Physiology Exam 3

Front 1

Bacteria

Back 1

-living
-produce toxins which attack cell

Front 2

Virus

Back 2

-unknown if living
-consists of DNA with protein code
-hacks into cells

Front 3

5 types of leukocytes

Back 3

neutrophils
eosinophils
monocytes
basophils
lymphocytes

Front 4

neutrophils

Back 4

engage in phagocytosis
-engulf and destroy unwanted materials

Front 5

Eosinophils

Back 5

-participate in allergic reactions
-destroy parasitic worms

Front 6

Monocytes

Back 6

-become macrophages to engage in phagocytosis

Front 7

Basophils

Back 7

release histamine and haparin
-involved in allergic reactions

Front 8

B Lymphocytes

Back 8

secrete antibodies that indirectly lead to the destruction of foreign material
-mature in the bone marrow
-differentiates into either plasma cell or memory cell

Front 9

T Lymphocytes

Back 9

destroys virus-infected and mutant cells by releasing chemicals that punch lethal holes in the victim cells

Front 10

Innate Immunity

Back 10

-nonselective
-already present in body
-1st line of defense
-rapid, but limited defense

Front 11

Processes of innate immunity

Back 11

inflammation
interferons
natural killer cells
complement system

Front 12

Adaptive Immunity

Back 12

organism adapts to attack specific invaders

Front 13

Two Types of adaptive immunity

Back 13

antibody mediated
cell mediated

Front 14

Inflammatory Response process

Back 14

1. stab hand
2. activation of monocytes to become macrophages, which begin eating excess tissue and bacteria (phagocytosis). Macrophages release cytokines which attract other phagocytes (neutrophils).
3. Mast cells (basophils) release histamine, which increases blood flow to bring more white blood cells
4. some cytokines release pyrogens, which travel to the hypothalamus and intitiate prostaglandin release, which produces fever

Front 15

NSAID's

Back 15

Non-Steroidal Anti-Inflammatory Drug
-inhibits prostaglandin to reduce fever

Front 16

Interferons

Back 16

interfere with viral replication

Front 17

Interferon process;

Back 17

1. virus invades cell and begins to replicate. Cell releases interferons
2. interferons travel to uninfected cells
3. Interferons bind to receptors on cells
4. receptors release inactive enzyme to prevent protein synthesis and viral RNA replication.
5. Virus invades cell and activates enzyme. Virus cannot reproduce to control cells.

Front 18

Natural Killer Cells

Back 18

-non-specific, they attack any virus-infected or cancer cell
-rapidly activated (no maturation period)
- are limited in response (fewer in numbers than activated T-cells)
-kill using granules.

Front 19

Complement System

Back 19

-made up of 9 proteins (C1-C9) -produced by the liver
-non-specific defense system
-complements the action of antibodies

Front 20

2 Complement system pathways

Back 20

alternate: nonspecifically binds to CHO chains
classical: binds to antibodies specific to a bacteria

Front 21

MAC

Back 21

membrane attack complex
MAC formation: membrane attack complex
-Activated by C1
-located in cell membrane
-made of proteins
-causes lysis of bacteria

Front 22

Clonal selection theory

Back 22

There are millions of B-cells present at birth, each of which recognized a different antigen. The B-cells, when activated, differentiate into either plasma cells or memory cells.

Front 23

Antibody

Back 23

-protein molecules produced by B cells in response to introduction of an antigen.
-can bind to two antigens, and are then recognized by phagocytes to be opsonized.

Front 24

Memory cell

Back 24

a cell that can cause rapid proliferation of antibodies upon a second encounter with a foreign invader
-dormant until second antigen invasion

Front 25

5 ways antibodies fight infections

Back 25

-agglutination (antibodies bind to bacteria; precipitate out of solution)
-neutralization (poisons in bacteria made non-toxic)
-activation of complement system
-opsonization (making bacteria more prone to phagocytosis)
-stimulation of Natural Killer Cells

Front 26

Primary Immune Response

Back 26

-first encounter with antigen
-slow response

Front 27

Second Immune Response

Back 27

-subsequent exposure to antigen -produces much larger and faster response

Front 28

Vaccinations

Back 28

1. Dead pathogen is injected
2. body mounts an immune response against the pathogen
3. memory cell production.
4. exposure to real pathogen
5. immune response is fast and powerful so that few symptoms occur.

Front 29

3 types of T-cells

Back 29

Cytotoxic T-cells
Helper T-cells
Suppressor T-cells

Front 30

Cytotoxic T-cells

Back 30

kills virus infected cells and cancer cells by direct contact
-contain receptors that bind to MHC on infected cell surface, and then release perforin

Front 31

Helper T-cells

Back 31

enhance activity of cytotoxic t-cells, b-cells, and macrophages by secreting cytokines

Front 32

Suppressor T-cells

Back 32

-The "brake" of the immune system
-suppresses antibody production

Front 33

MHC's

Back 33

Major Histocompatibility Complex
-major player in cell lysing (see cell lysing process card)
-presents antigens at surface of cell for cytotoxic t-cell recognition

Front 34

Cell lysing process

Back 34

1. MHC's present antigens at surface of cell,
2. antignes bind to cytotoxic t-cell receptors.
3. cytotoxic t-cells release perforin into the infected cell through exocytosis.
4. Calcium exposure causes perforin to turn dagger-shaped,
5. perforin pierces the cell membrane, causing the cell to lyse.
6. free virus eaten by microphages.

Front 35

traumatic pneumothorax

Back 35

-puncture in chest wall
-pressure between the atmosphere and the pleural cavity are the same, resulting in the lung collapsing

Front 36

spontaneous pneumothorax

Back 36

-hole in lung
-pressure between the pleural cavity and lung are the same, causing lung to collapse

Front 37

During inspiration:

Back 37

-diaphragm contracts and moves downward
-external intercostals contract, pulling ribs upward
-thoracic volume increases
-transmural pressure gradient causes lungs to expand (pressure is less in lungs than outside, so air rushes in)

Front 38

during passive expiration:

Back 38

-diaphragm relaxes, moving upward
-external intercostals relax, lowering ribs
-decrease in thoracic volume pushes air out of lungs

Front 39

during active expiration:

Back 39

-internal intercostals contract, pulling ribs in tighter
-abdominal muscles contract, pushing diaphragm up into thoracic cavity
-pressure becomes greater inside lungs, so air rushes out

Front 40

Boyle's law:

Back 40

P1 * V1 = P2 * V2

if pressure is cut by half, volume doubles. for example:
P1=2, V1=2. then, P2=1, so V2 has to = 4

Front 41

Tidal Volume (TV)

Back 41

volume of air in one normal breath.

Front 42

Inspiratory reserve volume

Back 42

volume that the lungs can still expand after a normal inspiration

Front 43

Inspiratory capacity

Back 43

tidal volume + inspiratory reserve volume
-The maximum volume of air that can be inspired at the end of a normal quiet expiration

Front 44

Expiratory reserve volume

Back 44

the extra volume of air that can be actively expired by maximally contracting the expiratory muscles beyond normal

Front 45

Residual Volume

Back 45

The minimum volume of air remaining in the lungs even after a maximal expiration

Front 46

Functional residual capacity

Back 46

ERV+RV,
The volume of air in the lungs at the end of a normal passive expiration

Front 47

Vital capacity

Back 47

TV + IRV + ERV
The maximum volume of air that can be moved out during a single breath following a maximal inspiration

Front 48

Total lung capacity

Back 48

TV + IRV + ERV + RV.
The maximum volume of air that the lungs can hold

Front 49

Minute Respiratory Volume

Back 49

Tidal volume X Respiratory rate

Front 50

Minute Alveolar Ventilation

Back 50

the amount of new air entering the alveoli each minute

- Rate (Tidal Volume - Dead Space)

Front 51

Calculate Minute Respiratory Volume and Minute Alveolar Ventilation when tidal volume is 500 ml, dead space volume is 150 ml, and the respiratory rate is 15 breaths/min

Back 51

MRV: (TV)*(RR) = 500 * 15 =7500

MAV: RR(TV-DS) = 15* (500 - 150) = 5250 ml/min

Front 52

What is the effect of increasing the rate of alveolar ventilation on CO2 and O2 partial pressures of the alveoli of the lungs?

Back 52

Decrease CO2 and Increase O2

Front 53

Partial Pressure

Back 53

the pressure exerted by that gas alone if all other gases were removed

found by multiplying percent of gas by total pressure

Front 54

2 ways oxygen is carried in blood

Back 54

-dissolved in blood (about .3 ml O2/ 100 ml blood)
-bound to hemoglobin (about 1.34 ml O2/ 1g hemoglobin)

Front 55

calculate the capacity of blood to carry oxygen when the hemoglobin concentration is 13 g/100 ml blood

Back 55

13g/100ml blood x 1.34ml/g = 17.42 ml O2/100ml blood

Front 56

Oxygen carrying capacity

Back 56

How much oxygen can the blood carry when all oxygen binding sites on Hb are occupied

Front 57

Oxygen content of blood

Back 57

How much oxygen the blood is carrying.
(Oxygen carrying capacity * % saturation of Hb)

Front 58

3 forms in which carbon dioxide is carried in the blood

Back 58

1.Dissolved in the blood (9%)
2.As bicarbonate (64%)
3.As carbaminohemoglobin (27%)

Front 59

Carbonic Anhydrase

Back 59

Helps in process of turning CO2 into HCO3

Front 60

3 basic renal processes

Back 60

1. Glomerular Filtration
2. Tubular Reabsorption
3. Tubular Secretion

Front 61

Tubular Reabsorption

Back 61

movement of solutes and water from the kidney tubules back into the blood of the peritubular capillaries

Front 62

Tubular Secretion

Back 62

active transport of substances into the lumen of the kidney tubules form the blood.
this mechanism makes it so H+ and K+ ions and drugs can be removed from blood.

Front 63

Plasma clearance

Back 63

Measure of the rate at which substances are cleared from the plasma (units are ml/min)

-(Rate of urine formation x urine conc)/ Plasma concentration

Front 64

Filtration Fraction

Back 64

the fraction of plasma flowing through the glomeruli that is filtered into the tubules. FF=GFR/RPF or FF=insulin clearance/PAH clearance

Front 65

2 mechanisms to control micturition

Back 65

-micturition reflex
-voluntary control

Front 66

micturition reflex

Back 66

1. stretch receptors within the bladder wall are stimulated.
2. Afferent fibers carry impulses into the spinal cord and eventually stimulate the parasympathetic supply to the bladder. 3.parasympathetic stimulation to the bladder causes it to contract. 4. Because of the contractions the internal sphincter is pulled open

Front 67

4 basic digestive processes

Back 67

Motility
Secretion
Digestion
Absorption

Front 68

Digestive processes in mouth

Back 68

Motility: teeth grind up food
Secretion: saliva produced by salivary glands
Digestion: none
Absorption: none

Front 69

Salivary Amylase

Back 69

breaks starch into maltose (two glucose)

Front 70

Functions of saliva:

Back 70

1. moisten and lubricate food
2. salivary amylase begins digestion of CHO
3. antibacterial action (lysozymes)
4. solvent to allow taste to occur
5. buffers acids (prevents caries)

Front 71

Digestive Processes in Stomach

Back 71

-motility: stores food. Contraction of smooth muscle mixes and grinds food into chyme.
-secretion: mucus, pepsinogen, HCl, intrinsic factor, gastrin, somatostatin, histamine
-digestion: salivary amylase continues to break down CHO. pepsinogen breaks down proteins
-absorption: NO food is absorbed. some drugs are.

Front 72

parietal cells

Back 72

secrete HCL and intrinsic factor

Front 73

intrinsic factor

Back 73

aids in vitamin B12 absorption

Front 74

functions of HCL in stomach

Back 74

-H is the primary active transport, Cl is the secondary active transport.
-activates pepsinogen,
-breaks down connective tissue and food particles,
-denatures proteins
-kills microorganisms.
-secreted into lumen

Front 75

Chief cells

Back 75

secrete pepsinogen, which, when activated, leads to protein digestion

Front 76

Pepsinogen

Back 76

-cleaved by HCL to become active pepsin

Front 77

Pepsin

Back 77

-breaks proteins into peptide fragments and begins protein digestion.
-cleaves more pepsinogen

Front 78

Digestive Processes in Small Intestine

Back 78

-Motility: peristaltic contractions and segmentation mixes and propels chyme; migrating motility complex cleans it out between meals
-Secretion: juice of intestine lubricates intestine
-Digestion: major site of digestion. accomplished by pancreatic secretions, bile, and brush border enzymes
-Absorption: the site of food absorption

Front 79

Pancreatic Secretions

Back 79

Bicarbonate
Proteolytic Enzymes:
-trypsinogen (--> trypsin)
-chymotrypsinogen (--> chymotrypsin)
-procarboxypeptidase (--> carboxypeptidase)
Pancreatic amylase
Pancreatic lipase

Front 80

Pancreatic Amylase

Back 80

converts polysaccharides into maltose

Front 81

Pancreatic Lipase

Back 81

converts triglycerides to 2 fatty acids and 1 monoglyceride

Front 82

Bicarbonate

Back 82

neutralizes chyme from stomach
-protects small intestine
-allows enzymes to work (they are inhibited by acid)

Front 83

Chemicals that stimulate pancreatic secretion

Back 83

-CCK
-secretin
--they are released from the duodenum

Front 84

2 functions of bile

Back 84

-excretion of bilirubin
-emulsification of fat

Front 85

CCK

Back 85

-stimulates pancreatic secretion
-stimulates bile secretion by contracting gallbladder

Front 86

brush border

Back 86

-lining of microvilli in small intestine
-contains
1.enterokinase
2. maltase, sucrase, and lactase
3. aminopeptidases

Front 87

Digestion Processes in the large intestine

Back 87

Motility: Haustral contractions mix feces; mass movements cause feces to move long distances
Secretion: alkaline mucus lubricates intestine; sodium bicarbonate neutralizes acid
Digestion: none
Absorption: water and salt (drying of feces)

Front 88

Defecation reflex

Back 88

1. mass movements force feces into rectum, stretching it.
2. stretch receptors initiate reflex
3. internal sphinctor relaxes
4. contraction of rectum muscle increases