Diabetes Mellitus Flashcards
1
Q
a broad term that refers to an abnormality in blood sugar stability
A
dysglycemia
2
Q
Blood glucose is controlled by ___ and ___
A
Insulin and Glucagon
3
Q
This biomolecule is not a fuel reservoir
A
Protein
4
Q
body proteins can be degraded protein during ___ and ___ and provide AA substrate for gluconeogenesis
A
starvation and periods of stress
5
Q
Most efficient form of energy storage in humans
A
triglycerides
6
Q
Excess glucose can be stored as
A
glyceride
7
Q
Largest reservoir of glycogen ____; Principal reservoir of glycogen ____
A
Skeletal muscles; liver
8
Q
Where production of glucose occurs
A
Liver
9
Q
Serves to spare the body’s use of protein as fuel source
A
Fatty acid oxidation and ketogenesis
10
Q
The two principal circulating fuel in humans
A
Glucose and FFA
11
Q
In the ___ state, nutrients are stored
A
Fed
12
Q
What happens to nutriends in the fasting state
A
they are oxidized for energy production
13
Q
Where will excess energy energy be deposited?
A
Liver, muscle, and fat
14
Q
In fed state, body has a preference for ____ over _____.
A
Glucose oxidation; fat oxidation
15
Q
Intermediary hormone in fed state
A
Insulin
16
Q
This state is associated with the release at times of requirement
A
Fasting state
17
Q
In fasting state, glycogen is transformed into ____ and triglycerides are transformed into ____
A
Glucose; FFA
18
Q
Body has a preference for ____ over ____ in Fasting sate
A
fat oxidation; CHO oxidation
19
Q
Intermediary hormone of Fasting state
A
Glucaon
20
Q
Function of insulin
A
helps glucose in the blood get into the cells
21
Q
Function of glucagon
A
works with insulin to control blood glucose levels
22
Q
In the fasting state, the presence of glucagon will cause glucose levels to go down. (T/F)
A
False
23
Q
Instead of causing the storage of energy, you will withdraw energy through ____ and ____ to produce ____. What state?
A
Gluconeogenesis; glycogenolysis; glucose; fasting state
24
Q
If insulin goes decrease, what will glucagon do?
A
Elevate blood sugar
25
Capacity for skeletal muscle to acutely shift its reliance between lipids and glucose during fasting in response to insulin
Metabolic Felxibility
26
After eating (fed state), we use the _____ as our energy source, but when we’ve used this up and haven’t eaten (fasting state), we convert ____ into energy
carbohyrates; stored fat
27
○ Suppression of fatty acid oxidation
○ Preference for glucose uptake, oxidation, and storage
State and metabolic flexibility or inflexibility?
Fed state; flexibility
28
○ Preference for the use of fatty acid oxidation in muscle ○ Suppressed glucose oxidation
State and metabolic flexibility or inflexibility?
Fasting state; flexibility
29
● Decrease or loss of flexibility is hypothesized to play a role in various disease processes (Kelley et al., 2000)
● This is not the typical condition experienced by a healthy individua
Metabolic Inflexibility
30
○ Less suppression of fatty acid
○ Blunted preference for glucose oxidation
State and metabolic flexibility or inflexibility?
Fed State (Metabolic Inflexibility)
31
Less suppression in beta oxidation
○ Blunted preference for fatty acid oxidation in muscle
State and metabolic flexibility or inflexibility?
Fasting state; inflexibility
32
The 2 cycles depict the interplay between the use of glucose and FFA
Randle and Reverse Randle
33
Aka the Glucose-Fatty Acid Cycle
Randle Cycle
34
Three mechanisms of Randle Cycle
Glucose, FFA, Joint pathway (Acetyl-COA to Malonyl Coa)
35
Similar to the Randle Cycle excpe thtat there is an increase in the ____ which will lead to the production of ____
Malonyl Coa Pathway; triglycerides
36
Results from the autoimmune destruction of β-cells of the endocrine
pancreas in the Islets of Langerhans
Type 1 Diabetes
37
How does Type 1 Diabetes occur?
The body’s immune system attacks and destroys the cells in the pancreas that make insulin which is needed to allow glucose to enter into the cells and produce energy
38
Increased thirst and urination ○ Increased hunger
○ Blurred vision
○ Fatigue
○ Unexplained weight loss
are symptoms of ____
Type 1 Diabetes
39
The body either fails to produce enough insulin to maintain normal glucose levels or resists the effects of insulin
Type 2 Diabetes
40
Pathoegenesis of Type 2 diabetes involve the ______ folloed by _____
Development of insulin resitance; progressive B- cell impairment
41
This disease occurs most often to those Aged 45 or older
| ○ With family history of diabetes ○ Who are overweight or obese
Type 2 Diabetes
42
T/F: Lifestyle plays a role in the devt of Diabetes type 2
T (Physical inactivity and certain health problems (i.e. high blood pressure, gestational diabetes during pregnancy) affect chances of Type II DM as well)
43
o Glucose increases insulin
o Entry of glucose in the skeletal muscle
o Hepatic glucose production is decreased o Thus, no elevation of blood glucose
Refer to the ___ postprandial response to insulin
Normal
44
Glucose increases insulin but because of resistance, the skeletal muscle
will not recognize it
o Glucose will not be absorbed in the muscles
o Muscles will send signals to the brain, then the brain will think that thebody is in the tfasting state
Brain will then e liver that they don’t have enough glucose o The liver will keep breaking down glycogen to produce glucose thus hyperglycemia happens
Refer to the ____ postprandial response to insulin
Abnormal
45
In insulin resistance (IR), insulin has no effect because?
IR prevents carbs from entering the cell and mitochondira
46
3 Sources of insulin resitance
Skeletal muscles
▪ Hepatocytes - parenchymal
cells in liver ▪ Adipocytes
47
caused by a decrease in mitochondrial biogenesis, reduced mitochondrial content, and/or decrease in the protein content and activity of oxidative proteins
Mitochondrial dysfunction
48
What happens if there is a mitochondrial dysfuction
Greater decrease in energy production
49
n effect of the dysfunction due to the oxidative stress
Reactive oxygen species
deteriorate -cell function and increase insulin resistance which leads to the aggravation of type 2 diabetes.
50
T/F: diabetes mellitus is an accumulation of both excess glucose and lipids
True
51
FFAs can have a dual impact on the liver and skeletal muscle (T/F_
True
● FFAs entering the skeletal muscle are converted to DAG due to mitochondria dysfunction
○ DAG and ROS from the mitochondria can activate PKCs
● This results in inhibition of the insulin receptor signaling and glucose uptake in the muscle cells
● In hepatocytes, DAG from FFA utilization can activate PKCs, leading to impairment of the insulin receptor signaling pathway
● In addition, less inhibition of the FOXO protein increases the production of gluconeogenic enzymes such as PEPCK and PC, leading to gluconeogenesis and elevation of blood glucose level
52
Why are PUFAs better to consume than monounsaturated fats?
More difficult to solidify;many molecules stick out ->> harder to stack
53
Theory of Whole Body Insulin Resistance
● During the early phases of insulin resistance, excess intake of nutrients stimulates insulin secretion
● This extra insulin production results in the liver producing more VLDL that can build up in skeletal muscle and the adipocyte
● The adipocyte experiences hypertrophy and results in increased TAG lipolysis to increase plasma FFA levels that can then go back to the pancreas to stimulate even more insulin secretion
● In the later phases of insulin resistance, the liver maximizes its production of VLDL, and there are elevations of lipolysis in skeletal muscle and adipocytes
● At the same time, there is an increase of hepatic gluconeogenesis. This in combination with the excessive plasma FFAs leads to over stimulation of the pancreas
● On the other hand, an excess of plasma FFAs will cause insulin resistance in tissues and organs, which establishes a vicious cycle and will eventually lead to β-cell failure and development of overt NIDDM
54
Social determinants of DM
Energy Balance, Individual Factors, Behavioral settings
55
Impaired Glucose Tolerance and Impaired Fasting Gucose are two indicators of ____
Pre-diabetes
56
Blood glucose level is higher than normal but is not high enough to be classified as diabetes
Impaired Glucose Tolerance
57
Blood glucose level is escalated during the fasting state but has not reached the diabetic stage
Impaired Fasting Glucose
58
Drugs tha help delay or prevent jabetis
Metformin, Acarbose, Pioglitazone, Orlistat
59
Eye, Kidney, Nerves are ____ complications of DM
microvascular
60
Brain, heart, extremities are _____ complicatios of DM
Macrovascular
61
diabetic patients without prior MI (MYOCARDIAL INFARCTION) are not at risk of MI compared to nondiabetic patients with previous MI.
False
62
Hyperglycemia leads to
Oxidative stress
Oxidative stress is an imbalance between free radicals and antioxidants in your body.
63
Normal fasting blood sugar would always change t/f
truw
64
With glucose buildup after meals, blood vessels will leak blood or fluid, distorting vision; treatment
Retinopathy; Anti- VEGF Injection Therapy
65
End stage renal disease; treatment
Nephropathy; Dialysis
66
LOPS (Loss of Protective Sensation)
| ▪ Not being able to feel pain from injury; treatment
Neuropathy; Amputation
67
Diabetics are 2-4x more likely to suffer from ischemic stroke
Brain
68
Mortality from coronary heart disease in subjects with
type 2 diabetes and in nondiabetic subjects with and without prior
myocardial infarction
Haffner Case
69
Diabetics’ extremities are often dismembered in the wards ○ Have to check the pulse of the feet as well
Extremities
70
TThe trend of escalating diabetes prevalence, with its impact on CVD, will no doubt lead to an immense financial burden in many countries, unless action is taken to prevent diabetes and its complications
true (pls read last page) :)
71
Who discovered insulin
Insulin was discovered by Sir Frederick G Banting (pictured), Charles H Best and JJR Macleod
72
He rediscovered the sweetness in urine and blood of patients; mellitues was added
Thomas Wellis
73
When was insulin discovered
July 27 1921
