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Diabetes Mellitus Flashcards

1
Q

Insulin is the primary _____ hormone of the body

A

anabolic

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2
Q

What processes does insulin regulate?

A

carbohydrate utilization/ storage
protein synthesis
lipogenesis

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3
Q

What hormones are counter-regulatory to insulin?

A

epinephrine
cortisol
growth hormone

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4
Q

Describe the regulation of glucose release from pancreatic beta cells

A
  • glucose is transported into the beta cell, enters glycolysis and generates ATP.
  • increased ATP closes an ATP-sensitive membrane potassium channel
  • K channel closure depolarizes the cell, which then opens voltage-dependent calcium channels and triggers insulin secretion.
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5
Q

Insulin response to a constant glucose simulus is _______

A

biphasic:

early peak and more prolonged second phase

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6
Q

What are initiators of insulin release?

A

glucose
some amino acids
sulfonylureas- stimulate closer of K channel

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7
Q

What are inhibitors of insulin release?

A

somatostatin
epinephrine
K channel openers ex diazoxide

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8
Q

What cell types do NOT have insulin receptors

A

kidney, nerve, retina

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9
Q

What are the four categories of DM?

A

type 1- autoimmune
type 2- metabolic syndrome
“other”
gestational

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10
Q

Diabetes mellitus is defined by the degree of _________

A

hyperglycemia

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11
Q

What kinds of deficits can cause “other” DM?

A 
defects in insulin action
defects in B cell function (MODYs)
drugs
infections- CMV, rubella
endocrinopathies
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12
Q

What are the diagnostic criteria for DM?

A
  • A1c > 6.5%
  • FPG > 125
  • two hour plasma glucose >200 for OGTT
  • any random plasma glucose >200 in symptomatic patient
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13
Q

What are the parameters for impaired fasting glucose (IFG)?

A

fasting glucose above 100 but below 126

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14
Q

What are the parameters for impaired glucose tolerance (IGT)?

A

plasma glucose between 140 and 200 two hours into OGTT

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15
Q

People with _____ are at increased risk for developing frank diabetes

A

pre-diabetes

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16
Q

People with _____ are at increased risk for developing frank diabetes

A

pre-diabetes

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17
Q

In type 1 diabetes, autoimmune destruction of B cells leads to:

A

absolute insulin deficiency

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18
Q

What HLA haplotypes are associated with type 1 diabetes?

A

DR3, DR4, DQ8

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19
Q

What antibodies can be found in type 1 diabetes?

A

insulin autoantibodies, islet cell antibodies, and anti-glutamic acid decarboxylase (GAD) antibodies

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20
Q

80-90% of beta cells are destroyed before ______ develops in type 1 diabetes

A

hyperglycemia

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21
Q

What is the renal threshold for glycosuria?

A

200

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22
Q

Describe effects of absolute insulin deficiency in type 1 diabetes

A

protein degradation, lipolysis, and inability to maintain body tissue, resulting in weight loss
osmotic diuresis

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23
Q

Type 1 diabetes symptoms are usually present for _____ before diagnosis

A

days- few weeks

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24
Q

What are the two major physiologic abnormalities in type 2 diabetes?

A

insulin resistance

impaired insulin secretion

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25
The pathophysiological manifestations of type 2 diabetes occur at the level of the ____ and ________
liver and peripheral tissues- adipose and muscle
26
What is the major cause of fasting hyperglycemia in people with type 2 diabetes?
insulin resistance causes increased hepatic glucose production via gluconeogenesis and glycogenolysis
27
As type 2 diabetes progresses, in addition to insulin resistance, there is a ____ in insulin secretion
decrease
28
Describe the patterns of insulin secretion in type 2 diabetes?
secretory defect in response to glucose- no first phase peak, prolonged second phase secretion normal response to other stimuli ex arginine
29
Insulin resistance is usually present for years before ________ develops
hyperglycemia
30
Describe the presentation of type 2 diabetes
- less acute/ dramatic than type 1 - weight gain - less notable polyuria and polydipsia
31
Who should be screened regularly for diabetes?
people over 45 yrs old | people with BMI>25 and other risk factors
32
Who should be screened regularly for diabetes?
people over 45 yrs old | people with BMI>25 and other risk factors
33
About 65% of people with DM2 die from ______ disease
cardiovascular
34
What are risk factors for gestational diabetes?
obesity family history of Dm2 previous history of GDM age >40
35
What is the acute complication of type 1 diabetes?
DKA
36
DKA is caused by a profound lack of ____ and increased counter-regulatory hormones
insulin
37
What are the symptoms of DKA
``` dehydration and electrolyte imbalances due to osmotic diuresis hyperglycemia acidosis ketosis glycogen depletion abdominal pain, NV lethargy, fatigue acetone breath ```
38
Describe the "vicious cycle" seen in DKA
volume contraction causes a decreased | GFR--> causes less glucose excretion--> more hypertonicity, volume losses, and further declining GFR
39
What is the effect of DKA on potassium?
acidosis causes shift out of cell serum levels can look normal even with total body potassium depletion --> must include potassium in treatment of DKA
40
What measures are necessary to manage the low bicarbonate levels in DKA?
None, should resolve when acidosis is treated
41
What are Kussmaul respirations?
deep fast breathing, compensation for metabolic acidosis
42
What is the most lethal complication of DKA?
cerebral edema
43
How is hyeprosmolar nonketotic syndrome different from DKA?
seen in DM2 | no acidosis or ketosis
44
Why does ketosis not develop in HNKS?
type 2 diabetics have enough insulin to suppress ketone formation
45
Why does ketosis not develop in HNKS?
type 2 diabetics have enough insulin to suppress ketone formation no Kussmaul respirations, less pronounced GI symptoms
46
What drugs are associated with the onset of HNKS
diuretics, esp K depleting niacin new anti psychotics glucocorticoids
47
What are the two categories of symptoms caused by hypoglycemia?
1. adrenergic: weakness, sweating, tachycardia, palpitations, tremor, nervousness, irritability earlier signs 2. neuroglycopenic: hypothermia, confusion, seizure, coma. later signs- hypoglycemic unawareness.
48
What can predispose to hypoglycemia?
``` excess insulin exercise missed meal/ snack low A1c diabetic gastroparesis alcohol impaired renal clearance of insulin sulfonylureas ```
49
What can predispose to hypoglycemia?
``` excess insulin exercise missed meal/ snack low A1c diabetic gastroparesis alcohol impaired renal clearance of insulin sulfonylureas ```
50
Constrast the Somogyi effect vs the Dawn phenomenon
Somogyi: fasting hyperglycemia that occurs as a rebound response from an overnight low (triggering a counter-regulatory response). Treatment – decrease PM insulin dose Dawn: fasting hyperglycemia due to the normal peaking of counter-regulatory hormones in the AM (e.g. cortisol) Treatment – increase PM insulin dose
51
What are the chronic complications of DM?
microvascular and macrovascular problems
52
Describe the stages of diabetic retinopathy
 Stage 1: non-proliferative retinopathy, characterized by microaneurysms, hard exudates, and dot and blot hemorrhages.  Stage 2: pre-proliferative retinopathy characterized by cotton wool spots and intra-retinal microaneuryms (IRMA).  Stage 3: proliferative retinopathy, characterized by neovascularization, new vessels tend to be weak and can rupture
53
The changes of diabetic retinopathy do not affect vision until there is _____
bleeding
54
How can proliferative diabetic retinopathy be treated?
laser photcoagulation
55
How can proliferative diabetic retinopathy be treated?
laser photcoagulation
56
_______ results from leaking capillaries in the macula and is the leading cause of blindness in DM2
macular edema
57
________ is the leading cause of ESRD
diabetic nephropathy
58
Describe the histologic changes seen in diabetic nephropathy
Basement membrane thickening Increased glomerular leakage Loss of glomerular charge selectivity Reduced size selectivity of the glomerular barrier
59
Early in the course of diabetes, there is _______ in the kidneys
hyperfiltration
60
The first clinical evidence of diabetic nephropathy is _______
microalbuminuria
61
Development of gross proteinuria is thought to represent ________ damage to the kidneys
irreversible
62
After development of gross proteinuria, it is usually about ____ years to the development of ESRD
8 years
63
What are the classes of diabetic neuropathy?
- peripheral - autonomic: GI, GU, CV - acute onset mononeuropathies, radiculopathies
64
What is the presentation of cardiac autonomic neuropathy?
resting tachycardia | orthostatic hypotension with supine hypertension
65
What are the macrovascular complications of diabetes?
damage to the large blood vessels resulting in coronary artery, cerebrovascular, and peripheral vascular disease.
66
In type 1 DM, ______ is an important determinant of risk of macrovascular complications
duration of DM- highest risk after about 25 years
67
What are cause of hypoglycemia in non-diabetic patients?
- excess insulin, ex insulinoma - substance other than insulin stimulating insulin receptors, ex IGF-2 in some tumors - non-insulin receptor mediated cause, hypoglycemia in the setting of low insulin. ex impaired GNG or glycogenolysis

Endocrine (19 decks)

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