Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endo > Diabetes mellitus Types 1 and 2 > Flashcards

Diabetes mellitus Types 1 and 2 Flashcards

1
Q

Diabetic ketoacidosis:

treatment (3)

A
  1. fluids (b/c of osmotic diuresis)
  2. insulin
  3. replace electrolytes lost from diuresis (esp K+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Diabetic ketoacidosis:

-describe mechanisms (2 main mechanisms)

A

Coma/shock is result of 2 main pathways:

  1. Ketone production

Lack of insulin results in increased glucagon. Glucagon stimulates lipolysis, resulting in liver conversion of free fatty acids to ketones. Ketones are important to supply the brain with energy in starvation state, but they cause acidosis.

  1. severe hyperglycemia
    - lack of insulin results in severe hyperglycemia, leading to osmotic diuresis and severe dehydration. This increases concentration of ketones.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

In general, why are pts with T2DM overweight, and pts with untreated T1DM underweight?

A

In T1DM, lack of insulin induces increased glucagon release. Glucagon stimulates lipolysis, proteolysis for gluconeogenesis.

In T2DM, there is still some insulin. This insulin keeps glucagon levels low (neg feedback), preventing glucagon’s chronic body wasting effects.

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

Insulin overdose symptoms:

  1. mild
  2. moderate
  3. severe
A

hypoglycemia stimulates sympathetic response:

  1. shakiness, headaches, dizziness, sweating, tachycardia
  2. confusion, slurred speech, poor coordination
  3. seizure, coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Your pt has HTN and diabetes

Is it safe to prescribe a beta blocker for his HTN?

A

With caution.

Dangerous because beta blockers remove the adrenergic warning signs of hypoglycemia (tachycardia, sweating, etc)

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

Names of Ketone bodies in DKA (2)

A
  1. beta hydroxybutyric acid
  2. acetoacetate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What levels to diagnose pre-diabetes:

  1. A1C
  2. fasting glucose
  3. glucose tolerance test, 2 hours
A
  1. 5.7-6.4%
  2. 100-125
  3. 140-199

“pre-diabetes” is a somewhat vague diagnosis, compared to actual diabetes

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

How does obesity cause type 2 diabetes mellitus?

A

Obesity induces a pro-inflammatory state that leads to insulin resistance.

Details:
-Adipocyte hypertrophy activates inflammatory cells (macrophages, T cells, etc), which increase production of cytokines (TNF, IL6, IL1, etc), which cause insulin resistance.

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

T2DM:

  • risk for what acute crisis?
  • mech
A

Hyperosmolar non-ketotic coma (DKA is in T1DM)

  • high glucose (>500) leads to life-threatening diuresis with hypotension and coma
  • ketones are absent b/c the small amount of insulin in T2DM counteracts glucagon’s lipolytic effect (which is also why T2DM remain fat and T1DM are skinny)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does diabetes cause peripheral neuropathy, retinopathy, and cataracts?

(explained well by pathoma)

A

Osmotic damage to cells.

Certain cells allow free entry of glucose and contain Aldose reductase. Aldose reductase converts glucose to sorbitol, which leads to osmotic cellular damage.

These cells are:

  1. schwann cells–peripheral nerve damage
  2. retinal blood vessel pericytes–retinopathy
  3. Lens–cataracts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Gestational diabetes

-mechanism

A

Fetus steals mom’s glucose:

During pregnancy, the placenta secretes hormones which cause insulin resistance in the mother–this way nutrients can be directed to the fetus.

This can unmask a woman’s existing predisposition to insulin resistance, causing gestational diabetes.

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

Insulin overdose treatment:

  1. mild hypoglycemia
  2. moderate
  3. severe
A
  1. juice, candy
  2. frosting, sugar-gel
  3. glucagon injections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List Diabetes mellitus long term complications:

  • microvascular (3)
  • macrovascular (2)
A

microvascular:

  1. retinopathy
  2. nephropathy
  3. neuropathy

macrovascular:

  1. coronary artery disease
  2. peripheral vascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

T1DM:

-mech/etiology of disease

A
  • autoimmune
  • Environmental damage (eg infection) to islet cells induces immune system to recognize beta islet cells as foreign. Immune system mounts a CD8 response to attack beta cells.
  • Type 4 hypersensitivity reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does diabetes cause macrovascular and microvascular damage?

A

non-enzymatic glycosylation (NEG)

-glucose deposits on vessel walls, causing damage that leads to atherosclerosis (big/med vessel) and hyaline arteriolosclerosis (small vessels)

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

T1DM

-etiology

A

Autotimmune beta-cell destruction by T cells

17
Q

Pt presents to ED with DKA

-classic clinical presentation

A
  • breathing heavily (Kussmaul respiration to breathe out acid)
  • fruity breath (caused by acetone ketone bodies)
  • dehydrated
  • mental confusion
18
Q

Basic progression of type 2 diabetes, from -20 years to +20 years

(Dr Raff’s “most important slide”)

A
  1. Insulin resistance develops many years before T2DM
  2. Beta cells compensate by increasing insulin secretion.
  3. Eventually, beta cells poop out and can’t keep up with increasing insulin resistance. This is onset of T2DM– insulin secretion decreases, and serum glucose increases
  4. eventually, there is a “point of no return”
19
Q

How are these electrolytes affected in untreated T1DM:

  • Na+
  • K+
  • HCO3
  • PO4
A
  1. hyponatremia–osmotic dilution of plasma
  2. hyperkalemia–insulin’s effect is to push K inside cells. However, there is net LOSS of total K+ because of osmotic diuresis
  3. low HCO3– acid from ketoacidosis is breathed out as CO2
  4. low PO4–osmotic diuresis
20
Q

What 2 types of foods are worst for diabetics and why?

A
  1. sugar:

sugar/simple carbs are absorbed too fast for insulin’s effect.

  1. Fat
    - fat absorbed too slowly, so insulin’s duration has ended before fat is complete absorbed.

So, pizza is bad for diabetics.

21
Q

What levels required for diagnosis of diabetes mellitus:

  1. A1C
  2. fasting glucose
  3. oral glucose tolerance test, 2 hours
  4. random glucose
A

You need only 1 of these to dx DM

  1. >6.5%
  2. >126
  3. >200
  4. >200
22
Q

Diabetes mellitus:

-why is there poor wound healing?

A

Result of diminished blood supply, caused by glycosylation damage of vessels.

23
Q

T2DM
-2 main physiologic defects

A
  1. insulin resistance
    - impaired suppression of glucose production
    - impaired glucose uptake
  2. inadequate insulin secretion
24
Q

Diabetes mellitus short-term complications

(5)

A
  1. electrolyte abnormalities, hyperosmolar hyperglyemic state (from osmotic diuresis)
  2. fatigue
  3. poor wound healing (impaired blood supply)
  4. impaired immune defense (hyperglycemia effect)
  5. DKA (lack of insulin leads to glucagon-stimulated lipolysis and ketone formation)

Endo (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions