGF) stimulates smooth wall muscle cells and fibroblasts to repair damaged blood vessel walls
Fibrynolysis: Plasmin (clot buster) digests fibrin threads and dissolved the blood clot

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72
Q

Thrombosis

A

Blood clot in a vessel supplying a vital organ (brain, heart)
leads to infarction: death of tissues which have blocked blood vessels

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73
Q

Artherosclerosis

A

Accumulation of fat in arterial linings
- fat can rupture and cause clot formation

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74
Q

Deep vein thrombosis

A

Clot formation due to pooling of stagnant blood, mainly in femoral or popliteal veins
Can lead to pulmonary embolism

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75
Q

Antigen

A

Molecule located on cell which identifies it

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76
Q

Antibody

A

Free floating protein that will act against foreign antigens

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77
Q

Agglutination

A

When RBCs come in contact with antibodies against them, they will agglutinate (clump together):
severe immune response (fever, seizures, heart attack)

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78
Q

Autorhythmic cells

A

A small fraction (1%) of cardiac muscle cells are autorhythmic cells
aka pacemaker cells
determine the heart rate

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79
Q

Contractile cells

A

Remaining 99% are contractile cells
determine the stroke volume

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80
Q

Location of heart

A

Within mediastinum posterior to sternum
Angled down left
Medial to lungs
Anterior to the vertebral column

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81
Q

Inferior/Superior location of heart

A

The base lies beneath the 3rd rib
Base: Broad flat posterior surface
The apex lies at the 5th intercostal space
Between 5th and 6th rib: “Apical Heartbeat”

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82
Q

pericardium

A

Heart is covered with tough double layered sac called pericardium

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83
Q

Fibrous pericardium

A

Outer cover, toughest, dense irregular connective tissue
protects heart
anchors heart to surrounding tissue
prevents overfilling (does not occur in healthy individuals)

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84
Q

Serous pericardium

A

Also has 2 layers
Forms fluid filled sac around heart
parietal pericardium
visceral pericardium (also called epicardium)
Between 2 serous layers –> pericardial cavity: filled with fluid

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85
Q

pericardial cavity

A

contains serous fluid which lubricates 2 membranes
- allows heart to work in friction free environment

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86
Q

pericarditis

A

inflammation of pericardium - roughing of serous membranes
- deep chest pain
- can be heart on stethoscope

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87
Q

Cardiac tamponade/ cardiac effusion

A

extreme inflammation fluid buildup in pericardial cavity

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88
Q

Layers of heart

A

epicardium (outer layer)
Myocardium
endocardium

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89
Q

Epicardium

A

Also called visceral pericardium
Thin layer of fat, thicker in elderly
Simple squamous epithelium
- contains coronary vessels

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90
Q

Myocardium

A

Middle layer, thickest layer
Composed of cardiac muscle tissue
arranged in spiral pattern

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91
Q

Endocardium

A

inner layer
forms thin continuous inner lining
epithelial and connective tissue
In all chambers, valves and vessels

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92
Q

Atria: ridges of muscle

A

Pectinate muscles
Increase volume/contraction strength
More prominent in RA

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93
Q

Features of ventricles

A

forms bulk of muscle tissue
trabeculae carne: increases strength of contraction, also ridges
Papillary muscles and chordae tendineae
Reinforce atrial valves during contraction

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94
Q

Heart valves 2 concepts

A

All 4 heart valves only allow blood flow in one direction
Valves open and close in response to pressure difference (not due to papillary muscle contraction)

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95
Q

SA node

A

Pacemaker; located in the right atrium
Initiates cardiac cycle
Starts with depolarization (contraction) of atria

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96
Q

AV node

A

Delays impulse
Allows atria to finish contracting and filling the ventricles with blood
Secondary pacemaker

97
Q

Bundle of His

A

Allows depolarization to travel from atria to ventricles
Only electrical connection between atria and ventricles

98
Q

Left and Right Bundle Branches

A

Located in septum of heart
Guide depolarization to apex

99
Q

Purkinje fibers

A

Large fibers: conduct impulses to ventricular myocardium
Tertiary pacemaker

100
Q

Abnormal EKGs: Atrial Fibrillation

A

Uncoordinated atrial depolarization
seldom reaches AV node
Causes: damaged Atrial Myocardium (ectopic depolarization)

101
Q

Abnormal EKGs: Junctional Rhythm

A

SA node is non-functional: no p-waves
AV node sets pace 40 - 60 bpm
Causes: damaged SA node

102
Q

2nd degree AV block

A

P-wave occasionally does not trigger QRS complex
- damaged AV node
Cause: Ischemia from blockade of coronary artery

103
Q

Prolonged QRS complex

A

Damage to Bundle of His
cause: ischemia from blockade of coronary artery

104
Q

Abnormal EKGs: Ventricular Fibrillation

A

Uncoordinated ventricular depolarization
cause: blocked coronary artery, toxic drugs, electrical activity, physical damage

105
Q

Coronary circulation drains into…

A

The coronary sinus
- large vein on posterior side of heart
- returns deoxygenated blood to right atrium
Great, Middle, and Small cardiac veins drain deoxygenated blood from myocardium

106
Q

Parasympathetic innervation of the heart

A

Muscarinic receptors:
- decreases excitability of SA node
- decreases HR

107
Q

Sympathetic innervation of the heart

A

Beta Adrenergic receptors:
- increases excitability of SA node/ventricles
- increases HR and SV

108
Q

What drives blood flow?

A

Pressure differences
body does not actually sense CO/blood flow, it only senses pressure

109
Q

Baroreceptors monitor…

A

They are sensors that monitor stretch (pressure) in the aortic arch and carotid sinuses

110
Q

MAP

A

mean arterial pressure (MAP)
weighted average of systolic and diastolic
MAP = CO * TPR

111
Q

What occurs if a decrease in stretch is sensed?

A

Activates sympathetic nervous system to restore pressure

112
Q

TPR

A

Total peripheral resistance
Sum of resistance in all vessels of body

113
Q

Vascular System Functions

A
  • Provide a conduit for blood to go from heart to organs
  • Regulation of both blood pressure and blood flow:
    — maintain enough resistance to ensure adequate BP in entire system
    — Match blood flow to metabolic demand of each organ system
114
Q

What occurs if BP is too low?

A

Vessel constricts to increase TPR
This will increase MAP to increase blood flow

115
Q

What generates initial pressure difference to drive blood flow?

A

The heart

116
Q

Tunica Intima

A

Inner layer of blood vessel
Contain endothelium; direct contact with blood
Simple squamous cells = low friction

117
Q

Tunica Media

A

Middle layer of blood vessel
Contain smooth muscle
Innervated by sympathetic nerve fibers –> controls diameter of blood vessels
Responds to circulating hormones, also effects diameter
Increase blood flow = vasodilate
Decrease blood flow = vasoconstrict

118
Q

Tunica Externa

A

Outer layer of blood vessel
Contains collagen fibers
Structural reinforcement/anchoring to surrounding tissues
large vessels = vasa vasorum

119
Q

2 major properties of arteries

A

Elasticity: elastic tissue in T. interna and Media can withstand high pressure
Contractility: smooth muscle in T.media (direct blood flow and limit bleeding - vascular spasm)

120
Q

2 types of arteries

A

Elastic arteries (conducting arteries) - act as a pressure reservoir
Muscular arteries (distributing arteries) - contribute to blood flow regulation

121
Q

Elastic Arteries

A

Thick wall of smooth muscle
Also contain elastin
Stretchiness acts as pressure reservoir
- maintains blood flow during diastole
Arteries distend during systole
- recoil during diastole
Recoil propels blood through artery

122
Q

Muscular Arteries

A

Most common type of artery
Thickest T.media (smooth muscle)
- good capacity for vasodilation/vasoconstriction
- plays a minor role in regulating blood flow to tissue
- most blood flow regulation is accomplished by arterioles

123
Q

Arterioles

A

Large arterioles contain all 3 tunics
Small = mainly smooth muscle surrounding endothelium
Contain loops of smooth muscle = precapillary sphincters

124
Q

Precapillary sphincters

A

Main determinant of vascular resistance (TPR)
contraction/relaxation of precapillary sphincters - adjust resistance to flow

125
Q

Extrinsic Flow Control

A

Activated by baroreceptors in response to decrease in MAP
- released epinephrine and norepinephrine
- non-specific - all organ systems are affected
Response determined by which the receptors the organ has

126
Q

Types of receptors of organs for extrinsic flow control

A

Alpha-adrenergic receptors = vasoconstriction
Beta-adrenergic receptors = vasodilation

Most non-essential organs have mainly alpha-adrenergic receptors

127
Q

Extrinsic flow control: sympathetic activation leads to…

A

Sympathetic activation increases vasoconstriction
increase TPR –> increases MAP
Problem: need to get blood into tissue that has a high metabolic rate

128
Q

Local (Intrinsic) Flow Control mechanisms

A

Control mechanisms at the site of the vessels themselves
Active hyperemia and flow autoregulation
- different cause but same effect = vasodilation

129
Q

Active hyperemia

A

Up Metabolic activity of Organ ->
Down O2, Up metabolites in organ interstitial fluid ->
Arteriolar dilation in organ ->
Blood flow to organ

130
Q

Flow autoregulation

A

Down arterial pressure in organ ->
Down blood flow to organ ->
Down O2, Up metabolites, Down vessel-wall stretch in organ ->
Arteriolar dilation in organ ->
Restoration of blood flow toward normal in organ

131
Q

Problem caused by intrinsic flow control

A

overall decrease in TPR
Blood flows out of arterioles faster than it is replaced in arteries
Drop in MAP = all organs get less blood

132
Q

How does body protect itself from decreases in pressure?

A

Baroreceptors activate the sympathetic nervous system -> Increases CO -> Vasoconstriction in non-essential organs (extrinsic flow control)

133
Q

Capillary

A

Smallest of all vessels
Huge surface area for nutrient delivery
Lack outer 2 tunic
- Thin T.lamina - single endothelial cell in thickness
Primary point of exchange between the blood and tissues

134
Q

Anatomy of capillary network through organ

A

Flow is regulated by arteriole precapillary sphincters
Nutrients/waste exchanged in capillary bed
Spent blood drains through venules

135
Q

How to get through capillary wall?

A

Diffusion occurs via 2 pathways
Transcellular - through endothelial cell
and Paracellular - around cells
Both pathways require concentration gradient

136
Q

Transcellular

A

Through endothelial cell
From apical to basolateral side
Aided by thin walls

137
Q

Paracellular

A

Around cells
Cells joined by tight junctions
Incomplete in capillaries
Gap = intercellular cleft

138
Q

Continuous capillaries

A

Intercellular clefts are gaps between neighboring cells
Skeletal and smooth, connective tissue and lungs

139
Q

Fenestrated capillaries

A

Plasma membranes have many holes
Kidneys, small intestine, choroid plexuses, ciliary process, endocrine glands

140
Q

Sinusoids

A

Very large fenestrations
Incomplete basement membrane
Liver, bone marrow, spleen, anterior pituitary, and parathyroid gland

141
Q

Major Functions of Venules and Veins

A

Low pressure/resistance path to return blood to heart:
- due to very large vessel lumen
Large blood reservoir
- sympathetic venoconstriction = increase venous return to the heart

142
Q

How much of blood volume is in veins?

A

60 % of total blood volume is in the veins

143
Q

Venule and Vein structure

A

Thinner walls than arteries - do have all 3 tunics
but very small venules = lack outer 2 (like capillaries)
Highly porous endothelium - allows for movement of WBC and other phagocytes
Tunica media less developed
- still vasodilate or constrict
Function as blood reservoir - highly distensible
Very large vessel lumen

144
Q

Venous valve systen

A

One way valves - only allows blood to flow back to heart
blood pressure in veins is very low
Lower body = pressure almost cannot overcome gravity - need to MOVE

145
Q

What is venous flow assisted by?

A

By the skeletal muscle pump mechanism working in combination with one-way valves

146
Q

Anastomoses

A

Union of 2 or more arteries supplying the same body region
Blockage of only one pathway has no effect
- Circle of Willis underneath brain
- coronary circulation of heart

147
Q

Collateral circulation

A

Alternate route of blood flow through an anastomosis is known as collateral circulation
- can occur in veins and venules as well

148
Q

End arteries

A

Arteries that do not anastomose
- occlusion of an end artery interrupts the blood supply to a whole segment of an organ, producing necrosis of that segment

Alternate route to a region can also be supplied by nonanastomosing vessels

149
Q

Minor roles of lymphatic system

A

Returning leaked proteins from interstitial fluid to plasma
Transporting dietary fats (intestinal villi)

150
Q

Major roles of lymphatic system

A

Return excess fluid from interstitial space back to plasma
Protection against infection
- House B- and T- lymphocytes in lymph nodes

151
Q

How does excess fluid get into interstitial space?

A

Fluid comes from capillaries in our tissue
Nutrient diffusion occurs via 2 pathways
- transcellular or paracellular
Fluid can exit capillaries via same pathways
- driven by Starling Forces
—- pressure gradient

152
Q

Hydrostatic pressure

A

Physical pressure pushing water through capillary wall

153
Q

Colloid Osmotic pressure

A

Non-penetrating proteins (colloids) that osmotically draws in fluid

154
Q

What happens to fluid that doesn’t get absorbed?

A

Enter lymphatic capillaries
Now called lymph
returned to venous circulation

155
Q

Structure of lymphatic capillaries

A

Very thin walled and permeable
contains overlapping flaps which form mini-valves to let fluid in
Flaps have anchoring filaments
- attaches them to surrounding tissue
- when fluid levels increase= flaps pull up to let more fluid in

156
Q

Where are lymphatic capillaries located?

A

Located everywhere except:
CNS, cornea, cartilage, and epidermis

157
Q

Lymphatic capillaries drain into…

A

Larger collecting vessels
- Have 3 main tunic but thin-like veins
- also have one way valves - like veins

158
Q

Collecting vessels drain into…

A

Collecting vessels unite and drain into lymphatic trunks named by body region

159
Q

Right Lymphatic Duct

A

Drains lymph from upper right torso, right arm, and right side of head
Returns lymph to circulation at junction of right subclavian and jugular vein

160
Q

Thoracic Duct

A

Drains lymph from rest of body including both veins
Return lymph to circulation at junction of left subclavian and jugular vein

161
Q

Cisternae chyli

A

In some individuals, the thoracic duct starts as an enlarged sac called the cisternae chyli

162
Q

What is lymph transport assisted by?

A

Like venous blood - assisted by skeletal muscle movement
One- way valves to prevent backflow
Pulsations from arteries and smooth muscle in lymph vessels assist lymph movement

163
Q

T-lymphocytes (T-cells)

A

When activated, coordinate immune response and directly attack infected cells

164
Q

B-lymphocytes (B-cells)

A

When activated, produce plasma cells which secrete antibodies
Antibodies mark foreign cells for destruction

165
Q

Macrophages

A

Phagocytize foreign objects and activate T-cells

166
Q

Dendritic cells (Antigen Presenting cell)

A

Capture foreign antigen and brings them to lymph nodes to alert other immune cells

167
Q

Primary lymphoid organs

A

Where B and T cells mature, but don’t encounter pathogens (immunocompetence and self-tolerance)
Thymus (between sternum and heart):
T-cell maturation
Red Bone marrow: B-cell maturation

168
Q

Secondary lymphoid organs

A

Where mature lymphocytes come in contact with and are activated by pathogens
- lymph nodes
- spleen
- mucosa associated lymphoid tissue

169
Q

MALT

A

mucosa-associated lymphoid tissue
- tonsils, peyer’s patches, appendix

170
Q

Lymph nodes

A

Small capsules located close to lymph vessels
Most dense in areas of body likely to encounter pathogens

171
Q

2 main functions of lymph nodes

A

Cleanse lymph: contain macrophages to phagocytize pathogens and debris
Activate the immune system: Antigen Presenting cells will bring antigens to lymph nodes to activate B and T lymphocytes

172
Q

Lymph Node Structure

A

Capsule: outer fibrous covering
Trabeculae: connective tissue extensions
- divides nodes into separate chambers
Outer layer: cortex
Inner chamber: medulla

173
Q

The flow of lymph in the nodes

A

Lymph enters via afferent vessels
- enters bag-like subscapular sinuses in cortex
—> contain macrophages attached to connective tissue fibers to filter lymph
Some lymph leaks into lymph follucle and germinal center
- activate rapidly dividing B-cells
Lymph move toward center (medulla) of node
- enters medullary sinus
- contains macrophages
- comes in contact with medullary cords
- contains both B and T cells waiting for activation
Cleansed lymph moves toward hilum (indentation) of node
Exits via efferent vessels

174
Q

Spleen

A

Site of lymphocyte proliferation and blood cleansing
Largest lymphatic organ
2 main components: red pulp and white pulp

175
Q

Red Pulp

A

Breaks down damaged RBCs and stores released iron
Stores platelets and monocytes for later use

176
Q

White Pulp

A

Where lymphocyte proliferation occurs

177
Q

MALT function

A

strategically located lymphoid tissue
Main function: gathers pathogens which enter body through air or diet
used for activation and creation of B/T memory cells before a severe infection ever occurs

178
Q

Locations of MALT

A

Tonsils - located throughout pharynx
peyer’s patches - clusters of lymph tissue in small intestine
Appendix

179
Q

Elephantiasis: clinical application

A

Parasitic worms infest lymphatic system - block fluid drainage.
Results in blocked lymph drainage, edema - accumulation (abnormal) of fluid beneath the skin

180
Q

Innate Immunity

A

Present at birth: responds to any foreign pathogen which has not been identified
Always vigilant and responds with minutes of invasion
Less effective than adaptive immunity

181
Q

Adaptive immunity

A

Only attacks identified pathogens
Extremely effective by takes longer to respond than innate immunity

182
Q

2 branches of Innate Immune

A

Surface Barriers - 1st line of defense
- skin and mucous membranes
Internal Defenses - 2nd line of defense
- only needed if surface barriers are breached
- phagocytes, NK cells, inflammation, antimicrobial proteins (complement), fever

183
Q

Skin as a Surface Barrier

A

Skin and mucous membrane are physically tough and have chemical defenses
Skin: outer keratinized layer is very durable and acidic
- acid (acid mantle) inhibits bacterial growth

184
Q

Mucous membranes as a Surface Barrier

A

Not as durable as skin but can have several types of defenses
- acid (stomach, eye, vagina, bladder/urine)…destroys microorganisms
- Enzymes - usually lysozymes which destroy microorganisms
- Mucin - mucous traps microorganisms
- filtering mechanisms (cilia or hairs) trap and physically remove pathogens

185
Q

Highly adapted mucous membrane: trachea

A

Trachea has most of the defense mechanisms associated with mucous membranes
- goblet cells create mucous: trap pathogens and contain lysozymes
- elongated cells are physically durable
- cilia (filter) - removes pathogens trapped in mucous

186
Q

When tissue is damaged, what occurs?

A

2 things-
Damaged tissue releases inflammatory chemicals
Immune cells are recruited to the area of damage

187
Q

How are immune cells recruited?

A

Attracted directly to inflammatory chemicals
Called by chemicals from cells with pattern recognition receptors

188
Q

TLRs

A

Major class of recognition receptors: toll-like receptors (TLRs)
These receptors generally identify foreign objects
If a pathogen is present, TLR containing cells release chemicals to attract more immune cells to the area

189
Q

How do immune cells get to site of infection/injury? (list)

A

1) Leukocytosis
2) Marginalization
3) Diapedesis
4) Chemotaxis

190
Q

How do immune cells get to site of infection/injury? : Leukocytosis

A

Neutrophils are released from bone marrow and enter bloodstream
- WBC count can increase 4-5x

191
Q

How do immune cells get to site of infection/injury? : Marginalization

A

Inflammatory chemicals cause endothelial cells in blood vessels and immune cells to sprout cell adhesion molecules (CAMs)
- causes passing immune cells to stick

192
Q

Cells recruited in an innate immune response

A

Neutrophils (WBC) 1st and Macrophages (2nd)
Macrophages are derived from monocytes which leave the bloodstream
Both are phagocytes

193
Q

Phagocytosis (the process)

A

1) Phagocyte must adhere to carbohydrate signature (glycocalyx) on pathogen!
2) Pathogen is engulfed to form a membrane enclosed phagosome
3) Phagosome fuses with lysosome to form phagolysosome
4) Enzymes from lysosome destroys pathogen

194
Q

How can phagocytosis fail?

A

Some pathogens can conceal their carbohydrate signature to avoid phagocytosis
Our defense: opsonization

195
Q

Opsonization

A

Free floating immune proteins called opsonins - a type of complement protein - can recognize foreign objects
— Usually an antibody - attaches to foreign objects and provides “handles” which phagocytes can grab onto

196
Q

Respiratory burst

A

Some pathogens are resistant to lysosome enzymes
Our defense: respiratory burst

197
Q

Certain lymphocytes can activate macrophages….

A

Certain lymphocytes can activate macrophages to produce additional enzymes
- Free radicals and oxidizing chemicals
break chemical bonds in bacterial cell wall
Increases acidity of macrophage

198
Q

NK cell

A

Natural killer cell - defense against virus infected and cancerous cells
NK cells scan for abnormalities in our cells
(example - lack of a self cell maker called a major histocompatibility (MHC) protein)
NK cell then functions like a friendly “hacker” - comes into contact with infected cell and triggers apoptosis

199
Q

While immune cells are being recruited to the area…

A

Inflammatory chemicals released from infected/damaged cells are doing the following:
- limiting the spread of the infection
- calling more immune cells
- clearing cell debris
- promoting healing

200
Q

Acute Inflammation

A

Cardinal signs: heat, redness, swelling, pain
Several major inflammatory chemicals - histamine, kinins, prostaglandins, complement proteins, cytokines

All have same general function: increase blood flow and increase capillary permeability

201
Q

How acute inflammation helps fight infection?

A

Increased blood flow (hyperemia) via arteriolar dilation increases delivery of immune cells and chemicals
- accounts for heat and redness
Increased capillary permeability helps deliver a fluid called exudate to site of infection
- accounts for swelling and pain
— excess fluid presses on nerve ending, prostaglandins cause pain

202
Q

Exudate

A

Excess fluid helps sweep foreign particles into the lymphatic system for destruction
Also contains:
- clotting factors - walls off infection and provides scaffolding for healing
- complement proteins - free floating proteins which “complement” innate and adaptive immune response

203
Q

Complement Proteins

A

Recognize and bind to carbohydrate layer on foreign cells
Opsonizes foreign cell - enhance phagocytosis
Forms a Membrane Attack Complex (MAC)
– it’s just a hole: punctured cell wall takes on water and cell is lysed

204
Q

Interferons

A

Protection against virus infection
Small proteins released by certain virus infected cells
- viruses must invade host cells because they lack their own replication machinery

Interferons trigger viral defense mechanisms in nearby cells which have not yet been infected by the virus
— halts protein production and degrades viral RNA - prevents replication of virus

205
Q

Fever (in relation to immunity)

A

Triggered by release of pathogens from immune cells when pathogens are encountered
Increases body temperature by acting on hypothalamus
Unclear how fever fights infection - higher temp may damage pathogens, increased metabolic rate of normal tissue may clear infection faster

206
Q

The adaptive immune response…

A

Takes longer to initiate
Utilizes T and B cells
Is specific: only attacked identified pathogens
Is systemic: not limited to the site of infection
Has memory: once it has encountered a pathogen, then next time it appears, it will be eliminated with much greater efficiency

207
Q

The 2 branches of Adaptive Immune System

A

Humoral (antibody mediated)
- utilizes free floating antibodies secreted by B-lymphocytes
- targets: extracellular (toxins, bacteria, free viruses)

Cellular
- utilizes T-lymphocytes to directly attack pathogens
- targets: cellular (virus/parasite infected cells, cancerous cells)
- T-cells can also indirectly attack by releasing inflammation enhancing chemicals

208
Q

Adaptive Immune System trigger

A

Antigens
- a marker used to identify a particle or cell
Some antigens encountered will be identified as foreign, which will initiate the immune response
2 types of antigen: complete and haptens

209
Q

Complete Antigen

A

2 requirement:
- reacts with activated lymphocytes and the antibodies they release
- must be immunogenic
— stimulates the production of more lymphocytes (examples - pollen, bacteria, fungi)

210
Q

Antigenic determinants

A

Only certain parts of the antigen are immunogenic, called antigen determinants
Located on antigen surface
these are what antibodies and lymphocytes bind to
Large antigen particles can have many determinants
Each one can bind a different lymphocyte/antibody

211
Q

Incomplete Antigens or haptens

A

Includes many types of very small molecules, peptides, and nucleotides
can be reactive, but not immunogenic on their own

212
Q

how do haptens antigens work?

A

Haptens bind to a friendly protein
Makes a combination the immune system marks as foreign
example - poison ivy toxin

213
Q

MHC proteins

A

Certain immune cells can only bind to antigens contained on Major histocompatibility complex (MHC) proteins
MHC proteins are located on the cell surface with a “pocket” for an antigen
- protein in the pocket can be a self-antigen or foreign antigen

214
Q

Adaptive IS: B-lymphocytes (B-cells)

A

Oversee humoral immunity

215
Q

Adaptive IS: T-lymphocytes (T cells)

A

Oversee cellular immunity

216
Q

Antigen presenting cells

A

assist T-cells in recognizing pathogens
- these cells will contain MHC proteins

217
Q

5 steps of B/T cell development

A

1) B/T cells originate in red bone marrow
2) migration to primary lymphoid tissue for maturation (B-cells to red bone marrow and T-cells to thymus)
3) Release of primary lymph tissue and seeding of secondary lymph tissue
- here they likely encounter pathogens
4) antigen encounter and activation
- lymphocytes which have never seen a pathogen = naive
- pathogen binding activates the lymphocyte
5) once activated, B/T cells proliferate and differentiate (proliferation helps fight more of the same pathogens)

218
Q

B/T cells can differentiate into 2 main types:

A

Effector cells: fighting force
Memory cells: respond quickly to same pathogen

219
Q

2 Important abilities granted by maturation phase (B/T cell development)

A

Immunocompetence - develops receptors which can bind to one specific antigen
- all receptors on the same lymphocyte are the same
- each lymphocyte is committed to recognizing only one type of pathogen

Self-tolerance - must be unresponsive to self-antigens

220
Q

Test of lymphocytes

A

Tested for the 2 properties, those which fail the test are destroyed
- only about 2 % of lymphocytes survive

221
Q

How APCs work

A

1) Ingest foreign antigen
2) Embed a fragment of the antigen within their MHC protein
3) present the fragment to a naive T-cell to activate its cell which can act as APCs: dendritic cells, macrophages, B cells

222
Q

Humoral Immunity

A

Occurs when a B cell encounters an antigen that can bind its unique receptors
Causes that B-cell to proliferate or create clones of itself - called clonal selection

223
Q

clone differentiation

A

Some will become effector cells called plasma cells
- Plasma cells secrete 2000 antibodies/sec which bind to the encountered antigen
- marks the antigen for destruction by both innate and adaptive immune cells

The other will become memory cells
- survive for years and can mount an immediate immune response if the same antigen shows up again

224
Q

Memory cells causing immunological memory

A

When a B-cell first encounters the antigen, the proliferation and differentiation which occurs is called the primary immune response
- 3-4 day lag before antibody production ramps up
If the same antigen appears the second time, the memory cells immediately mount a secondary immune response
- little to no lag period
- more rapid antibody production

225
Q

Active humoral immunity

A

Antigens activate B-cells via natural infection or from a vaccine
- memory cells maintain the immunity

226
Q

Passive humoral immunity

A

Pre made antibodies are directly introduced into body
- can be naturally passed from mother to fetus or administered (snake anti-venom)
- these antibodies are degraded, providing only short-term immunity

227
Q

How do antibodies work?

A

When antibody binds with its recognized antigen, it forms an immune complex
- formation of the complex inactivate the pathogen in several ways
—neutralization
—precipitation
—agglutination
all 3 enhance phagocytosis

228
Q

Neutralization

A

binding sites on viruses and bacterial toxins are blocked

229
Q

Precipitation

A

like agglutination for small soluble molecules, not cells

230
Q

Cellular immunity

A

Mainly provides defense against virus/bacteria infected cells and foreign or cancerous cells
Involves activation of T-lymphocytes rather than B-cells

231
Q

Differences between B and T cells

A

All T-cells are activated only by antigens presented to them on MHC proteins, not free floating antigens
2 types of naive effector T-cells: CD4 and CD8 cells

232
Q

CD4 and CD8 cells

A

When activated by APCs, CD4 and CD8 cells differentiate into different effector cells

233
Q

Activated CD4 cells can becomes 2 possible effector cells

A

T-helper cell: activate B cells, other T cells, macrophages, and APCs
T-regulatory cell: moderates immune response
- dampens the immune response to prevent auto-immune conditions

234
Q

Activated CD8 cells become…

A

cytotoxic T cells: these cells directly destroy anything harboring a foreign antigen
- bind to and give infected cells a “death hug”
- release perforins and granzymes
- granzymes enter perforin pore and activate apoptosis

235
Q

Role of MHC proteins in antigen presentation

A

Antigens embedded within MHC proteins are “read” by T-cells to determine if that cells is healthy or infected, foreign or friendly

236
Q

MHC I proteins

A

found in almost all “self” cells
In its pocket, it has an antigen made of proteins from inside that cell (endogenous antigen)
if a self-cell becomes infected or cancerous, the antigen on its MHC I protein changes
- activate specifically naive CD8 cells
- signals cytotoxic T cells to destroy it

237
Q

MHC II proteins

A

Other type of MHC proteins
Found mainly on APCs - specifically activate CD4 cells
MHC II proteins can only contain in their pocket an antigen made from proteins engulfed by the APC
- these are exogenous antigens

238
Q

Dendritic cells

A

Unique type of APC
Contains both MHC I and MHC II proteins which are used to activate both CD4 and CD8 cells
- after it engulfs a foreign antigen, a piece of it gets embedded in both its MHC I and II proteins

239
Q

what do only dendritic cells do?

A

Only type of immune cell which can display an exogenous antigen in its MHC I complex
- allows them to activate both CD4 and CD8 cells

Anatomy (4 decks)

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