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Pharm 1 - SP19 > 31 - diabetes > Flashcards

31 - diabetes Flashcards

1
Q

blood sugar, hypo or hyperglycemia?

nervous, shakey, dizzy, condused, headache, cold clammy, fast heart beat, irritability

A

hypoglycemia

low blood sugar

below 80mg/dl

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2
Q

blood sugar, hypo or hyperglycemia?

weak, tired, frequent urination, increased thirst, decreased appetite, blurry vision, itchy dry skin, breath smells fruity

A

hyperglycemia

high blood sugar

above 120mg/dl

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3
Q

blood sugar level chart

fasting - 80-120
just ate 170-200
3 hours after meal 120-140

normal pre-diabetic or diabetic ?

A

normal

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4
Q

blood sugar level chart

fasting - 101-125
just ate 190-230
3 hours after meal 140-160

normal pre-diabetic or diabetic ?

A

pre-diabetic

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5
Q

blood sugar level chart

fasting - 126+
just ate 220-300
3 hours after meal 200+

normal pre-diabetic or diabetic ?

A

diabetic

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6
Q

Hypoglycemia presents an acute problem

_ uses glucose almost exclusively as its source of
chemical energy to supply ATP

A

Brain

Glc yeilds CO2 and water + ATP

Brain only has a few minutes worth of glucose stored.
Need sufficient glucose in bloodstream

moderate hypoglycemia - brain dysfunction

severe hypoglycemia - death

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7
Q

high levels of blood sugar
(hyperglycemia) is also not good for you

Bottom line: your body goes to great lengths to regulate
_ levels

A

blood glucose levels

have to be regulated can’t be too high or too low

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8
Q

When fasting, the body maintains glucose
in blood at 70 – 100 mg/dl
When you eat, the level of glucose in your blood _.
This triggers insulin
release from the pancreas. Insulin (acting through its receptor) does some
things that lower blood sugar levels.

A

when you eat, the level of glc rises

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9
Q

After a meal, 2/3 of the glucose in the blood is removed and stored in the _ and _ as glycogen

Once glycogen stores are filled, glucose is converted to _ in the liver and stored as
triglycerides in fat cells

A

liver
and skeletal muscle

fatty acids

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10
Q

During times of need, glucose is liberated from glycogen and released from
the _ to the blood in order to keep blood glucose levels appropriate.
Glucose (stored as glycogen) in _ is not released but is used within the
muscle as needed

A

liver releases Glc when needed

in muscle - not released

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11
Q

The _ is responsible for keeping the blood glucose level

where it needs to be

A

liver

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12
Q

If blood glucose is high, the liver (and muscle) store it as glycogen

_ = glucose -> glycogen

A

glycogenesis

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13
Q

If blood glucose is low, the liver releases it from glycogen

_ = glycogen -> glucose

A

glycogenolysis

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14
Q

If the liver runs out of glycogen but still thinks glucose levels are low, it will make
glucose by a process known as _

A

gluconeogenesis

glycogenolysis until glycogen stores are depleted then if bloodglc is still low, gluconeogenesis occurs

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15
Q

Hormones produced by the pancreas are entrusted with regulating
blood glucose levels

_ cells - secrete somatostatin

_ cells - secrete glucagon

_ cells - secrete insulin

A

δ cells: secrete somatostatin

α cells: secrete glucagon

β cells: secrete insulin

islets of Langerhans are the regions of the pancreas that contain its endocrine (hormone-producing) cells

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16
Q

_ and _ are
the principal hormones
regulating blood sugar
levels

A

Glucagon - alpha cells -

Insulin - beta cells

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17
Q

_ hormone stimulates breakdown of glycogen and raises blood glucose levels

A

glucagon - alpha cells

raises blood sugar

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18
Q

_ hormone stimulates the formation of glycogen

stimulates glucose uptake from blood

A

insulin - beta cells - lowers blood sugar

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19
Q

high blood sugar promotes

glucagon or insulin release from pancreas

A

high blood sugar - promotes insulin release

low blood sugar promotes glucagon release

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20
Q

Glucagon or insulin?

acts through a
G protein coupled
receptor (coupled to Gαs)
to elevate cAMP levels
and activate protein
kinase A.
A

glucagon

this initiates a
kinase cascade leading to
liberation of glucose from
glycogen, mainly in liver
and skeletal muscle.
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21
Q

Glucagon or insulin?

acts through a tyrosine kinase receptor

A

insulin

  1. decreases blood glc levels
  2. promotes storage of fat
  3. enhances protein anabolism
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22
Q

3 major effects of insulin

  1. decreases blood sugar - how?

A rise in blood sugar levels triggers insulin release from β cells. Insulin
mobilizes cells to utilize the glucose and store the glucose.

A
  1. decreases blood sugar levels - Stimulate glucose uptake by liver, muscle, adipose,

increases glycogen synthesis,

decreases gluconeogenesis

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23
Q

3 major effects of insulin

Insulin promotes storage of fat - how

A

Promotes fatty acid and triglyceride synthesis (liver)

Increase fatty acid transport into adipose cells (storage)

Increased conversion to triglycerides (adipose)

Decreases breakdown of triglycerides (adipose)

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24
Q

3 major effects of insulin

enhances protein anabolism - how

A

Increases amino acid transport into cells

Increases general protein synthesis

Decreases general protein degradation

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25
Q 
_ is a group of
metabolic disorders in which there are
high blood sugar levels over a
prolonged period. There are three
common types.
A

Diabetes mellitus (DM),

NOT - Diabetes insipidus (DI) is a condition
characterized by large amounts of dilute urine
and increased thirst.
Caused by damage to pituitary gland leading to loss of
antidiuretic hormone (vasopressin) release.

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26
Q

a form of diabetes mellitus in which
not enough insulin is produced.
This results in high blood sugar
levels in the body.

A

DM TYPE 1

Type 1 diabetes happens when your
immune system destroys cells in your
pancreas called β cells. They’re the ones
that make insulin.
Some people get a condition called
secondary diabetes. It’s similar to type 1,
except the immune system doesn’t
destroy your β cells. They’re wiped out
by something else, like a disease or an
injury to your pancreas
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27
Q

_ a longterm metabolic disorder that is
characterized by high blood sugar,
insulin resistance, and relative lack
of insulin

A

DM type 2

The causes of type 2 diabetes are
not completely understood.
Obesity and a sedentary lifestyle
clearly play roles. Genetic
predisposition factors, only some
of which are known, also play a
role
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28
Q 
a condition in
which a woman without diabetes
develops high blood sugar levels during
pregnancy. Gestational diabetes
generally results in few symptoms;
however, it does increase the risk of preeclampsia, depression, and requiring a
Caesarean section. Babies born to
mothers with poorly treated gestational
diabetes are at increased risk of being
too large, having low blood sugar after
birth, and jaundice. If untreated, it can
also result in a stillbirth. Long term,
children are at higher risk of being
overweight and developing type 2
diabetes
A

Gestational diabetes

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29
Q 
_ diabetes usually
begins before age 40,
although there have been
people diagnosed at an
older age. In the United
States, the peak age at
diagnosis is around 14
A

Type 1

pancreas cannot produce insulin

autoimmune disease that
leads to the destruction of β cells

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30
Q

_ diabetes can be thought of as hyperglycemia*
associated with ‘relative’ insulin deficiency**
* High levels of blood glucose
**Not enough insulin to do the job it needs to do

A

Type II

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31
Q

Type II diabetes develops over time. Genetics play a role but _ and _ are key contributors. Development of cellular resistance to insulin is a key. This insulin
resistance is part of a series of problems known as metabolic syndrome

A

genetics - some role

obesity and sedentary lifestyle - main role

metabolic syndrome - insulin resistance, high BP, high triglyceride levels, low HDLs

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32
Q

3 principle targets of insulin

A

liver
skeletal muscle
adipose

33
Q 
Key tissues less responsive to insulin than they
need to be. 
Less glucose stored and utilized by
tissues, more glucose in blood. 
Metabolic
changes to compensate for _
A

insulin resistance

Changes in signaling
events will
contribute
mightily to
insulin
resistance
34
Q

_ is the process of glycogen synthesis, in which

glucose molecules are added to chains of glycogen for storage

A

Glycogenesis

Liver and
skeletal
muscle are
the primary
sites of
glycogen
storage
35
Q

what does hexokinase enzyme do

A

glucose metabolism

converts glucose to Glc-6-P

36
Q

glycogenesis can occur in

liver, muscle, adipose?

A

liver and muscle

37
Q

When blood glucose drops, glycogen in is
broken down and glucose is released to the
bloodstream. This process is called glycogenolysis

liver, muscle, adipose?

A

liver

skeletal muscle
has little glucose
6-phosphatase.
It utilizes
glucose 6-
phosphate but
does not export
glucose
38
Q

describes the production of glucose
from pyruvate

liver to convert excess amino acids,
glycerol, and lactate (all through
pyruvate) to glucose

A

gluconeogenesis

It is not identical to glycolysis running in reverse, but close

39
Q 
More important (in the context of blood
sugar control), gluconeogenesis provides
a way for the liver to basically convert
amino acids (derived from muscle
protein) into glucose in times of need

first intermediate of pyruvate is _

A

oxaloacetate

in mitochondria

40
Q

In times of crisis in muscle: some protein is degraded to amino acids

Through transamination
reactions, _ aminoacid leaves
the muscle and goes into
the blood stream

A

alanine which is converted to pyruvate

In the liver, the alanine
is converted to pyruvate
\+ urea (to get rid of the
nitrogen)
The pyruvate is converted to
glucose (via gluconeogenesis)
where it gets sent to the blood
stream and used where
required.

In essence: proteins are
broken down in muscle in
order to provide glucose

41
Q

Fatty acids are
metabolized by β
oxidation into _ which is metabolized by the TCA cycle and oxalactetate is the last step and gets converted to pyruvate

A

Acetyl CoA is metabolized by the TCA cycle

42
Q

Free fatty acids can be
transported in the blood to
most tissues, where they can
provide energy

exceptions?

A

Exceptions are
brain (FA’s can’t
cross blood brain
barrier)

and red
blood cells (no
mitochondria)

43
Q 
Much of the metabolism of
fatty acids is taking place in
the liver during times of need.
If the liver is also working
to provide blood glucose
through gluconeogenesis a
problem can arise

The liver will only oxidize the
fatty acid to acetyl CoA and will
convert the acetyl Co A to
_

A

‘ketone’ bodies. Ketone bodies

are not good (ketoacidosis)

44
Q

If metabolism through TCA cycle is not possible, acetyl CoA from _ in the liver will be converted to ‘ketone bodies’ (acetone,
acetoacetate, β-hydroxybutyrate)

A

β
oxidation

In times of crises, oxaloacetate
gets diverted from the TCA
cycle to gluconeogenesis

If the liver needs to make glucose
through gluconeogenesis (body is
hypoglycemic), oxaloacetate can be
depleted

45
Q

If metabolism through TCA cycle is not possible, acetyl CoA from _ in the liver will be converted to ‘ketone bodies’ (acetone,
acetoacetate, β-hydroxybutyrate)

A

β
oxidation

In times of crises, oxaloacetate
gets diverted from the TCA
cycle to gluconeogenesis

If the liver needs to make glucose
through gluconeogenesis (body is
hypoglycemic), oxaloacetate can be
depleted

46
Q

You eat and then store food as glycogen, protein, and fat. Later, blood sugar begins to
drop. Troublesome because the brain is totally dependent on glucose as an energy source.
Body starts by using glycogen stores in liver to crank out glucose to the blood. At some
point fat cells will be liberating fatty acids. This is good news for many tissues but not
brain. fatty acids can not be converted to glucose (no path from acetyl CoA).
Thus, if glucose levels drop in the blood, this must be fixed. Body will start degrading
protein and basically turn amino acids into glucose. β-oxidation of fatty acids will be used
to generate ATP (not in brain). Liver is using fatty acids and also trying to crank out glucose
into the blood via gluconeogenesis. It can deplete itself of _, leaving acetyl
CoA stuck (no TCA cycle). Liver starts cranking out ketone bodies.

A

oxaloacetate

The liver cranking out ketone bodies is a possibility any time the body is
relying too heavily on β oxidation of fatty acids (Metabolism via the TCA cycle
is insufficient to handle the amount of acetyl Co A being produced). As noted
before, one way for this to happen is when a person becomes hypoglycemic

47
Q

Normally, high
glucose levels stimulate insulin production and insulin stimulates
glucose uptake and utilization by cells. If insulin fails to be made or
cells fail to respond to insulin,
β oxidation of _ is liable to
increase substantially, even though there is plenty of glucose around.
In this case, excess acetyl CoA can be produced, and formation of
ketone bodies increased. In essence, the liver is fooled to act as if it
needs to make glucose (and consequently ketone bodies) even
though it really doesn’t.

A

fatty acids

48
Q

What are the acute complications of diabetes

3 things

A
  1. Diabetic ketoacidosis
  2. Hyperosmolar hyperglycemic state
  3. Hypoglycemia
49
Q

Symptoms of _

Hyperglycemia
Ketosis
Metabolic acidosis (drop in pH in blood)

A

diabetic ketoacidosis (DKA)

Insulin action normally suppresses breakdown of triglycerides to fatty acids (FA’s)
and glycerol in adipose cells. Increase in FA’s leads to production of ketone bodies by the
liver

More common in type one diabetes with poorly managed use of insulin

50
Q

Tx of diabetic ketoacidosis (DKA)

dilute urine, bed wetting, rapid HR, light headed upon standing
kussmaul breathing - deep and labored

A

fluids - normal saline before ER hospital

insulin - this will start in the ER– must control electrolyte problems first

more common in type 1

51
Q

Hyperosmolar hyperglycemic state is a metabolic complication of diabetes mellitus (DM)
characterized by

severe hyper/hypo? glycemia,
extreme _,
- plasma,
altered _.

A 
severe hyperglycemia,
 extreme dehydration, 
hyperosmolar plasma, 
and
altered consciousness

It most often occurs in type 2 DM, often in the setting of
physiologic stress.
HHS is diagnosed by severe hyperglycemia and plasma hyperosmolality
and absence of significant ketosis. Treatment is IV saline solution and insulin. Complications
include coma, seizures, and death.

52
Q

Poor glucose utilization coupled with liver cranking out glucose. Severe
dehydration.

A

Hyperosmolar hyperglycemic state

complications with DM

53
Q

Low blood sugar, also known as hypoglycemia, can be a
dangerous condition.

Low blood sugar can happen in people with
diabetes who take medicines that increase insulin levels in the
body. Taking too much medication, skipping meals, eating less
than normal, or exercising more than usual can lead to low blood
sugar for these individuals.

Over medication and/or poor eating.

type 1 or type 2?

A

Both type one and type two diabetes

54
Q 
Chronic complications of diabetes: The result of _
neuropathies
retinopathies
nephropathies
macrovascular
complications
ulcers
infections
GI disturbances
A

hyperglycemia

vascular system (vessels) affected most

These vascular complications are thought to be principally
mediated through diabetes-induced endothelial cell
dysfunction.

Reactive oxygen species (ROS) are thought to be important
mediators of the damage to the endothelium that results in
endothelial dysfunction.

chronic hyperglycemia is thought to enhance
production of ROS

55
Q

The_ test measures glycation of hemoglobin (a long lasting
protein in the blood). It provides a window into the average blood
sugar of an individual over a period of months

Why red bloods cells and hemoglobin are good for this?

A

A1C

red blood cell have a mean t1/2 of 115 days
red blood cell are anucleated and do not synthesize protein.
Thus, the glycation of hemoglobin that is measured
reflects a mean value averaging events over several
months.

56
Q

good A1c test score?

A

6 or lower - excellent

7-8 good

9 or more acting suggested

57
Q

_ Test is the
preferred test for Type 1 and Type 2
diabetes or pre-diabetes.

A

The Fasting Plasma Glucose

Patient will
fast overnight (at least 8 hours) Draw
blood in the morning (It is best to
have this test done in the morning
because afternoon results tend to be
lower).
58
Q

Casual (random) glucose blood test

A couple of hours after a meal, a normal blood glucose level would be no
higher than _

A

140 mg/dl

healthy adults - Glc levels remain relatively stable - still true even is varied diet, stress, and meals

DM and preDM - glucose levels can vary widely over the course of
the day. This is particularly true if the disease is not well-managed. In these people,
random test results will vary widely. Tests may also be consistently high. A random test is
one performed outside your normal testing schedule. Random testing is an important part
of diabetes management. If random glucose levels are acceptable, the therapeutic strategy
is probably working. Wide swings in levels suggest a need to change the management
plan.

59
Q

Oral glucose tolerance test

  1. Draw blood for fasting (baseline) level
  2. Ingest glucose (75 g).
  3. Draw blood after 1 and 2 hours.
A

normal < 6.1 mM (110mg/dL) – 1 hou - less than 10; 180, 2 hours less than 7.8 and 140

preDM - 6.1-7; 110-125, 2 hr - 11.1; 200

DM - >7;125 2hr >11.1; 200

60
Q

drugs to tx DM

A

insulin - type 1 pretty much starts and ends here - goal is to manage blood sugar levels to mimic natural physio - type 2 usually don’t start with insulin but eventually have to take it

secretagogues - sulfonylureas standard of care - help Beta cells produce insulin - Must have functional β cells for the drugs to work

61
Q

Liver cells and pancreatic β cells are designed to be glucose sensors (2 reasons)
Blood glucose levels average around 5 mM

A

Reason 1. The glucose transporter on liver and β cells (GLUT2) has a Km of 15-20 mM. It will let glucose in
at a rate that is dependent on its concentration in blood.

Reason 2. Liver and β cells have glucokinase. Its Km is 10
mM. This means glucose will be converted at a rate that
is roughly linearly proportional to the blood glucose
level.

62
Q

_ is present in most cells. Its Km for glucose is
0.2 mM. This means that the glucose inside these cells
will be maximally converted to gluc-6-phosphate across
the whole range of blood glucose levels

A

Hexokinase

63
Q

_ makes decisions on what to do metabolically based on
this information.

_ make decisions on whether to secrete insulin based
on this information.

A

Liver - what to do metabolically

β cells - whether to secrete or nah

64
Q

Pancreatic β cells have a _ channel that is sensitive to the ratio of [ATP/ADP] inside.

The channel functions when the ratio is _. This keeps the cell hyperpolarized (inside -70
mV relative to the outside). If the ratio [ATP/ADP] is high, the channel is blocked, leading to
depolarization of the cell (inside becomes approximately -40 mV relative to the outside).

A

potassium

fxns when ratio is low - so hyperpolarizing - no AP

Hexokinase is present in all cells except liver and β
cells. Its Km for glucose is 0.2 mM. Glucokinase is
present in liver and β cells. Its Km is 10 mM.
Liver and β cells will only convert glucose to pyruvate and form ATP when glucose
levels are high enough for glucokinase to work. Thus, they can be glucose sensors.

65
Q

Glucose levels are linked to the [ATP/ADP] ratio in _

high ratio?
low ratio?

A

β cells

β cell remains
hyperpolarized when glucose levels are low and becomes partially depolarized when
glucose levels are high.

high ratio - glucose comes in - glycolysis - glucokinase

low ratio - doesn’t work but channel is working

Voltage sensitive Ca++ channels respond to membrane depolarization

66
Q

Secretagogues

A K+ channel regulates insulin release from β cells by sensing _

A

ATP/ADP

β cells are metabolically
designed to be especially
sensitive to glucose levels in
the blood and respond by
adjusting their ratio of
ATP/ADP
67
Q

ATP/ADP low (fasting), K+ channel open, cell hyperpolarized, L-type
Ca++ channels closed,

insulin secreted or nah .

A

insulin not secreted

68
Q

ATP/ADP high (after a meal), K+ channel closed, cell depolarized, Ltype Ca++ channel open,

insulin secreted or nah .

A

insulin secreted

69
Q

More rapid onset of action, shorter duration of action
than sulfonylureas. Used before meals. Hypoglycemia a
concern if drug is taken and person doesn’t eat. Add on
drugs.

A

Meglitinides

Some subtle mechanistic distinctions between sulfonylureas and
meglitinides but both work to promote insulin release by
inhibiting K+ efflux from ATP/ADP regulated K+ channels

70
Q 
Glucagon like
peptide 1* (GLP-1) and
Glucose dependent
insulinotropic
polypeptide* (GIP) act
at the GLP-1 receptor
on β cells and stimulate
insulin release. )

Exenatide is a GLP-1 agonist. Sitagliptin inhibits GLP1 and GIP degradation

A

Incretins

minor add on to standard of care

71
Q

_ drug for diabetes

increase glucose uptake in skeletal
muscle (diminish insulin resistance)

reduce glucose production in liver

reduce intestinal absorption of glucose

anti-oxidant properties on vascular
endothelial cells

modest weight loss

A

Biguanide (metformin

usually first line of tx for DM type 2

combo with exercise and weight loss

immediate release
and extended release - for patient with GI probs

72
Q

_ drug for diabetes

usually 1st medication combo with exercise and diet

improves glycemic control (lowers blood
glucose),

less risk of hypoglycemia than
insulin or secretagogues

A

metformin (diguanide)

73
Q

why is metformin so good

does not stimulate _ secretion

many patients loss _

will lower HbA1c by about 1.5%

less risky - no hypoglycemia

A

insulin sparing - does not stimulate insulin secretion

inhibit mitochondrial glycerol-3-phosphate
dehydrogenase (flavoprotein dehydrogenase), thereby disrupting the
glycerophosphate shuttle

74
Q

Metformin drug for diabetes

inhibit mitochondrial glycerol-3-phosphate
dehydrogenase (_), thereby disrupting the
glycerophosphate shuttl

The net result of this shuttle is cytosolic
NADH is converted to NAD+ and
mitochondrial FAD is converted to
FADH2. Your body does this as a means
to utilize NADH produced by glycolysis
to produce ATP through oxidative
phosphorylation/electron transport

Inhibiting this process has two
important consequences as it relates
to liver production of glucose.

A

inhib flavoprotein dehydrogenase

  1. [NADH/NAD+] increases so less pyruvate
    becomes available for gluconeogenesis.
  2. [NADH/NAD+] increases so less
    glycerol (from triglyceride breakdown)
    goes down the path of gluconeogenesis
    (via DHAP).

this inhibits gluconeogenesis by liver

75
Q

metformin

inhibition of mitochondrial glycerol-3-phosphate
dehydrogenase by metformin inhibits _ by the liver

A

gluconeogenesis

76
Q

metformin inhibs gluconeogensis

inhibits the
mitochondrial respiratory
chain complex I

This could increase glucose utilization
through glycolysis

This could also decrease levels of ATP and
increase levels of ADP and AMP. This is very
important because it could activate _

A

AMP
dependent protein kinase (AMPK)

AMP activated
protein kinase can
sort of be thought of
as the ‘anti-glucagon’

increase glc uptake, glycolysis, fatty acid oxidation,

decrease fatty acid synthesis, sterol syntheis, glycogen synethis, protein synthesis

77
Q

_ decrease insulin resistance
These drugs are agonists of the peroxisone
proliferator-activated receptor γ. (PPAR-γ)

A

Thiazolidinediones

These effects by
PPAR-γ agonists
diminish insulin
resistance.

78
Q

_ is a pathological condition in which cells fail to respond to the normal actions of the hormone insulin
the body produces insulin under conditions of insulin resistance, the cells in the body are resistant to the insulin and are unable to use it as effectively, leading to high blood sugar, this is a compnent of diabetes

_ regulates fatty acid storage and glc metabolism, the genes activated by _ stimulate lipid uptake and adiopgenesis by fat cells

A

insulin resistance

PPAR-γ agonist - thiazolidinediones

decrease inflammation,

79
Q

These drugs act by inhibiting the digestion of
glucose

delay digestion and absorption of carbs in GI tract

A

α-glucosidase inhibitors

this enzyme breaks down starch and disaccharides to glucose - so we inhib it

Pharm 1 - SP19 (26 decks)

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