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Endocrinology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Insulin action on glucose, protein and fat?

A

Glucose : Decrease HGO
-Increase muscle uptake

Protein : decrease proteolysis

Fat : decrease lipolysis
decrease ketogenesis

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2
Q

GLUT 4 transporter characteristics?

A

Common in myocytes and adipocytes

Highly insulin responsive

Lies in vesicles

Recruited and enhanced by insulin

7 fold increases glucose uptake

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3
Q

Effects of insulin on Muscle cell metabolism?

A

Fed state: inhibits protein –> gluconeogenic AAs
* Cortisol also aids this inhibition

Fasting state: stimulates gluconeogenic AAs production
* GH, IGF-1 also aids this pathway

AAs can leave cell once created to create glucose

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4
Q

Effects of Insulin and Glucagon on the Liver?

A

Fed state : inhibits gluconeogenesis of AAs to glucose and promotes AAs to turn into proteins = decreasing HGO

Fasting state : Glucagon stimulates AAs to be transported into hepatocytes, protein –> AAs conversion and Gluconeogensis into glucose
* Gluconeogenesis aided by Cortisol = increased HGO

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5
Q

Effects of Insulin on Triglycerides

A

LPL enzyme breaks them down into fatty acids and glycerol.
This relies on insulin activating the enzyme

Fed state: Insulin Stimulated glucose uptake by transporters into adipocytes –> NEFAs
Insulin then stimulates NEFAs –> triglycerides

Fasting state: Insulin Inhibits triglyceride breakdown into NEFAs
* GH and Cortisol promotes Triglycerides –> Glycerol + NEFAs

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6
Q

How does blood circulation aid insulin release quickly?

A

Due to Hepatic Portal vein connecting gut to liver directly = can detect increased glucose levels

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7
Q

Can HGO increase due to lipid metabolism?

A

Gluconeogenesis can occur by triglycerides

Glycerol can travel in or Hepatocyte triglycerides can be converted to Glycerol-3P –> Glucose

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8
Q

What are the cerebral energy type requirements?

A

Glucose primarily

Or ketone bodies

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9
Q

In a fasting state, what does glucagon encourage in liver? (Fatty Acyl - CoA)

A

NEFAs transported into hepatocytes
Glucagon stimulates fatty Acyl-CoA –> Ketone bodies ( Acetyl CoA/ Acetoacetate/ Acetone + 3 OH-B ) == Ketone bodies released from liver

  • in the fed state insulin inhibits ketone body production
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10
Q

What is Hepatic Glycogenolysis?

A

The generation of glucose from stored glycogen in liver during fast state:

Glucose –> Glucose-6-P –> Glycogen ( this is stored by insulin )

Glucagon stimulates Glucose-6-P production from Glycogen which turns to Glucose = Increased HGO

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11
Q

Can muscle cells release glucose?

A

No, glycogen created will be used in the muscle cell by conversion to glucose, then to Acetyl CoA = Oxidative phosphorylation ( Carbon dioxide release )

*GH also inhibits glucose uptake alongside Glucagon during Fasting

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12
Q

In a fasted state what happens to
NEFA levels?
Amino acid levels?

A
  • Triglycerides lysis increased so NEFA increase

- Increase at first by increased proteolysis then decrease when prolonged fast

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13
Q

What occurs in the Fed state?

A 
Stops HGO
Increase Glycogen
Decrease gluconeogenesis
Increase protein synthesis
Decrease proteolysis
Increase Lipogenesis
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14
Q

How do diagnose Diabetes Mellitus?

A

High levels of glucose

Fasting glucose : 7+
Random glucose : 11.1+

Oral glucose tolerance test:
2-hour glucose

  • HbA1c test

Need two positive tests to diagnose or 1 test and symptoms

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15
Q

Characteristics of type 1 diabetes?

A
  • Autoimmune condition
  • Absolute insulin deficiency

Diabetic ketoacidosis : serious acute compilation due to increased ketone bodies

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16
Q

Clinical presentation of Type 1 diabetes?

A
  • Weight loss
  • Hyperglycaemia
  • Glycosuria with osmotic symptoms
  • Ketones in bood and urine

Diagnostic tests : (tell you more likely to be type 1 )

  • Antibodies GAD, IA2
  • low C-peptide
  • Presence of ketones
  • Need to watch out for other autoimmune diseases that can occur or already have
17
Q

What happens when too much insulin is administered?

A

No glucose hepatic output

Muscle glucose input

18
Q

What are counterregulatory responses to hypoglycaemia?

A
  • increased Glucagon
  • increased Catecholamines
  • increased Cortisol
  • increased Growth hormone
    = Increased HGO + Lipolysis

Impaired awareness of hypoglycaemia due to loss of counterregulatory response until it is very low

19
Q

Symptoms and signs of hypoglycaemia?

A 
(Autonomic)
Sweating
Pallor
Palpitations 
Shaking
(Neuroglycopenic)
•Slurred speech
•Poor vision
•Confusion
•Seizures
•Loss of consciousness
20
Q

Characteristics of type 2 Diabetes?

A

Insulin resistance resides in liver, muscle and adipose tissue

*Have enough insulin to suppress ketogenesis and proteolysis

( you can have insulin resistance before having diabetes)

21
Q

What pathways are activated by insulin - which one is affected by insulin resistance?

A

P13K-Akt pathway ( metabolic action ) = this is where insulin resistance occurs

MAPK pathways ( growth and proliferation

22
Q

Presentation of symptoms of type 2 diabetes?

A
  • Hyperglycaemia
  • Overweight
  • UTI due to glucose in urine
  • Less osmotic symptoms
  • Complications
  • Insulin resistance
  • Later insulin deficiency
  • Dyslipidaemia (disturbances in fat metabolism cause changes in the concentrations of lipids in the blood)
23
Q

What are the risk factors for type 2 diabetes?

A

Age, PCOS, high BMI, Family History, Ethnicity, Inactivity

24
Q

Complications caused by diabetes?

A

Retinopathy
Neuropathy
Nephropathy
Cardiovascular

25
Q

Dietary recommendations?

A
  • Total calories control
  • Reduce calories as fat and refined carbs
  • Increase complex carb calories
  • …
26
Q

How is type 1 managed?

A
  • Exogenous insulin (basal-bolus regime)
  • Self-monitoring of glucose
  • Structured education
  • Technology
27
Q

How is type 2 managed?

A
  • Diet
  • Oral medication
  • Structured education
  • May need insulin later
28
Q

How is type 2 managed?

A
  • Diet
  • Oral medication
  • Structured education
  • May need insulin later
29
Q

What are the medical terms for the following:

Feeling thirsty:
Passing urine frequently:
Getting up at night to pass urine:
Painful when it pees:

A
  • Polydipsia
  • Polyuria ( glucose in urine = can lead to UTI )
  • Nocturia
  • Dysuria ( due to UTI )

Endocrinology (22 decks)

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