Tbr Biology Modules 1-5

Front 1

What are the 4 types of tissues

Back 1

1. Epithelial-makes up the layers
2. Nervous- innervate
3. Connective- holds in place
4. Muscle-helps movement of organ

Front 2

3 main types of specialized junctions

Back 2

1. Tight Junctions- Permiability
2. Desmosomes- Secure position
3. Gap junctions- pore like structures that allows H20 and solution molecules to equlibrate.

Front 3

Define: Endo-

Back 3

Endo means directly released into blood

Front 4

Define: Exo-

Back 4

Exo means released via a duct

Front 5

5 main steps of conducting a nerve impulse

Back 5

1. Stimulus: Resting nerve is -80m. There is a THRESHOLD that must be reached as an ALL OR NOTHING signal
2. Depolarization: Na+ flows in
3. Repolarization: K flows out. Nerve is -60
4. Hyperpolarization: K flows in
5. Refractory: Na+ chaneels close- no other AP

Front 6

Name to 5 actions that take place at the POST synaptic cleft to propagate an action potential

Back 6

1. The action potential opens the Ca2+ inonophore
2. Ach binds post synaptic cleft and released into the cleft
3. Ach goes to membrane and binds Pre synaptic cleft
4. New action potential is propagated
5. Ach-esterase breakes Ach back to Acetyl- Co

Front 7

What are the following:
1. Triangle
2. Star
3. Heart
4. Lightening Bolt
5. Diamond

Back 7

1. Triangle: A band- Myosin (thick)
2. Star: Z disc
3. Heart: M line
4. Lightening Bolt: I band- Actin (thin)
5. Diamond: H zone

Front 8

Describe how muscle contractions work

Back 8

1. Relaxed- Myosin is 45degrees. Troponin hiding the myosin heads.
2. ATP binds and myosin releases the Actin
3. ATP is hydrolyzed to ADP and Pi
4. Ca2+ floods our from the Sarcoplasmic reticulum and shifts the tropomyosin into place
5. Myosin and actin bind
6. Inorganic phosphate leaves and ADP leaves= POWERSTROKE and moves it forward
7. ATP binds and causes myosin to release the actin again

Front 9

Describe the following part of the brain:
1. Paretial
2. Temporal
3. Frontal
4. Occipital

Back 9

1. Paretial- touch
2. Temporal- Hearing
3. Frontal- Personality
4. Occipital- Vision

Front 10

Components of Forebrain

Back 10

1. Cerebrum- Cerebral cortex
2. Thalamus- Visual and auditory
3. Hypothalamus- Visceral
4. Pituitary- Master Endocrine

Front 11

Components of Brainstem

Back 11

Midbrain: Movement and pleasure
Cerebellum: Coordination
Pons/Medula: Visceral
Reticular Formation: alerts and shut off to sleep

Front 12

Example of a Monosynaptic Pathway

Back 12

Extensor Muscles

Front 13

Example of Polysnaptic Pathway

Back 13

Flexor

Front 14

starch

Back 14

glucose polymer w/alpha linkages, found in plants

Front 15

glycogen

Back 15

branched polymer of glucose with alpha linkages

Front 16

cellulose

Back 16

glucose polymer w/beta linkages, found in plants. not digestable by animals.

Front 17

competitive inhibitors

Back 17

take up active site [Efree] but not permenantly. can be overcome by high conc of substrate
Vmax same
Km looks to increase

Front 18

Noncompetitive inhibitors

Back 18

bond to enzyme at nonactive site [Efree] and [ES], change its shape to make it less effective.
Vmax decreases
Km stays the same

Front 19

glycolysis

Back 19

breaks 6-carbon glucose into 2 3-carbon pyruvates, 2 molecules ATP and 2 NADH. occus in cytosol.

Front 20

aerobic respiration

Back 20

produces 36 ATP incl glycolysis. 1 NADH = 3ATP, 1FADH2 = 2ATP.

Front 21

krebs cycle

Back 21

pyruvate->acetyl CoA turns cycle 2x. Cycle produces 1ATP, 3NADH, 1FADH2.

Front 22

Enzymes exhibit saturation kinetics.. =

Back 22

as the conc of substrate increases, the rate of the rxn also increases until Vmax (max rate). Vmax is proportional to enzyme concentration.

Front 23

Protein Structure:
Primary
Secondary
Tertiary
Quaternary

Back 23

Primary: sequence of amino acids that determines basic secondary structure of protein (B mercampenol experiment)

Secondary: α helix, β sheet

Tertiary: Twisted polypeptide, interactions within itself (Zinc Finger and Leucine Zippers)

Quaternary: multiple polypeptide, interactions between subunits

Front 24

Factors that effect enzymes

Back 24

Temperature

PH

Front 25

Where does most glycolysis occur in humans?

Back 25

Cytosol of Liver Cell

Front 26

Aerobic Respiration occurs where?

Back 26

In the mitochondria

Front 27

Which are the Purines

Which are the Pyrimidines

Back 27

Adenine, Guanine

Cytosine, Thymine, Uracil

CUT the Py

Front 28

Pathway of Eye

Back 28

Cornea
Anterior Cavity
Pupil
Iris
Lens (connected to ciliary muscle)
Retina (rods and cones)

Front 29

Pathway of Ear

Back 29

Tympanic Membrane
Malleus, Incus, Stapes
Oval Window
Cochlea
Hair cells

Front 30

Stomach (4 major cell types)

Back 30

Mucous Cells- makes mucous
Chief Cells- Synthesis Pepsinogen
Parietal Cells- Est. a H+ gradient
G Cells- Secretes Gastrin

Front 31

Pancreas- 6 major enzymes

Back 31

1)Trypsin
2)Chymotrypsin
3)pancreatic amylase
4)lipase
5)ribonuclease
5)deoxyribonuclease

Front 32

Autonomic- Sympathetic

Parasympathetic

Back 32

flight or fight (epinephrine and norepinephrine)

rest and digest (acetylcholine

Front 33

Give the divisions of the PNS

Back 33

I. Peripheral Nervous System
a. Somatic Nervous System (Voluntary)- Ach
b. Autonomic Nervous System (Involuntary)- Ach and Noroepi

Front 34

Parasympathetic Nervous System

Back 34

PNS (Rest and Digest):
a. Origin-Sarcal+ Midbrain
b. Pre Ganglion- long (ACh)
c. Post Ganglion- Short, near the organ it affects (ACh)
d. ex. Vagus Nerve

Front 35

Sympathetic Nervous System

Back 35

SNS (Fight or Flight):
a. Origin- Thoraic and Lumbar
b. Pre Ganglion- short, into a trunk with diff fates. (ACh)
c. Post Ganglion- long, far from organ to affect (Noroepi)
d. ex. Adrenal Medula has no post ganglion

Front 36

Non Polar Amino Acids (Hydrophobic)

Back 36

Glycine, Alanine, Valine, Leucine, Isoleucine, Proline, Methionine, Phenylalanine, Tryptophan

Front 37

Polar Charged Amino Acids (Hydrophilic)

Back 37

Serine, Theronine, Cysteine, Tyrosine, Asparagine, Glutamine

Front 38

Polar Charged amino Acids

Back 38

Aspartate, Glutamate, Lysine, Arginine, Histadine

Front 39

Henderson Hassalbach Equation

Back 39

pH=pKa+ log [A-]/[HA]

Front 40

Henderson Hassalbach Trick
Relationship between pH-pKa to [A-]/[HA]

Back 40

Front 41

Isoelectric Point

Back 41

pI=[pKa1+pKa2]/ 2

pH>pI- migrate to anode (+)
pH<pI- migrate to cathode (-)

Front 42

Explain a titration curve and which is the best buffering region.

Back 42

pH is 1 unit from the pKa is the best buffer region.

Front 43

Give characteristics of alpha helix/B pleat of Protein folding.

Back 43

Front 44

Formula for sterioisomers

Back 44

2^n where n is the number of sterioisomers,

(this typically excludes the first and last carbons, and the carbon that is the keytone, therefore 5 carbon carb has only 3 sterioisomers)

Front 45

Alpha vs Beta Glucose

Back 45

Front 46

Give the 2 oxidizing agents used to see the carbohydrate functional groups (aldose, ketose)

Back 46

1. Tollen's Agent (Ag+)- Silver precipitate
2. Benedict's Reagent (Cu2+)- Brick Red precipitate

Note: these only detect reducing sugars such as Lactose (hemiacetal and hemiketal, not acetal and ketals)

Front 47

Formula for carbohydrate

Back 47

(CH2O)n

-Aldehyde/Keytone + 2 or more alcohols

Front 48

Define and give the properties for Saturated Fatty Acids

Back 48

Saturated: All carbons have max number of H's

increased Wanderwalls, increased melting point, decreased fluidity, solid at RT.

Front 49

NTP binding and strenght

Back 49

A=T (U)
C≡G

Front 50

Types of RNA

Back 50

mRNA: message to synthesize protiens
tRNA: transfers amino acids in ribosome
rRNA: makes up the ribosome

Front 51

Types of Membrane Transport

Back 51

1. Simple Diffusion
2. Facilitated Diffusion
3. Primary Active Transport
4. Secondary Active Transport

Front 52

Simple Diffusion

Back 52

Moves down a concentration gradient- from high concentration to low concentrations

Front 53

Facilitated Diffusion

Back 53

Moves down a concentration gradient, but needs some help (a membrane protein).
a. Uniport- one thing at a time
b. Symport- 2 things at a time in the same direction
c. Antiport- 2 things at a time in opposite directions

Front 54

Primary Active Transport

Back 54

Goes against a concentration gradient, from low concentrations to high concentrations. Uses energy directly from the hydrolysis of ATP

Only 2 known
1. Na+-K+ pump: Antiport 2 K+in 3Na+ out
2. Ca2+ ATPase: 2Ca+ out into the cytosol for every ATP

Front 55

Secondary active transport

Back 55

Goes against a concentration gradient, from low to high.
Uses ionic gradient established by primary active transport.

ex. Glucose and Na+ in the kidney: increased Na+ in the cell already but once glucose and Na+ bind the symport lets them both in. The Na-K pump only reads the Na+ levels (1 active transport) but the glucose piggybacks in secondary transport

Front 56

Describe the Michaelis-Menten Enzyme Inhibition for competitive and non competitive inhibition

Back 56

Panel A: Original
Panel B: Competative Inhibitor (same Vmax different Km)
Panel C: Non-competative Inhibitor (different Vmax same Km)
Panel D: Uncompetative inhibitor (Paralell to original)

Front 57

Relationship between Km (K2/K1) and ES binding

Back 57

As Km increases= decreased ES binding
As Km decreases= increased ES binding

Km=K2/K1

Front 58

Define zero order and first order kinetics

Back 58

First order: V proportional to [S]= As [S] increases V (rate) increases

Zero order: V independent to [S]= As [S] increases V doesn't change

Front 59

Name the 4 check points for regulation of glycolysis

Back 59

1. Increased ATP= Decreased Phosphofructose Kinase (PFK).

2. Increased AMP= increased PFK.

3. Increased Citrate= Decreased PFK

4. Increased H+= decreased PFK functionality.

Front 60

How does pH affect PFK functionality?

Back 60

Increased H+= This decrease in pH augments ATP inhibition of PFK. This assumes lactic acid buildup so decreased PFK functionality.

Front 61

How does citrate buildup affect PFK functionality?

Back 61

Increased Citrate= This means that there is a lot of citrate buildup from the citrate acid cycle. There is no more need to commit more glucose for degredation. Decreased PFK

Front 62

How does AMP affect PFK functionality

Back 62

Increased AMP= AMP reverses the inhibition from ATP. Therefore increased PFK. PFK activity increases as ATP/AMP ratio is lowered.

Front 63

How does ATP affect PFK functionality

Back 63

Increased ATP= Decreased Phosphofructose Kinase (PFK). ATP alosterically inhibits PFK. PFK activity increases as ATP/AMP ratio is lowered.

Front 64

Starting at Glucose name the essentials thru glycolysis and Krebs

Back 64

Front 65

What is gluconeogeneisis

Back 65

Gluconeogenesis is synthesis of glucose. It takes place in the liver.

Front 66

Explain what happens in the muscle cell and liver cell respectively in terms of glycolysis.

Back 66

Front 67

What drives Krebs and Gluconeogenesis

Back 67

Increased Acetal CoA= Increased Pyruvate Carboxilate= increased oxaloacetate which drives Krebs and Gluconeogensis

Front 68

Overall Net ATP of Gycolysis and Gluconeogenesis

Back 68

Glycolysis = 2ATP
Gluconeogensis=6ATP therefore NET -4 ATP

Front 69

True or False: Gluconeogensis is the reverse of Glycolysis

Back 69

False, it is not the exact reversal because there are irreversible steps in glycolysis (where ATP) have been spent, that are bypassed in glyconeogensis to prevent spending ATP to undo it.

Front 70

How many ATP are the following worth
a. 1 FADH
b. 1 NADH

Back 70

a. 1FADH=2 ATP
b. 1NADH=3 ATP

Front 71

Give a general overview of the urea cycle

Back 71

Front 72

What are the parts of the Kidney's nepheron and the journey through it.

Back 72

a. Proximal Convoluted Tubule
b. Loop of Henley
c. Distal Convoluted Tubule
d. Collection Duct

Front 73

Describe how the Proximal convoluted tubule (a) works

Back 73

Decreased regulation.
100% absorption of Glucose, Protein, and Vitamins.
80% Absorption of H20 and Na/Cl

Front 74

Describe how the distal convoluted tubule (b) works.

Back 74

Close to the loop of Henley.
Impermeable to urea and H20
Lets ions out
Increased dilution of the urine

Front 75

Describe how the loop of henely (c) works.

Back 75

There are three parts to the Loop of Henely.

*= H20 can leave. Urea and NaCl cannot. Increase concentration of urine.

**= Urea can leave, but NaCl and H20 can not. Decrease concentration of urine.

***=Actively transports ions (NaCl) out. H20 and urea can not leave. Further dilutes urine.

Front 76

Describe how the collecting duct (D) works

Back 76

ADH- increased release of ADH causes increased H20 reabsorption which causes increased urine concentration

Aldosterone- increased aldosterone means increased Na in epithelials and increase K+ in lumen.

Front 77

Explain how ADH can be used to counteract a drop in BP due to a hemorrhage for example

Back 77

Premise: Blood pressure drops therefore decreased blood volume

1. ADH- Atria--> Hypothalmus to release vassopressin (ADH)
2. This works in the kidneys to increase H20 resorption into the blood thereby increasing blood volume.
3. This leads to increased blood molarity as well because ADH is circulating in the blood.

B.

Front 78

Explain how the renin-angiostensin-aldosterone system can be used to counteract a drop in BP due to a hemorrhage for example

Back 78

1. When BP drops renin is released into the blood stream.
2. Renin floats around and converts inactive forms of angiotensin (produced by liver) into angiotensin I
4. Most angiotensin I is converted to angiotensin II this then
a. directly causes vasoconstrition in the arterioles (thereby increasing BP) and
b. causes aldosterone to be released from the cortex. Aldosterone increases Na+ reapsorbtion into the blood therefore increasing blood osmolarity and so H20 will flow there and this increases blood volume and thereby increases BP.