choroid plexus (brain)

proximal convoluted tubule (kidney)

epithelial cell brush border of the small intestine

skeletal muscle

adipocytes (fat cells)

Hydrolysis of macromolecules

metabolism into acetyl COA

oxidation of acetyl

& oxidative phosphorylations

are all examples of what type of reaction?

what hormones do alpha cells release?

what do these hormones do?

glucagon

secreted when glucose is gone

what hormone do beta cells release?

what do they do?

insulin

when glucose is abundent in the blood

what changes in blood chemistry first appear in the progression of DM

last?

first: high glucose in the blood

last: lipolysis

in gestational DM

what hormone causes the raise in blood glucose?

what drugs stimulate insuline sensitivity?

good for DMI

glucotrol

micronase

acarbose

(alpha- glucosidase inhibitors)

high fluctuations in blood sugar verry high/ verry low

(bad insulin control)

severe dehydration

high blood sugar

confusion

no ketosis

observed in undiagnosed DMII

believed that some insulin inhibits lipolysis

-allows glucose to enter skeletal muscle, and adipose tissue

1inhibit breakdown of lipids of adipose tissue

inhibits breakdown of glycogen in liver

timulated synthesis of glycogen in liver

NAD

NADH

NADP+

NADPH

AMP

COA (substrate)

NAD+ (substrate)

ATP (product)

Actyl COA (product)

NADH (product)

through physphorylation

when a P is added, PD is inactive

it is irreversible

so we can't convert most fatty acids into glucose

how much ATP does

NADH

FADH2

yield?

NADH: 3

FADH2: 2

how much ATP is yielded by aerobic breakdown of 1 glucose?

Glycolysis: 8

Pyruvate dehydrogenase: 6

Citric Acid: 12

total 36-38 ATP

citrate synthase

isocytrate dehydrogenase

alphs-ketogluterate dehydrogenase

(where NADH starts)

4 H+ are pumped out

Ubiquinone

a nonpolar lipophylic carrier which diffuses through the membrane

(where FADH starts)

succinate dehydrogenase

(also present in the TCA)

(a cytochrome with heme like group)

2 H+ are pumped out, as electrons pass through

(cytochrome with heme like group)

a water soluble protein loosely associated with the membrane

(cytochrome with heme like group)

4 H+ are pumped out as electrons pass through

CN

CO

how many protons channeled into the cell for oxidative phosphorylation gives enough energy to turn ADP into ATP

hoe many protons does NADH and FADH2 pump 

3 protons = 1 ATP

NADH pumps 10 Protons

FADH2 pumps 6 protons

present in oxidative phosphorylation

3 H+ enter, 1 ATP made

1.) Hexokinase (glucokinase in the liver)

2.) phosphofructokinase-1

3.) pyruvate kinase

cycle where lactic acid is sent to the liver.

the liver turns the lactate into pyruvate through lactate

dehydrogenase

and then turns the pyruvate into glucose through gluconeogenesis and releases the glucose back into the blood

Hexokinase/Glucokinase

how is it regulated?

by adding a p to glucose it traps it in the cell.  (this is not a comiting step of glycolysis)

phosphorylated glucose can still do other stuff like make glycogen.

Hexokinase

where:

is it activated by high Glucose?

Vman/Km

Hexokinase is housekeeping in ALL cells

it is always on, and is not activated by high glucose.

Low Vmax, Low Km

Glucokinase

where:

is it activated by high glucose?

Vmax/Km

Glucokinase

in liver; pancreas beta cells

activated by high glucose

high Vmax, high Km

Phosphofructokinase-1 (PFK-1)

what is it?

what does it do?

sctivstors:

inhibitors:

PFK-1

a large enzyme that converts fructose 6 phosphate with ATP into fructose 1,6 bisphosphate and ADP

Activators: AMP, fructose 2,6 biaphosphate

Inhibitors: ATP, Citrate, low PH

Pyruvate kinase

where:

what:

Pyruvate Kinase

in liver

turns phosphoenol pyruvate and ADP into pyruvate and ATP

what makes:

lactic acide

amino acids

glycerol

lactic acid: from anaerobic resperation

amino acids: from dietary proteins

glycerol: from tryasal glyceral neutral fat.

cytosol of liver

cortex of kidney.

what is the "nemesis" of hexokinase/glucokinase?

(present in gluconeogenesis)

glucose 6 phosphatase

it turns glucose 6 phosphate into glucose

what is the nemesis of PFK-1

present in gluconeogenesis

it's + and negative effectors

Fructose 1,6- bisphosphatase

+: citrate

-: F-2,6-BP and AMP

turns fructose 1,6 BP into fructose 6 p

what is pyruvate Kinase's nemesis?

present in gluconeogenesis

1.) pyruvate Carboxylase.  it turns 2 pyruvate into 2 oxaloacetate. (needs biotin)

+: acetyl COA

-: ADP

2.) Phosphoenol Pyruvate Carboxykinase.  it turns oxaloacetate into phosphoenol pyruvate.

-: ADP

when is glycolysis turned on, and gluconeogenesis turned off?

when is gluconeogenesis turned on, and glycolysis turned off

at the present of this molecule or absence of it

when F-2,6 BP is present, liver glycolysis occurs

when F-2,6 BP is absent, liver gluconeogenesis occurs.

when "then enzyme" that deals with Fructose-2,6-BP is phosphorylated, which kinase is active?  what does it do ti F-2,6-BP?

when the enzyme is phosphorylated, the FBPase-2 domain is active.  this degrades F-2,6-BP.  this enzyme is phosphorylated when protein kinase A is activated (by epinepherine/glucogon)

ultimately favors gluconeogenesis

When "the enzyme" that deals with F-2,6-BP is dephosphorylated, what domain is active?

what does it do to F-2,6-BP?

PFK-2 domain is active when "the enzyme" is dephosphorylated. 

this makes F-2,6-BP.  this enzyme os dephosphorylated when insuline is abundent. 

ultimately results in liver glycolysis.

of these, which does the muscle not have receptors for?

1.) insuline

2.) epinepherine

3.) glucogon

does high alcohol intake result in hypoglycemia or hyperglycemia

why?

high alcohol = hypoglycemia.

ethanol metabolism results in high NADH which favors gluconeogenesis.

glucose (starches)

galactose (milk)

fructose (honey)

lactose (galactose + fructose in milk)

Sucrose (fructose + glucose in table sugar)

alpha amylase (ptyalin)

which cleaves bonds.  some sugar can be absorbed through the mucous membrane.

the acidity of the stomach (1.0-3.0)

denatures alpha amalase from the mouth, but also cleaves bonds of polysachurides into monosachurides.

the PH of the SI is 6.0 to 7.o

when food enters, the low PH triggers secretion of secretin which triggers the pancreas to secrete bicarbonate to buffer. 

pancreatic amylase hydrolizes starch and glycogen. 

found in all cells

high concentration in liver (10% of wet weight)

and muscle (1-2% of weight).

there is 2X more glycogen in muscle than in liver.

core of every glycogen. 

has an oligosachuride chain of glucose added in ER.

adds 8 more glucose to itself.

glucose-6-phosphatase (in liver only, not in muscle)

cleaves the phosphate from glucose-6-phosphate allowing the liver to generate glucose for the body.

what are the

activators of glycogen phosphorylase?

inhibitors?

activator: Ca++ (muscle only), AMP (muscle only)

inhibitor: ATP

tyrosine binding to it's receptor involves

(old exam)

tyrosine phospforylation of insuline receptor substrates

(old exam)

the comiting step of glycolysis is catalyzed by

(old exam)

phosphofructokinase-1

(old exam)

what allosteric regulators regulates liver glycolysis or gluconeogenesis through hormones like insuline or glucagon?

(old exam)

fructose 2,6 bisphosphate

(old exam)

how does glucophage work?

(old exam)

decreases glucose production by liver

(old exam)

phosphorylation of an enzyme is catalized by

(old exam)

a protein kinase

(old exam)

scalene

sternocleidomastoid

forced inspiration & expiration

has pre-botzinger

NTS

ventrolateral:

Lateral

dorsal medial

Ventrolateral: DRG

Lateral: pripheral chemoreceptors & pulmonary stretch receptors

dorsal medial: arterial baroreceptors

apneustic center

where

what

pons

prolongs inspiration by effecting pre botzinger

Pneumotaxic

where:

what:

pons

''fturn off inspiration, effects apneustic and prebotzinger

caroted body

aortic body

sense Pao2, sends messages to lateral NTS

if Pao2 falls below 60, increase ventilation

type I send out dopamine when low Pao2

minute by minute control

ventrolateral medulla

high CSF CO2 -> low PH ECF -> chemoreceptor -> medula to increase ventilation

smooth muscle of lungs prevents overstretch

Breuer-herring reflex

airway epithelial

cause bronchoconstriction

cough/sneeze

pulmonary C fiber

j receptors

near alviolar capilaries

interstitial edema -> apnea -> rapid shalow breathing

irritant

cough/bronchoconstriction/apnea/larynx spasm

regardless of Po2 if Pco2 high: hyperventilation

body more responsic\ve to pco2 when hypoxic

increasing alveolar ventiltion and unchanged metabolism

Po2

Pco2

Po2: increase

Pco2: decrease

Po2: decrease

Pco2: increase

increased metabolism, unchanged alveolar ventilation

Po2

Pco2

Po2: decrease

Pco2: increase

Word suffix

itis

suffix

agia/dynia

suffix

centesis

suffix

megaly

suffix

tripsy

suffix

esis/ism

Prefix

dys

ab= away

ad= to

prefix

ante

prefix

dia

prefix

juxta

meso

juxta: near

Meso: middle

colors

cyano

cosin/rube

cirh/xantho

cyano: blue

cosin/rube: red

cirh/xantho: yellow

suffix

oid

pnea

oid: resembling

pnea: breathing

suffix

cele

ectasis

emia

iasis

malacia

cele: hernia

ectasis: dilation

emia: blood

iasis: formation of

malacia: softening

suffix

plasia

ptosis

rrhagia

rrhexis

plasia: formation

ptosis: downward displacement

rrhagia: discharge

rrhexis: rupture

suffix

desis

pexy

desis: binding

pexy: suspension

suffix

tomy

stomy

tomy: incision

stomy: creating an opening

criminal: person vs society

civil: person vs person

FDA

controls:

controls:

manufacture/trials

drug lables

prescription status

diet pills

2 years

unless certified before 1/1/08

6 months

(5 refills)

1 RX per form

quantity written and spelled out

must be written Rx (or written givin within 7 days after verbal)

pharmacist sign each Rx

limits on pseudaphed

per day

per month

30 hours every 2 years