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Pathophysiology > Final: Ch 33 DM & Metabolic Syndrome > Flashcards

Final: Ch 33 DM & Metabolic Syndrome Flashcards

1
Q

fasting level of blood glucose

A

80-90mg/dl

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2
Q

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

A

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

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3
Q

carbohydrates are stored as ________ in the ______ and ______ _______

A

glycogen, liver, skeletal muscle

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4
Q

excess glucose is converted to what

A

fat and stored in adipose

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5
Q

a low blood glucose stimulates release of what

A

glucagon –> glycogenolysis and gluconeogenesis

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6
Q

what are triglycerides used for

A

energy or stored in adipose

glycerol + 3 FA

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7
Q

excess aa are used for what

A

energy

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8
Q

glycogenolysis

A

glycogen –> glucose

when blood sugar is low

stimulated by glucagon to raise blood sugar

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9
Q

glycolysis

A

glucose –> pyruvate

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10
Q

gluconeogenesis

A

aa or FA –> glucose

by liver

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11
Q

the exocrine pancreas produces what

A

digestive enzymes

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12
Q

endocrine pancreas has what types of cells

A

islets of langerhans - hormone production

alpha cells - glucagon

beta cells - insulin

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13
Q

is release of insulin biphasic?

A

yes

immediately with a meal and then hrs later

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14
Q

3 ways insulin lowers blood sugar

A

raises glucose uptake, glycolysis, glycogen synthesis

lowers lipolysis, glycogenolysis

lowers gluconeogensis

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15
Q

insulin promotes ___ storage by increasing….

A

fat, increasing glucose uptake by adipose

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16
Q

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

A

insulin, C-peptide

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17
Q

how does insulin reach the liver

A

portal circulation

1/2 used or degraded

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18
Q

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

A

alpha-subunits

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

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19
Q

GLUT4 transporter

A

gets translocated to membrane to take in glucose

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20
Q

glucagon

A

produced by alpha-cells

released when blood sugar falls

maintains blood sugar during fasts

stimulates glycogenolysis, gluconeogenesis, lipolysis

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21
Q

somatostatin

A

secreted by delta cells in response to food

inhibits insulin and glucagon release –> slow GI activity

prolongs energy availibility

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22
Q

counter-regulatory hormones

A

catecholemines: stim glycogenolysis/lipolysis

GH: lowers glucose uptake

steroids: stimulate gluconeogenesis

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23
Q

classifications of DM

A

Type 1: Beta-cell destruction

Type 2: 9/10 cases - insulin resistance

gestational: glucose intolerance beginning in pregnancy

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24
Q

Dx of DM

A

depends on stages of glucose intolerance

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25
Q

pre-diabetes 3 levels

A

fasting plasma glucose 100-125mg/dl

plasma glucose 140-199 2 hrs after oral glucose load

hemoglobin A1C 5.7-6.4

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26
Q

type 1 DM

A

autoimmune destruction of beta-cells

absolute lack of insulin

requires insulin to avoid ketosis

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27
Q

progression of type 1 DM

A

triggering event activates immune system

anti-insulin and B-cell Ab appear

GTT abnormal

overt DM

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28
Q

is there genetic predisposition in type 1 DM

A

some

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29
Q

type 2 DM

A

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

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30
Q

early insulin resistance causes…

A

more insulin secretion, which further increases insulin resistance

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31
Q

patients with type 2 DM are usually

A

older and obese

but young people get it now too

strong genetic (not HLA) links

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32
Q

risks for type 2 DM

A

central obesity/lack of activity

high free fatty acids (FFA)

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33
Q

3 effects of high FFA on type 2 DM

A

increases insulin secretion –> B-cell failure

block peripheral glucose uptake

lower hepatic insulin sensitivity

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34
Q

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

A

yes, metabolic syndrome

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35
Q

metabolic syndrome

A

central obesity

high triglycerides

low HDL

HTN

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36
Q

other causes of DM

A

endocrine: cushing’s syndrome or pheochromocytoma
meds: streptomycin, diuretics, antiretrovirals

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37
Q

gestational DM

A

glucose intolerance 1st detected in pregnancy

after pregnancy, woman has higher risk of getting real DM

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38
Q

risks for gestational DM

A

family history of DM

glucosuria

obesity

previous large baby

previous stillbirth/miscarraige

39
Q

Rx of gestational DM

A

close observation

nutritional counseling

insulin

40
Q

symptoms of DM

A

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
Q

fasting blood glucose normal/DM

A

normal: less than 100mg/dl

DM: greater than 126

42
Q

casual blood glucose DM

A

greater than 200mg/dl w/ symptoms

43
Q

OGTT

A

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

44
Q

glycosalated Hb

A

Hb acquires glucose during life of RBC

normal is 4-6%

recommendation is less than 7%

45
Q

urine tests

A

ketones?

46
Q

self-monitoring of blood glucose

A

lancet to obtain blood

drop of blood on test strip

put strip in meter

record results in a log

47
Q

dietary management goals

A

maintain normal blood glucose and lipids

attain reasonable weight

restrict fat/Na to avoid cardiovascular complications

48
Q

type 1 DM dietary management

A

assess food and adjust insulin

49
Q

type 2 DM dietary management

A

weight loss

lower blood glucose/lipids

50
Q

low affinity glucose transporter

A

GLUT2 found in beta cells

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

51
Q

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

A

2

insulin secretogogues

biguanides

alpha-glucoside inhibitors

thiazolidendones

incretin-based agents

52
Q

biguanides

A

metformin

lowers hepatic glucose output

53
Q

alpha-glucoside inhibitor

A

acarbose

slow carb metabolism in small intestine

54
Q

thiazolidendones

A

lower insulin resistance by up-regulating GLUT4

55
Q

sodium glucose cotransporter 2 (SGLT2) inhibitors

A

glucose diffuses out of the cell

56
Q

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

A

1, 2

57
Q

short acting insulin

A

works in minutes

action for 5 hrs or less

58
Q

intermediate acting (NPH) insulin

A

onset in several hours

action for up to a day

59
Q

multiple daily injections (MDI) of insulin

A

long or intermediate acting insulin 1-2x per day

short-acting before meals

60
Q

continuous subcutaneous insulin infusion (CSII)

A

insulin pump

basal and bolus injections

61
Q

acute complications of DM

A

ketoacidosis

hyperosmolar state

hypoglycemia

62
Q

ketoacidosis is most common in which type

A

1

63
Q

ketoacidosis

A

FA converted to ketones by liver

metabolic acidosis (pH and bicarb low)

intracellular acidosis –> K+ shift out of cells

64
Q

Symptoms of ketoacidosis

A

fruity breath

tachycardia

hypotension

65
Q

Rx of ketoacidosis

A

give insulin and IV fluids + K+

66
Q

hyperosmolar hyperglycemic state (HHS)

A

extreme hyperglycemia (BG > 600mg/dl)

plasma osmolarity > 310mOsm/L

extreme cellular dehydration

can exist without ketoacidosis

67
Q

symptoms of hyperosmolar hyperglycemic state

A

neuro from aphasia

hallucinations to seizures

68
Q

treatment of hyperosmolar hyperglycemic state

A

replace water carefully to avoid hypokalemia and cerebral edema

grave prognosis

69
Q

hypoglycemia

A

usually seen in people with DM who use insulin

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

70
Q

precipitating factors of hypoglycemia

A

increased exercise

missing a meal

decrease in insulin requirement

alcohol (reduces gluconeogenesis)

71
Q

symptoms of hypoglycemia

A

headache

decreased mentation

anxiety

tachycardia, sweating, shaking

72
Q

treatment of hypoglycemia

A

eat 15-20g of concentrated glucose

73
Q

Somogyi effect

A

hypoglycemia increases stress hormones –> hyperglycemia

people at risk for hyperglycemia after an episode of hypoglycemia

74
Q

Dawn effect

A

high blood glucose early in the morning

circadian GH release

75
Q

microvascular complications of chronis DM

A

nephropathies

retinopathies

76
Q

macrovascular complications of chronic DM

A

CHD

stroke (CVA)

PVD (PAD)

77
Q

other complications of chronic DM

A

neuopathies

foot ulcers

infections

78
Q

sorbitol pathway in hyperglycemia

A

glucose –> sorbitol within cells

breakdown is slow

excess –> swelling of lens

depletes ATP

causes schwann cell damage/neuopathy

79
Q

advanced glycation end products

A

hyperglycemia –> higher glycoproteins

glycoproteins damage basement memb of small vessels

80
Q

neuropathies in DM

A

schwann cell damage

damage to nerve nutrient vessels

81
Q

somatic neuopathies

A

distal and symmetric

stocking-glove pattern

sensory loss

painful

82
Q

autonomic neuopathies

A

low cardiac, GI, GU, sexual function

83
Q

nephropathies

A

leading cause of end stage renal disease

thickening of capillary basement membrane

sclerosis of glomerulus

84
Q

risks for nephropathies

A

HTN (goal is 130/80)

poor glycemic control

microalbuminura

85
Q

prevention of nephropathy

A

BP control using ACEI or ARB

glycemic/A1C control

stop smoking

treat hyperpilidemia

86
Q

retinopathies

A

DM is #1 cause of new blindness

microaneurysm

neovascularization

bleeding/scarring

cataracts

87
Q

other risks of macrovascular complications

A

high BP, lipids, glucose, CRP

poor endothelial function

88
Q

type 1 DM macrovascular complications

A

develop with age

89
Q

type 2 DM macrovascular complications

A

often have at diagnosis

90
Q

prevention of macrovascular complications in DM

A

manage risk factors aggressively

BP/lipid management

stop smoking

91
Q

diabetic foot ulcers

A

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

common cause of amputation

92
Q

distal symmetric neuropathy

A

major risk factor for foot ulcers

sensory loss allows tissue damage without pain

pressure points common at sites of ulcers

93
Q

prevention of diabetic foot ulcers

A

foot exams

test sensory function of the feet

check feet for infection

stop smoking

94
Q

infections in DM

A

more serious and common in DM

sensory loss –> people ignore symptoms

hyperglycemia stimulates bacterial growth

Pathophysiology (24 decks)

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