waver Carbohydrates Lipids
a glucose a
glucose
CH - OH
Aft-di-polar
CH - OH CH - OH CH - OH
I condensation
molecule I I I
eY
-
Oi
o
onYL
H -
Lipids
-
ins
-
H
HH Galy acid
Y Ybit
:
I
jo
in
- I I
most
bit
H
Hi
↳
H H
gr
OH
hydrogenDandeene E
I
I
-
I I
soluble
ji
·
↑ it hydrolysis it ji ↑ it ji fary acid
I ↓ Re
Hf
+
monosaccharide 1
glycoside
e
-
H2o removed
, -
-
acid
disaccharide falty H
Properties 2 (1 4)
a
glucose maltose
hydrophobic
=
x ,
B
glucose galactore
lactose
DI saccharides
dipolar
+ =
-
Cohesive because they are
a glucose
+ tructure :
sucrose
surface cohesion flow
good for transport Formation of
triglyceride
-
lots of glucose (1 4)
a ,
=
amylose
-Solvent good at
transporting around the
body glucose (1 AND 6)
4 1 lots of side branches amylopectin
IPOLY
H ① H
d
a
saccharides
+
=
, ,
glycogen (1 , 4 AND 1 6) + LOTS of side branches :
glycogen I
I
HO R
,
- -
H -
C -
OH H C -
0
mass transport system STARCH mixture of amylose +
amylopectin ②
=
11
-compact :
good for
storage H-C OH HO-C R H C 0
-
-
- -
side branches
glucose
released quickly
- :
-
raw materials
exchange organs from
Carry -
insoluble :
doesn't let water in
good for storage
H C OH
O ③
lungs/digestive system
-
to
-
e
g. .
body cells , main energy fore in
plants H0-C
19
-
R
H -
c -
0
-Remove metabolic waste e
g CO2 i H
↓
.
GLYCOGEN
.
a
glucose (1 , 4 and 6) IOB of side branches
fatty acids
=
1 +
,
In mammals mass transport system =
-
side branches quick energy release
:
glycerol
H20 released triglycer
,
-compact storage
=
circulatory system .
-
insoluble : doesn't cause cels to well by osmosis
large molecule lots of energy sto red
:
.
main crore in animals
aort a energy
ven
cuperior
car a -- ↑
↓ E pulmonary
ARTERIES
LIFESTYLE HEALTH AND RISK
↓
↑W artery
I - ·
-
W
left atrium
-
I
↓/~
j
↳ Risk factors
R thick muscular walls of CVD
-
- endothelium
Damage inflammatory response
-
to
:
↳ -[
-
pulmonary Memmm u m
folded endothelium (expands
↓
veins White blood cells lipids clump together
-
- +
Diet (high saturated fat
-
-
/
7 j2
right ~
under pressure) Time =
more build up =
plaque= atheroma =cholesterol
:
at heromal
small lumen
-
atrium
L Plaque partially blocks lumen :
restricted blood How -High
I
blood pressure
endothelium)
VEINS :
high blood pressure . damage to
(carbon monoxide
Smoking
-
left
Hardening of arteries atherosclerosis
:
- I
right thin oxygen in blood/tissu
umm reduces
ventricle muscular walls
rentricle
-values (backflow) : heart attack/stroke Nicot
B lood clot formation
.
makes platelets sticky bloo
11
=
RHS deoxygenated lumen
large
=
-
numm e
clot Also reduces antioxidan
prothrombin
.
Dr
inferior LHS
=
oxygenated =celldamage
=
Atheroma)
CAPILLARIES
ven a cara -
Genetics
aorta
one cell thich (diffusion) - THROmOPI e
-Age (plaque builds up over
Librinogen
-
/Y
- -Gender (men
i ↑ ~↑
likely
-I↑
metabolic
W exchange
L more
- :
-
- =
&
pulmonary- bestrogen levels
=
R
-
arvery ↳ semi-lunar THROMBIN I
good' cholesterol)
values
I I-
e e
perior
W - pulmonary atria ventricles
-
L
vena cara
"
I arvery Librin
L
Treatment of CVD
&
->
W
W ⑪ ② ③ + platelets #
a S red
rea blood
-1
I ~
CeIIS
cellS -Antihypertensives= reduc
= +
a glucose a
glucose
CH - OH
Aft-di-polar
CH - OH CH - OH CH - OH
I condensation
molecule I I I
eY
-
Oi
o
onYL
H -
Lipids
-
ins
-
H
HH Galy acid
Y Ybit
:
I
jo
in
- I I
most
bit
H
Hi
↳
H H
gr
OH
hydrogenDandeene E
I
I
-
I I
soluble
ji
·
↑ it hydrolysis it ji ↑ it ji fary acid
I ↓ Re
Hf
+
monosaccharide 1
glycoside
e
-
H2o removed
, -
-
acid
disaccharide falty H
Properties 2 (1 4)
a
glucose maltose
hydrophobic
=
x ,
B
glucose galactore
lactose
DI saccharides
dipolar
+ =
-
Cohesive because they are
a glucose
+ tructure :
sucrose
surface cohesion flow
good for transport Formation of
triglyceride
-
lots of glucose (1 4)
a ,
=
amylose
-Solvent good at
transporting around the
body glucose (1 AND 6)
4 1 lots of side branches amylopectin
IPOLY
H ① H
d
a
saccharides
+
=
, ,
glycogen (1 , 4 AND 1 6) + LOTS of side branches :
glycogen I
I
HO R
,
- -
H -
C -
OH H C -
0
mass transport system STARCH mixture of amylose +
amylopectin ②
=
11
-compact :
good for
storage H-C OH HO-C R H C 0
-
-
- -
side branches
glucose
released quickly
- :
-
raw materials
exchange organs from
Carry -
insoluble :
doesn't let water in
good for storage
H C OH
O ③
lungs/digestive system
-
to
-
e
g. .
body cells , main energy fore in
plants H0-C
19
-
R
H -
c -
0
-Remove metabolic waste e
g CO2 i H
↓
.
GLYCOGEN
.
a
glucose (1 , 4 and 6) IOB of side branches
fatty acids
=
1 +
,
In mammals mass transport system =
-
side branches quick energy release
:
glycerol
H20 released triglycer
,
-compact storage
=
circulatory system .
-
insoluble : doesn't cause cels to well by osmosis
large molecule lots of energy sto red
:
.
main crore in animals
aort a energy
ven
cuperior
car a -- ↑
↓ E pulmonary
ARTERIES
LIFESTYLE HEALTH AND RISK
↓
↑W artery
I - ·
-
W
left atrium
-
I
↓/~
j
↳ Risk factors
R thick muscular walls of CVD
-
- endothelium
Damage inflammatory response
-
to
:
↳ -[
-
pulmonary Memmm u m
folded endothelium (expands
↓
veins White blood cells lipids clump together
-
- +
Diet (high saturated fat
-
-
/
7 j2
right ~
under pressure) Time =
more build up =
plaque= atheroma =cholesterol
:
at heromal
small lumen
-
atrium
L Plaque partially blocks lumen :
restricted blood How -High
I
blood pressure
endothelium)
VEINS :
high blood pressure . damage to
(carbon monoxide
Smoking
-
left
Hardening of arteries atherosclerosis
:
- I
right thin oxygen in blood/tissu
umm reduces
ventricle muscular walls
rentricle
-values (backflow) : heart attack/stroke Nicot
B lood clot formation
.
makes platelets sticky bloo
11
=
RHS deoxygenated lumen
large
=
-
numm e
clot Also reduces antioxidan
prothrombin
.
Dr
inferior LHS
=
oxygenated =celldamage
=
Atheroma)
CAPILLARIES
ven a cara -
Genetics
aorta
one cell thich (diffusion) - THROmOPI e
-Age (plaque builds up over
Librinogen
-
/Y
- -Gender (men
i ↑ ~↑
likely
-I↑
metabolic
W exchange
L more
- :
-
- =
&
pulmonary- bestrogen levels
=
R
-
arvery ↳ semi-lunar THROMBIN I
good' cholesterol)
values
I I-
e e
perior
W - pulmonary atria ventricles
-
L
vena cara
"
I arvery Librin
L
Treatment of CVD
&
->
W
W ⑪ ② ③ + platelets #
a S red
rea blood
-1
I ~
CeIIS
cellS -Antihypertensives= reduc
= +
