4.7 Diabetes Mellitus Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Which is more common: T1DM or T2DM?

A

T2DM (90% of cases)

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

Describe T1DM pathophys

A
  • Immune mediated reduction of the insulin secreting capacity of beta cells of the pancreas
  • Blunted/absent insulin response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe T2DM pathophys

A
  • Body becomes resistant to normal levels of insulin
  • Impaired release of insulin
  • Blunted/absent insulin response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the effects of “incretin” hormones? Where are they released from?

A
  • Promote release of insulin
  • Released from duodenum and small intestine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the two incretin hormones? Which type of cells secrete them?

A
  • Gastric inhibitory peptide (GIP): K cells (Dr K likes this one)
  • Glucagon like peptide-1 (GLP-1): L cells (semaglutide is an L)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why might insulin be higher from oral glucose than IV glucose?

A
  • Oral glucose goes through the stomach
  • This stimulates incretin hormones; much bigger insulin response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the final straw that causes frank diabetes?

A
  • Failure of insulin secretion in response to increased resistance
  • This leads to much higher blood glucose levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is C-peptide? Is it high or low in T1DM vs T2DM?

A
  • Byproduct released during insulin secretion
  • Low in T1DM
  • Normal/high in T2DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What’s the mech for how T1DM can cause diabetic ketoacidosis

A
  • No insulin
  • No suppression of Hormone-Sensitive Lipase
  • More FFAs in blood
  • Excess are converted into ketones; lowers pH; acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the two most common precipitating factors for diabetic ketoacidosis

A
  • Infection
  • Deliberate insulin manipulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hyperosmolar hyperglycaemic syndrome (HHS) pathophys. Which type of diabetes is it associated with?

A
  • Relative insulin deficiency
  • Incr. gluconeogenesis
  • Hyperglycaemia
  • Diuresis
  • Hyperosmolarity :(
  • Primarily associated with type 2 diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Precipitating factors for HHS

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

What are the four tiers, in order, that the body uses to prevent hypoglycaemia as BGL lowers?

A
  1. Insulin suppression
  2. Glucagon + adrenaline
  3. Growth hormone
  4. Cortisol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

List four autonomic symptoms of hypoglycaemia

A
  • Palpitations
  • Shaking
  • Sweating
  • Hunger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Basic treatment algo for hypoglycaemia

A
  • If responsive/cooperative, give high-sugar foods like jelly beans
  • If not, give IV glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the two classifications of chronic diabetes complications?

A
  • Microvascular
  • Macrovascular
17
Q

What are the three categories of macrovascular complications of diabetes?

A
  1. Heart
  2. Brain
  3. Extremities
18
Q

What are the three categories of microvascular complications of diabetes?

A
  1. Retino
  2. Nephro
  3. Neuropathy
19
Q

How do you test for microvascular renal complications of diabetes?

A
  • Urinalysis
  • High albumin levels indicate protein leakage -> nephro referral
20
Q

What are the three types of diabetic foot ulcers, as classified according to their causes?

A
  • Neuropathic
  • Ischaemic
  • Neuroischaemic
21
Q

What is the proposed link between DKA and pancreatitis?

A
  • Elevated lipids
  • Parenchymal inflammation
  • Ischaemic damage of tissue
22
Q

Proposed link between DKA and DVT

A
  • DKA causes hypercoagulability
  • Incr. DVT risk
23
Q

Proposed link between DKA and resp. disturbance

A
  • Acidosis
  • Body tries to blow off CO2
  • Kussmaul breathing
24
Q

Proposed link between DKA and cerebral oedema

A
  • High BGL sucks fluid from brain via osmosis
  • When insulin is given, there’s a rebound rush of fluid into the brain