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

Final: Ch 33 DM & Metabolic Syndrome Flashcards

(94 cards)

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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
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

Pathophysiology (24 decks)

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