Brainscape's Knowledge GenomeTM

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


See full index

Endocrinology > Chronic Complications of Diabetes Mellitus > Flashcards

Chronic Complications of Diabetes Mellitus Flashcards

1
Q

Pt with _____ usually have significant insulin resistance and are USUALLY older.

A

T2D

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

Pt with ___ are prone to have episodes of DKA which may have long tern effects on a variety of organs.

A

DKA

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

What are the 3 organs most commonly and dramatically affected by diabetes?

A

eyes (retinopathy), nerves (neuropathy), kidneys (nephropathy)

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

What is the most common cause of death in a diabetic pt?

A

atherosclerotic vascular disease

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

What is the most common cause of death in T1D before 40 years old?

A

renal failure

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

What are 6 metabolic abnormalities contributing to chronic complications of diabetes?

A
  1. Increased metabolism–> increased ROS
  2. Def in myo-inositol–> abnormal phosphoinositide metabolism
  3. Increased metabolism of glucose through sorbitol pthwy
  4. Non-enzymatic glycosylation of proteins, RNA, DNA
  5. Abnormal ECM, increase in collagen and fibronectin, decrease in heparan sulfate
  6. Metabolic syndrome has added impact of adipose derived tissue components: leptin, TNFa, Ang II, PAI-1, FFA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

T or F The development of complications in pt with insulin resistance begins after hyperglycemia develops.

A

F- BEFORE

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

What are the major enviornmental factors in T2D?

A

development of obesity and reduced exercise

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

What is the significance of visceral fat in metabolic syndrome?

A

Secretes excessive amounts of FFA, leptin, TNF-a, ATII, PAI-1, decrease secretion of adiponectin

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

Excessive oxidation generates ROS that activates _______ and damages ______.

A

Serine-threonine kinase such as PKC; many cellular mechanisms including proteins, FA, DNA, RNA

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

SO can be generated via coenzyme _____.

A

Q10

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

How does excess oxidation of glucose or FFA cause generation of SO from CoQ10?

A

Excessive H is pumped into mitochondria by ETC. High [H] inhibits cytochrome from accepting electron from CoQ10. CoQ10 diverts these electrons to oxygen and generates excess amounts of SO.

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

ROS, kinases, and gene products (cytokines, chemokines, etc.) produce _________ that lead to diabetic complications

A

ischemia, cellular proliferation, matrix accumulation and dysfunction, cellular necrosis, apoptosis

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

SO ______ the synthesis of NO.

A

inhibits

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

_____ is the primary endogenous inhibitor of Nfkb and platelet aggregation.

A

NO

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

What does deficiency of NO cause?

A

allows inflammation to proceed unchecked. It is an important vasodilator and its deficiency contributes to vasoconstriction and ischemia.

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

What is auto-oxidation?

A

method by which excess glucose generates additional SO

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

____ is a fatty acid that is a direct inducer of NO.

A

Ceramide

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

T or F NO induces apoptosis.

A

T

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

When is apoptosis good and when is it bad?

A

Plaque: good–> shrinkage
Islets: bad

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

_____ is a substrate for the pro-inflammatory prostaglandins that contribute to the destruction of islets.

A

Arachidonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is beta-oxidation?

A

oxidation of FFA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Excessive oxidation and ROS changes the redox state. What are detrimental effects of this?

A
  1. Inhibits further glucose and fatty acid oxidation–> partially degraded FA bound to carnitine –>
  2. inhibiting transfer of more FA into mitochondria and toxic accumulation in cytoplasma.
  3. Increased glyceraldehyde 3P–> major intracellular glycosylator of proteins
  4. GAP–> DAG–> PKC
  5. Equilibrium shifted to lactate (from pyruvate)–> acidosis
24
Q

T or F SO is a potent activator of PKC

A

TRUE (this is bolded and underlined in the document so its probably not important….)

25
Q

3 additional ways SO is generated

A
  1. NADPH oxidase stimulated by oxidized LDL, TNFa, ATII
  2. auto-oxidation
  3. Neutrophils and macrophages
26
Q

In cells that have aldose reductase, glucose is converted to ____.

A

sorbitol and then fructose

27
Q

T or F Glucose is a more potent glycosylating agent than fructose

A

False- Fructose is

28
Q

What happens to sorbitol that causes osmotic swelling of cells?

A

accumulates in cytoplasm

29
Q

What does hyperosmolarity activate?

A

AMP kinase–> DAG synthase–> DAG –> PKC (inflammation) and JNK and MAPK which induce apoptosis

30
Q

Sorbitol is structurally similar to _____.

A

myo-inositol (ringed)

31
Q

Myo-inositol is a 2nd msger in the _____ pathway.

A

phosphatidylinositol

32
Q

Why is an abundant supply of intracellular myo-inositol required?

A

PI turn over is very fast

33
Q

What does sorbitol and probably glucose do to the transport pathway of myo-inositol?

A

Blocks- When sorbitol/glucose levels are high, PI pathway is starved- nerves are susceptible

34
Q

How does the PI pathway normally function?

A

PI–> PIP-2–> activation of PKC–> IP3 and DAG
IP3–> stimulates release of Ca–> Na/K ATPase and calcium chanels
DAG–> activates PKC, metabolized to PG like PGE1 that is pro-inflammatory

35
Q

In order for NaK ATPase to function normally and play its role in normal nerve impulse propagation, is one or both arms of the PI pathway required?

A

both

36
Q

What happens when glucose comes in contact with protein or DNA molecule?

A

covalently linked via aldehyde group on glucose and terminal amino groups on arginine, lysine, and nucleic acids

37
Q

What is the initial step in non-enzymatic glycosylation reactions? What is the slow rearrangement step?

A

formation of schiff base; Amadori product

38
Q

How is non-enzymatic glycosylation measured?

A

hemoglobin A1C

39
Q

The degree of non-enzymatic glycoyslation is determined by ____

A

simple mass action

40
Q

T or F glycosylation can create novel binding sites to create new binding sites

A

true

41
Q

Glycosylated proteins can undergo an extensive series of oxidation-dehydration reactions and rearrangements to form _________

A

AGE-products

42
Q

What is the most important reaction in formation of AGE products?

A

cross links between proteins and/or DNA- prevent normal degradation

43
Q

Are AGE-products reveresible?

A

negative ghost rider

44
Q

GAP, other glyolytic intermediates, and fructose are all potent ______

A

glycosylators

45
Q

_________ express RAGE. When bound, they activate ______.

A

macs and enothelial cells; PKC

46
Q

Collagen synthesis is stimulated by _____ and inhibited by _____. What happens to these in diabetes?

A

TGF B- increased thanks to PKC

NO- reduced

47
Q

Heparan sulfate binding is inhibited by ______

A

glycosylation

48
Q

Hall mark of diabetic tissue annddd GO!

A

massive increase in ECM that is unable to provide a physiological barrier

49
Q

How is glomerular perfusion pressure affected?

A

WITHIN DAYS, control of arterioles becomes dysfunctional and pressure INCREASES accompanied by an increase in GFR

50
Q

What happens to GFR, perfusion pressure, and kidney size at the beginning of diabetes?

A

All increase

51
Q

What happens if nephropathy progresses?

A

micro-albuminuria–> proteinuria
Matrix material dysfunction–> crowding–> fall in GFR
Toxic filtered protein–> tubular cells die
HTN, loss of EPO, anemia,

52
Q

How does nephropathy lead to secondary hypoparathyroidism

A

loss of VD, decreased Ca absorption, increase PTH (pro-inflammatory)

53
Q

Retinopathy affects ___% of diabetics.

A

80

54
Q

2 types of clinical presentations of retinopathy

A

macular edema and/or neo-vascularization…..This is bolded and underlined soooo yea

55
Q

The accumulation of fluorescein in vitreous is due primarily to _____

A

dysfunctional pigment epithelial cells

Endocrinology (31 decks)

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