Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Endocrinology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is the boundary for hypoglycaemia

A

<4-5MM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What can hypoglycaemia cause

A

Impaired brain function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can happen when glucose level is under 3mM

A

unconsciousness, coma , death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which hormones control glucose regulation

A 
Insulin
Glucagon
Cortisol
Catecholamines
Somatrophin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is type 1 DM

A

Elevated glucose levels where insulin is required to prevent ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is type 2 DM

A

More common. Defined in terms of glucose but is also related to hypertension and dyslipidaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When does hypoglycaemia occur

A

Imbalance between diet, exercise and insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does treatment aim to help

A

Symptoms, complications (morbidity) and mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is common in DM treatment

A

Diet, insulin and capillary glucose monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How much of the pancreas do langerhans take up and what does the rest of the pancreas do

A

2%

Involved in exocrine secretions via pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What cell junctions can you find between langerhans cells

A

Gap junctions to allow small molecules to pass and tight junctions to form small intercellular spaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the types of langerhans cell

A

alpha - glucagon
beta - insulin
delta - somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the principal actions of insulin

A

Increased glycogensis
Increased glycolysis
Increased glucose transport into cells via GLUT4
Decreased lipolysis
Increased lipogenesis
Increased amino acid transport and increased protein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the principal actions of glucagon

A 
Increased hepatic glycogenolysis
Increased blood glucose
Increased amino acid transport to the liver
Increased gluconeogenesis
Increased lipolysis
Increased gluconeogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which factors regulate the release of insulin

A

Increasing blood glucose
Certain amino acids
Certain gastro intestinal hormones (GLP)
Sympathetic control (-) and parasympathetic (+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What factors regulate the release of glucagon

A

Decreasing blood glucose
Certain amino acids
Certain gastro intestinal hormones
Sympathetic (++) and parasympathetic (+) control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the beta-cell sensing mechanism of glucose

A

Glucose -> G-6-P -> Metabolic pathways -> insulin synthesis and release.
Glucokinase/ hexokinase IV is the “glucose sensor” as it is in the rate limiting step

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the process of insulin secretion

A
  1. glucose enters via GLT 2
  2. conversion to G-6-P by glucokinase
  3. ATP blocks the ATP sensitive K+ channel
  4. Voltage dependent Ca+ channel opens
  5. Insulin secreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the insulin receptor

A

Mostly on muscle, can be on liver
not responsible for type II DM
Made of alpha and beta subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does the alpha subunit of the insulin receptor do

A

Recognises the 3D insulin structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does the beta subunit of the insulin receptor do

A

Has tyrosine kinase domains where phosphorylation occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is GLP-1

A

Glucagon-like peptide 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does the GLP-1 do

A

Gut hormone that is secreted in response to nutrients in the gut. Stimulates insulin secretion and glucagon suppression. Increases satiety.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the half life of GLP-1

A

Short half life due to rapid degeneration from enzyme dipeptidyl peptidase-4 (DPPG-4)

25
How is GLP-1 produced
Transcription product of proglucagon gene, mostly from the langerhans cells
26
What is the effect of insulin on glucose
Decreased hepatic glucose output and increased muscle intake
27
What is the effect of insulin on protein
Decreased proteolysis
28
What is the effect of insulin on lipids
Decreased lipolysis and decreased ketogenesis
29
What is GLUT-4
A receptor that allows glucose uptake through the membrane. They lie in vesicles and become incorporated into the membrane by insulin resulting in a 7 fold increase in uptake
30
What does cortisol stimulate
Proteolysis
31
Which hormones stimulate protein synthesis
Insulin and IGF I
32
What is the main short term energy store
Glycogen
33
After short-term fasting what is used to maintain glucose levels
gluconeogenesis using proteins
34
Describe the formation of glycerol and NEFA from TAG
1. Triglyceride is broken down by lipoprotein lipase, promoted by insulin 2. Glucose enters through GLUT-4, stimulated by insulin 3. Glucose can be broken down and two components can be used to form triglyceride, these being glycerol-3-p and NEFA, again promoted by insulin 4. This can be used to stop the break down of triglyceride into glycerol and NEFA
35
Describe the circulation glycerol
1. Glycerol reaches the liver 2. It enters the cell and is phosphorylation 3. Formation o triacyl glycerol 4. This can be used to synthesise glucose (hepatic glucose output)
36
What is the importance of the way glycerol circulates
Blood flows through the gut before the liver, allowing for food to be processed before entering the liver. Adipocytes in the central circulation of different those in the limbs
37
What can eat brain utilise as an energy source
Glucose and ketone bodies (NOT fatty acids)
38
What is fat used for in metabolism
Broken down and used in Krebs> Non-esterified fat cannot be used to synthesise glucose
39
How are ketone bodies formed
1. Fatty acids enter the liver 2. Fatty acids are broken down into segments 3. Formation of ketone bodies (acetoacetate and 3-hydroxybutarate)
40
Which molecule can be used as an indication of insulin
Ketone bodies as insulin inhibits their formation
41
What occurs during fasting
``` Low insulin to glucose ratio Increasing non-esterified fatty acids Increase in proteolysis and lipolysis Break down of glycogen Gluconeogenesis ```
42
What occurs during prolonged fasting
Decrease in amino acids Increased ketogenesis Brian uses ketone
43
Which molecules do the muscle and brain use
``` Muscle = lipids Brain = glucose ```
44
What occurs when one is fed
Stored insulin is released then a second phase insulin release High insulin to glucagon ratio Hepatic glucose output is stopped Increase in glycogen formation Decreases in gluconeogensis and proteolysis Increase in protein synthesis and lipogenesis
45
What are the signs and symptoms of type 1 DM
``` Weight loss Hyperglycaemia Glycosuria with osmotic symptoms Ketonuria Given an intramuscular injection of insulin ```
46
What causes weight loss in T1 DM
Proteolysis and lipolysis
47
What is the difference between T1 and T2 DM
``` T1 = absolute insulin deficiency T2 = insulin resistance ```
48
Where does insulin resistance reside
Adipose, muscle and liver
49
Why don't T2 DM patients lose weight
There is enough insulin to suppress proteolysis and lipolysis
50
What are the two pathways that occur when insulin meets its receptor
MPAK or PI3K-Akt
51
How does insulin resistance affects the pathways
PI3-Akt is inhibited so the MAPK pathway is enhanced
52
What are the two pathways responsible for
``` MAPK = growth, proliferation, growth in utero, blood pressure and dyslipidaemia PI3-Akt = metabolic actions (glucose, fat and amino acids) ```
53
What are the effects of hyperinsulinaemia via the MPAK pathway
Excess stimulation of the mitogenic pathway Low LDL cholesterol and high HDL Smooth muscle hypertrophy -> high blood pressure Ovarian function (polycystic ovary syndrome) Clotting Energy expenditure
54
What are the effects of the insulin resistance via IP3-Akt
Glucose, protein and lipid metabolism affected
55
What happens to lipoproteins in humans with T2 DM
Predominantly abnormal lipoproteins that is lipid carriage in the circulation, contributing to damage to the artery
56
What is insulin resistance associated with
Hyperglycaemia Greater waist circumference High blood pressure High triglyceride and low LDL
57
What can patients with T2 DM present with
``` Obesity (60-80%) Dyslipidaemia Hyperglycaemia Insulin resistance and later deficiency Complications due to central adiposity Less osmotic symptoms ```
58
Describe the features of a diet for patients with DM
``` Total calorie control Reduce calories as fat and as refined carbohydrate Increase calories as complex carb Increase soluble fibre Decrease sodium intake ```

Endocrinology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions