Final: Ch 33 DM & Metabolic Syndrome Flashcards Preview

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Flashcards in Final: Ch 33 DM & Metabolic Syndrome Deck (94):
1

fasting level of blood glucose

80-90mg/dl

2

a high blood glucose (like after a meal) stimulates release of what

insulin release --> increased uptake and use of glucose and aa

3

carbohydrates are stored as ________ in the ______ and ______ _______

glycogen, liver, skeletal muscle

4

excess glucose is converted to what

fat and stored in adipose

5

a low blood glucose stimulates release of what

glucagon --> glycogenolysis and gluconeogenesis

6

what are triglycerides used for

energy or stored in adipose

glycerol + 3 FA

7

excess aa are used for what

energy

8

glycogenolysis

glycogen --> glucose

when blood sugar is low

stimulated by glucagon to raise blood sugar

9

glycolysis

glucose --> pyruvate

10

gluconeogenesis

aa or FA --> glucose

by liver

11

the exocrine pancreas produces what

digestive enzymes

12

endocrine pancreas has what types of cells

islets of langerhans - hormone production

alpha cells - glucagon

beta cells - insulin

13

is release of insulin biphasic?

yes

immediately with a meal and then hrs later

14

3 ways insulin lowers blood sugar

raises glucose uptake, glycolysis, glycogen synthesis

lowers lipolysis, glycogenolysis

lowers gluconeogensis

15

insulin promotes ___ storage by increasing....

fat, increasing glucose uptake by adipose

16

insulin is produced as proinsulin and cleaved to _____ and _-______ prior to release

insulin, C-peptide

17

how does insulin reach the liver

portal circulation

1/2 used or degraded

18

insulin binds to the _-subunits of the membrane insulin receptor

alpha-subunits

causes beta-subunits to be autophosphorylated (activated kinase activity)

19

GLUT4 transporter

gets translocated to membrane to take in glucose

20

glucagon

produced by alpha-cells

released when blood sugar falls

maintains blood sugar during fasts

stimulates glycogenolysis, gluconeogenesis, lipolysis

21

somatostatin

secreted by delta cells in response to food

inhibits insulin and glucagon release --> slow GI activity

prolongs energy availibility

22

counter-regulatory hormones

catecholemines: stim glycogenolysis/lipolysis

GH: lowers glucose uptake

steroids: stimulate gluconeogenesis

23

classifications of DM

Type 1: Beta-cell destruction

Type 2: 9/10 cases - insulin resistance

gestational: glucose intolerance beginning in pregnancy

24

Dx of DM

depends on stages of glucose intolerance

25

pre-diabetes 3 levels

fasting plasma glucose 100-125mg/dl

plasma glucose 140-199 2 hrs after oral glucose load

hemoglobin A1C 5.7-6.4

26

type 1 DM

autoimmune destruction of beta-cells

absolute lack of insulin

requires insulin to avoid ketosis

27

progression of type 1 DM

triggering event activates immune system

anti-insulin and B-cell Ab appear

GTT abnormal

overt DM

28

is there genetic predisposition in type 1 DM

some

29

type 2 DM

impaired insulin secretion (B-cell failure)/insulin resistance

hepatic release of glucose is high

uptake of glucose by tissues is low

plasma glucose is high

30

early insulin resistance causes...

more insulin secretion, which further increases insulin resistance

31

patients with type 2 DM are usually

older and obese

but young people get it now too

strong genetic (not HLA) links

32

risks for type 2 DM

central obesity/lack of activity

high free fatty acids (FFA)

33

3 effects of high FFA on type 2 DM

increases insulin secretion --> B-cell failure

block peripheral glucose uptake

lower hepatic insulin sensitivity

34

is insulin resistance linked to other metabolic abnormalities in addition to hyperglycemia

yes, metabolic syndrome

35

metabolic syndrome

central obesity

high triglycerides

low HDL

HTN

36

other causes of DM

endocrine: cushing's syndrome or pheochromocytoma

meds: streptomycin, diuretics, antiretrovirals

37

gestational DM

glucose intolerance 1st detected in pregnancy

after pregnancy, woman has higher risk of getting real DM

38

risks for gestational DM

family history of DM

glucosuria

obesity

previous large baby

previous stillbirth/miscarraige

39

Rx of gestational DM

close observation

nutritional counseling

insulin

40

symptoms of DM

polyuria: a lot of urine b/c glucose is an osmotic diuretic

polydipsia: thirst (diuresis --> dehydration)

polyphagia (type 1): cells depleted of nutrients

hyperglycemia: blurred vision, fatigue, skin infections

41

fasting blood glucose normal/DM

normal: less than 100mg/dl

DM: greater than 126

42

casual blood glucose DM

greater than 200mg/dl w/ symptoms

43

OGTT

test plasma glucose 1-2 hrs after 75g of glucose

44

glycosalated Hb

Hb acquires glucose during life of RBC

normal is 4-6%

recommendation is less than 7%

45

urine tests

ketones?

46

self-monitoring of blood glucose

lancet to obtain blood

drop of blood on test strip

put strip in meter

record results in a log

47

dietary management goals

maintain normal blood glucose and lipids

attain reasonable weight

restrict fat/Na to avoid cardiovascular complications

48

type 1 DM dietary management

assess food and adjust insulin

49

type 2 DM dietary management

weight loss

lower blood glucose/lipids

50

low affinity glucose transporter

GLUT2 found in beta cells

high blood glucose increases glucose entry into beta cells and metabolism for ATP

51

oral (non-insulin) hypoglycemics are used mostly in type what

2

insulin secretogogues

biguanides

alpha-glucoside inhibitors

thiazolidendones

incretin-based agents

52

biguanides

metformin

lowers hepatic glucose output

53

alpha-glucoside inhibitor

acarbose

slow carb metabolism in small intestine

54

thiazolidendones

lower insulin resistance by up-regulating GLUT4

55

sodium glucose cotransporter 2 (SGLT2) inhibitors

glucose diffuses out of the cell

56

insulin is always required in type __ and sometimes needed in type __

1, 2

57

short acting insulin

works in minutes

action for 5 hrs or less

58

intermediate acting (NPH) insulin

onset in several hours

action for up to a day

59

multiple daily injections (MDI) of insulin

long or intermediate acting insulin 1-2x per day

short-acting before meals

60

continuous subcutaneous insulin infusion (CSII)

insulin pump

basal and bolus injections

61

acute complications of DM

ketoacidosis

hyperosmolar state

hypoglycemia

62

ketoacidosis is most common in which type

1

63

ketoacidosis

FA converted to ketones by liver

metabolic acidosis (pH and bicarb low)

intracellular acidosis --> K+ shift out of cells

64

Symptoms of ketoacidosis

fruity breath

tachycardia

hypotension

65

Rx of ketoacidosis

give insulin and IV fluids + K+

66

hyperosmolar hyperglycemic state (HHS)

extreme hyperglycemia (BG > 600mg/dl)

plasma osmolarity > 310mOsm/L

extreme cellular dehydration

can exist without ketoacidosis

67

symptoms of hyperosmolar hyperglycemic state

neuro from aphasia

hallucinations to seizures

68

treatment of hyperosmolar hyperglycemic state

replace water carefully to avoid hypokalemia and cerebral edema

grave prognosis

69

hypoglycemia

usually seen in people with DM who use insulin

rapid onset when BG less than 50-60mg/dl

70

precipitating factors of hypoglycemia

increased exercise

missing a meal

decrease in insulin requirement

alcohol (reduces gluconeogenesis)

71

symptoms of hypoglycemia

headache

decreased mentation

anxiety

tachycardia, sweating, shaking

72

treatment of hypoglycemia

eat 15-20g of concentrated glucose

73

Somogyi effect

hypoglycemia increases stress hormones --> hyperglycemia

people at risk for hyperglycemia after an episode of hypoglycemia

74

Dawn effect

high blood glucose early in the morning

circadian GH release

75

microvascular complications of chronis DM

nephropathies

retinopathies

76

macrovascular complications of chronic DM

CHD

stroke (CVA)

PVD (PAD)

77

other complications of chronic DM

neuopathies

foot ulcers

infections

78

sorbitol pathway in hyperglycemia

glucose --> sorbitol within cells

breakdown is slow

excess --> swelling of lens

depletes ATP

causes schwann cell damage/neuopathy

79

advanced glycation end products

hyperglycemia --> higher glycoproteins

glycoproteins damage basement memb of small vessels

80

neuropathies in DM

schwann cell damage

damage to nerve nutrient vessels

81

somatic neuopathies

distal and symmetric

stocking-glove pattern

sensory loss

painful

82

autonomic neuopathies

low cardiac, GI, GU, sexual function

83

nephropathies

leading cause of end stage renal disease

thickening of capillary basement membrane

sclerosis of glomerulus

84

risks for nephropathies

HTN (goal is 130/80)

poor glycemic control

microalbuminura

85

prevention of nephropathy

BP control using ACEI or ARB

glycemic/A1C control

stop smoking

treat hyperpilidemia

86

retinopathies

DM is #1 cause of new blindness

microaneurysm

neovascularization

bleeding/scarring

cataracts

87

other risks of macrovascular complications

high BP, lipids, glucose, CRP

poor endothelial function

88

type 1 DM macrovascular complications

develop with age

89

type 2 DM macrovascular complications

often have at diagnosis

90

prevention of macrovascular complications in DM

manage risk factors aggressively

BP/lipid management

stop smoking

91

diabetic foot ulcers

caused by a combination of neuropathy, vascular lesions, and infections

common cause of amputation

92

distal symmetric neuropathy

major risk factor for foot ulcers

sensory loss allows tissue damage without pain

pressure points common at sites of ulcers

93

prevention of diabetic foot ulcers

foot exams

test sensory function of the feet

check feet for infection

stop smoking

94

infections in DM

more serious and common in DM

sensory loss --> people ignore symptoms

hyperglycemia stimulates bacterial growth