Endo 15: Type I Diabetes Mellitus Flashcards Preview

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Flashcards in Endo 15: Type I Diabetes Mellitus Deck (31)
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1
Q

What acts as a marker for insulin function?

A
  • C PEPTIDE

- -> it is linked to insulin production

2
Q

What causes T1DM ?

A
  • destruction of Beta cells

Autoimmune destruction of islet cells

3
Q

What is a histological feature of T1DM?

A
  • there is a lot of lymphocyte infiltration of the beta cells
  • -> which destroys B-cells
  • -> so they can no longer release insulin
4
Q

What is the importance of the autoimmune basis of T1DM?

A
  • increased prevalence of other autoimmune disease
  • risk of autoimmunity in relatives
  • more complete destruction of B-cells
  • autoantibodies can be useful clinically
  • immune modulation offers possibility of novel treatments
5
Q

What are 2 most significant marker for clinically defining someone who might have T1DM?

A
  • Islet cell antibodies (ICA)
  • Glutamic Acid Decarboxylase antibodies (GADA) –> neurotransmitter

others:
- insulin antibodies (IAA)

6
Q

What are some symptoms of T1DM?

A

Symptoms:

  • polyuria
  • nocturia
  • polydipsia
  • blurred vision
  • weight loss
  • fatigue
  • thrush (due to increased risk of infections)
7
Q

What are signs of T1DM?

A

Signs:

  • dehydration
  • cachexia
  • hyperventilation (may have metabolic acidosis)
  • smell of ketones
  • glycosuria
  • ketonuria
8
Q

What is the effect of Insulin on:

HGO:
Glucose uptake:
Proteolyic breakdown:
Glycerol release from fatty tissue:

A

HGO: decrease
Glucose uptake: increase
Proteolyic breakdown: decrease
Glycerol release from fatty tissue: decrease

9
Q

Describe the mechanism of diabetic ketoacidosis in T1DM

A
  • glucose = isn’t taken up into cells + utilized
    so most energy = from fatty acids
  • if you have insulin deficiency, fatty acids come out of adipocytes –> into circulation (instead of glycerol)
  • then fatty acids go to the liver
  • and is converted to ketones
  • there is no insulin to inhibit this process
  • -> so you get ore ketone bodies produced by the liver
10
Q

What are main aims of treatment of T1DM?

A
  • reduce early mortality
  • avoid acute metabolic decompensation
  • identify requirement for exogenous insulin
  • prevent longterm complications such as retinopathy, neuropathy, nephropathy etc.
11
Q

note: increase in ketone = insulin DEFICIENCY

A

-

12
Q

How would you control diet in T1DM?

A
  • reduce fat
  • reduce refined carbohydrate
  • increase complex carbs
  • increase soluble fibre
13
Q

What are some treatments for T1DM?

A

with meals:

  • short acting insulin
  • human insulin
  • insulin analogues e.g lispro, aspart etc

background insulin:

  • long acting
  • non-C bounds to zinc or protamine
  • insulin analogues e.g glargine, determir, degludec

note: type + dose = dependent on how much patient eats in each meal and when they eat.

14
Q

How do insulin pump act as a method of treatment for T1DM?

what are disadvantages of it?

A
  • provides continuous insulin delivery
  • has preprogrammed basal rates + bolus for meals

DSADV:

  • doesn’t measure glucose
  • no completion of feedback loop
15
Q

How do islet cell transplants act as a method of treatment for T1DM?

what are disadvantages of it?

A
  • islet cells = harvested/isolated/injected into liver

DSADV:

  • risk of rejection
  • long waiting list

note: transplant if there is severe hypoglycemia + can’t be controlled by insulin pump

16
Q

How do capillary monitoring act as a method of treatment for T1DM?

what are disadvantages of it?

A
  • prick finger tips
  • capillary glucose levels
  • -> reflects venous blood glucose
  • patients can titrate insulin dose according to reading
17
Q

Long term blood glucose control is monitored by measuring:

A

HbA1c

  • HbA1c red cells react with glucose
  • high HbA1c = high glucose level in blood
  • lower HbA1c = lower risk of microvascular complication

note: not that useful in those with renal failure/ Hb Opathy

18
Q

What are the major acute complications associated with T1DM? (rapid decompensation)

A
  • hyperglycemia

- metabolic acidosis

19
Q

Why would hyperglycemia occur in T1DM?

A
  • reduced glucose utilisation in tissues –> causes increased hepatic glucose production
20
Q

Why would metabolic acidosis occur in T1DM?

A
  • increased ketone body production in liver
  • causes increase in circulating acetoacetate + hydroxybutyrate
  • causes osmotic dehydration _ poor tissue perfusion
21
Q

Define hypoglycemia

+

severe hypoglycemia

A

hypoglycemia = condition when the plasma glucose level = < 3.6 mmol/L

severe hypoglycemia = hypo requiring help of another person to treat

22
Q

what are some Hypoglycemia symptoms + signs?

A

Increased autonomic activation:

  • palpitations
  • tremor
  • sweating
  • cold extremities
  • anxiety

Impaired CNS function:

  • drowsiness
  • confusion
  • coma
23
Q

How would you treat hypoglycemia orally?

A
  • feed patient glucose as solution/ tablets

- give complex CHO

24
Q

How would you treat hypoglycemia parenterally?

A

if consciousness = impaired:

  • give IV dextrose
  • 1mg Glucagon IM
25
Q

What is Honeymoon phase

A

period of time following diabetes diagnosis when the pancreas is still able to produce amount of insulin to reduce insulin needs and aid blood glucose control.

26
Q

What is the primary genetic marker of diabetes ?

A

in HLA chr 6

- DR3/4

27
Q

note:
insulin tries to prevent glucose leaving liver
(no insulin –> increase plasma glucose

insulin can also increase glucose absorption by muscle
(no insulin –> increase plasma glucose level)

insulin prevents fatty cells from breaking up
(because glycerol from fatty cells can be used to produce glucose in liver)

A

-

28
Q

What are some long term complication

A
  • retinopathy
  • nephropathy
  • neuropathy
  • vascular disease
29
Q

note: basal insulin = constantly released throughout the day

A

-

30
Q

What are the different methods of monitoring diabetes in patients?

A
  • capillary monitoring

- continuous glucose monitor

31
Q

hypoglycemia is usually associated with patients with low/high HbA1c

A

hypoglycemia is usually associated with patients with low HbA1c