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Clin Med - Endocrine > Lecture 12 - DM > Flashcards

Lecture 12 - DM Flashcards

1
Q

Diabetes Mellitus definition

A

a chronic disorder characterized by hyperglycemia resulting in acute metabolic alterations and propensity towards the development of specific ophthalmic, renal and neurologic complications as well as increased risk of atherosclerotic vascular disease

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2
Q

Diabetes is the number 1 cause of what 3 health conditions?

A

blindness
renal failure
amputation

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3
Q

What is the difference in incidence between type 1 and 2 diabetes?

A

type 1 is 0.2-0.5% while type 2 is >9%

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4
Q

What is the difference in age of onset between type 1 and type 2 diabetes?

A

type 1 starts typically <30 years of age

type 2 starts >40 years of age

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5
Q

Ketosis is more common with type 1 or type 2?

A

Type 1

rare with type 2

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6
Q

Type 1 or type 2 has islet autoantibodies present?

A

Type 1

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7
Q

How does insulin secretion differ between type 1 and type 2?

A

type 1 is absent or severely impaired

type 2 is progressively impaired

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8
Q

Which type of DM is commonly associated with insulin resistance?

A

Type 2

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9
Q

LADA

A

late onset type 1 diabetes

Latent autoimmune diabetes in adults

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10
Q

What is the typical pt for type 1 1/2 DM?

A

young, obese, AA man presenting with DKA, but without permanent insulin requirement after stabilization

DKA is a marker for type 1

but these pts don’t need insulin

basically these are type 2 DM pts that present with characteristics of type 1

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11
Q

MODY

A

maturity onset diabetes of the young

autosomal dominant syndromes due to single gene mutations affecting beta cell function

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12
Q

How does age relate to DM?

A

Prevalence of DM increases with age

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13
Q

What metabolic effects does diabetes have on the muscle and fat?

A

decrease glucose uptake

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14
Q

What metabolic effects does diabetes have on the liver?

A

increase hepatic glucose production

all leading to hyperglycemia

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15
Q

What is the definition of insulin resistance?

A

impaired cellular response to the physiological effects of insulin

for ex. decreased glucose uptake by muscle in response to insulin

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16
Q

Insulin resistance in the presence of functioning beta cells

A

insulin resistance in the presence of functioning beta cells results in hyper-insulinism and only mild glucose abnormalities

17
Q

When does insulin resistance start in DM pts?

A

Roughly 10 years before they get dx

beta cell failure continues after dx

18
Q

sxs of hyperglycemia in type 1

A

polydipsia
blurred vision
weight loss

19
Q

What are some of the less obvious risk factors for type 2 DM?

A

PCOS
gestational DM

more obvious ones: 
HTN 
obesity 
family hx 
sedentary lifestyle
20
Q

Type 2 DM can present less obviously, with what sxs?

A

UTI, cellulitis, vaginal yeast

21
Q

What are the dx criteria for diabetes in nonpregnant adults?

A

fasting plasma glucose >/= 126 mg/dl (on 2 occasions)
or
HbA1c >6.5%
or
random plasma glucose >200 mg/dl together with sxs of hyperglycemia (polyuria, polydipsia, weight loss, blurred vision)
or
2 hour plasma glucose >200 75g OGTT

22
Q

How an you distinguish between type 1 and 2 DM?

A

Type 1 has GAD antibody

this is a better test than C-peptide because it doesn’t change with change in glucose

23
Q

If you have a DM pt who is having seizures, what must their blood glucose level be?

A

lower than 30

24
Q

HgA1C can tell you about the glucose levels over the past ____months

A

2-3 months

25
Q

What is happening in DKA?

A

glucagon gets released
lipolysis (d/t no glucose being in the cells so the cells turn to a different form of energy)
lipolysis gives rise to free fatty acids which get broken down into ketone bodies that are used for energy but also make the blood acidic

26
Q

What is the treatment for DKA?

A

fluids
insulin
electrolytes

trying to reverse the acidosis

27
Q

Who do we see DKA more with?

A

Type 1 DM (more commonly with people who didn’t know they had DM but it can still be seen with known DM pts)

28
Q

How does DKA occur in pts with known DM?

A

it states of stress the body will produce epi and epi stimulates glucagon which increased blood glucose but these pts are still unable to get that glucose into the cells

29
Q

Insulin resistance

A

body doesn’t respond to insulin

30
Q

What are risk factors to insulin resistance?

A

obesity
HTN
lack of exercise

31
Q

HHS

A

hyperosmolar hyperglycemic state
MC seen in type 2 b
basically the EXTREMELY high blood glucose levels make the osmolarity of the plasma so high that water leaves the cells to enter the plasma —dehydrating the cells

32
Q

Why is DKA less common in type 2 DM?

A

glucagon and insulin are in balance in type 2 DM since they still are able to produce insulin, just not respond well to it

Clin Med - Endocrine (13 decks)

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