Brainscape's Knowledge GenomeTM

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


See full index

Therapeutics 2 - Exam 2 > Pathophysi of Diabetes > Flashcards

Pathophysi of Diabetes Flashcards

hockerman

1
Q

criteria for diagnosis of diabetes (ADA)

A

A1C ≥ 6.5%
Fasting plasma glucose (FPG) ≥ 126 mg/dL (7.0 mmol/L)
2 hour plasma glucose ≥ 200 mg/dL (11.1 mmol/L) during OGTT (oral glucose tolerance test)
a random plasma glucose ≥ 200 mg/dL (11.1 mmol/L) with symptoms of diabetes

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

other names of T1DM

A

Insulin Dependent Diabetes Mellitus (IDDM)
Juvenile Onset Diabetes Mellitus (JODM)

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

prevalence of T1DM

A

10% of diabetic population

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

cause of T1DM

A

autoimmune response targeting pancreatic beta cells (may be triggered by viruses, chemicals, etc in genetically predisposed individuals)

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

typical treatment of T1DM

A

dependency on exogenous insulin

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

characterization of T1DM

A

no functional insulin-secretion
near complete loss of pancreatic beta cells
glucose interolance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

common complication of T1DM

A

tendency towards ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

mean age of onset T1DM

A

12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

is family history often a factor in T1DM?

A

family history often negative

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

ICA

A

islet cell cytoplasmic antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

IAA

A

insulin autoantibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

presence of ICA or IAA

A

means the immune system has initiated a response against the pancreatic beta cells

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

after initiation of autoimmune response, what happens to BCM?

A

gradual loss of BCM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what happens to FBG after initiation of autoimmune response?

A

FBG levels remain normal until about 70% of BCM is lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

C-peptide

A

a product of endogenous insulin that is a marker for insulin secretion in the presence of exogenous insulin

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

stage 1 of autoimmune response

A

normal glucose-stimulated insulin release
normal FBG
ICA-positive
IAA-positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

stage 2 of autoimmune response

A

progressive loss of glucose-stimulated insulin release
normal FBG
abnormal OGTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

stage 3 of autoimmune response

A

overt diabetes
high FBG
C-peptide present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

autoantibodies associated with T1DM

A

islet antigen 2 (IA-2)
phogrin (IA-2B)
Zinc transporter (ZnT-8)
Glutamic acid decarboxylase (GAD65)
Voltage-gated Ca++ (Cav 1.3)
Vesicle-associated membrane protein-2 (VAMP-2)
antibodies against one or more B-cell proteins signals an increased risk for developing diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

IA-2 accuracy

A

57% sensitivity –> 57% of non-diabetics who have it will develop type 1 diabetes
99% selectivity –> 99% of type 1 diabetics have Abs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

prevalence of non obese T2DM

A

10%

22
Q

prevalence of T2DM

A

80%

23
Q

age of onset of non-obese T2DM

A

often under 25

24
Q

age of onset of obese T2DM

A

usually over 30

25
Q

another name of T2DM

A

Non-insulin dependent diabetes mellitus (NIDDM)
Maturity onset diabetes of the young (MODY)
Adult onset DM

26
Q

is family history often a factor in T2DM?

A

yes

27
Q

insulin secretion in response to glucose challenge (non-obese)

A

low

28
Q

insulin secretion in response to glucose challenge (obese)

A

low for body mass

29
Q

cause of non-obese T2DM

A

mutations in specific proteins

30
Q

cause of obese T2DM

A

insulin resistance
decreased BCM

31
Q

consequence of lack of insulin

A

hyperglycemia
glucosuria
hyperlipidemia
uninhibited glucagon

32
Q

source hyperglycemia due to lack of insulin

A
  1. decreased glucose uptake in cells where glucose uptake is insulin-dependent
  2. decreased glycogen synthesis (process in the liver where glucose is stored for later release into the blood stream)
  3. increased conversion of amino acids to glucose (in the absence of insulin there is nothing to inhibit gluconeogenesis)
33
Q

source of glycosuria due to lack of insulin

A

high glucose concentration in renal filtrate, overwhelming of glucose transporters in the kidneys, glucose spills into the urine

34
Q

source of hyperlipidemia due to lack of insulin

A

increased fatty acid mobilization from fat cells (lipids are broken down to fatty acids and distributed through the body to use for fuel instead of carbs)
increased fatty acid oxidation (ketoacidosis)

35
Q

ketoacidosis

A

high rate of B-oxidation and accumulation of their byproduct, ketone bodies
leads to a large amount of acid in the body

36
Q

source of uninhibited glucagon due to lack of insulin

A

increased glucagon levels in the presence of increased blood glucose levels, this process is usually inhibited by insulin

37
Q

complications of hyperglycemia (CV)

A

micro and macro angiopathies
leads to compromised blood flow to parts of the body

38
Q

complications of hyperglycemia (NS)

A

neuropathy

39
Q

cause of neuropathy

A

high BG level
increase utilization of polyol pathway
water accumulation in neurons/reduced protection from oxidative damage

40
Q

complications of hyperglycemia (eye)

A

cataracts
retinal micro aneurysms
hemorrhage

41
Q

complications of hyperglycemia (infections)

A

increases susceptibility to infections

42
Q

goal of insulin therapy historically

A

reduce acute symptoms (polyuria, dehydration, ketoacidosis)

43
Q

current goals of insulin therapy

A

keep an average blood glucose level below 150 mg/dL
prevent/delay onset of complications
A1C ≤ 6 (ideal) or <7 (goal)

44
Q

risk of insulin therapy with aggressive goals

A

increased risk of hypoglycemia

45
Q

why is glucose so toxic?

A

oxidation products of glucose react irreversibly with proteins –> forms advanced glycation end products (AGEs) –> loss of normal protein function and acceleration of aging process

Theorized to account for many long-term complications of diabetes

46
Q

RAGE

A

receptors for advanced glycation end products
when peptides containing CML (glyoxal) and CEL (methylglyoxal) bind, inflammation is promoted

47
Q

polyol (aldose reductase) pathway

A

glucose –> sorbitol –> fructose

48
Q

effect of increased glucose in polyol pathway

A

increased accumulation of sorbitol –> increases the osmolality of the cell –> swelling and damage

49
Q

increased glucose in hexosamine pathway

A

increased formation of energized glucosamine-6-P (UDP-GIcNAc) which can diminish function of proteins/genes

50
Q

increased glucose in protein kinase C pathway

A

leads to excess of various signaling

Therapeutics 2 - Exam 2 (10 decks)

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