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Endo > SM_185-186b: Diabetes I and II > Flashcards

SM_185-186b: Diabetes I and II Flashcards

1
Q

Normal is fasting glucose of ____ and 2 hour plasma glucose of ____

A

Normal is fasting glucose of < 100 and 2 hour plasma glucose of < 140

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2
Q

Diabetes is fasting glucose of ____ and 2 hour plasma glucose of ____

A

Diabetes is fasting glucose of ≥ 126 and 2 hour plasma glucose of ≥ 200

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3
Q

Probability of fasting glucose and 2 hour plasma glucose begins to rise above levels of ____

A

Probability of fasting glucose and 2 hour plasma glucose begins to rise above levels of 116-185

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4
Q

Attachment of glucose to hemoglobin (glycation) is directly proportional to ___

A

Attachment of glucose to hemoglobin (glycation) is directly proportional to amount of glucose in the blood over time

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5
Q

Red blood cells circulate for 3-4 months so irreversible glycation of hemoglobin reflects ____ in the blood for the previous several months and indicates the degree of diabetes of control

(HbA1c correlates with self glucose monitoring)

A

Red blood cells circulate for 3-4 months so irreversible glycation of hemoglobin reflects the average levels of glucose in the blood for the previous several months and indicates the degree of diabetes of control

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6
Q

Type 1 diabetes is ____ usually leading to ____

A

Type 1 diabetes is beta-cell destruction usually leading to absolute insulin deficiency

(immune mediated or idiopathic)

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7
Q

Type 2 diabetes ranges from ___ to ___

A

Type 2 diabetes ranges from predominant insulin resistance with relative insulin deficiency to predominantly secretory defect with insulin resistance

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8
Q
A
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9
Q

Type 1 diabetes occurs due to ___

A

Type 1 diabetes occurs due to autoimmune destruction of beta cells in pancreatic islets

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10
Q

Describe immunologic history of Type 1 diabetes

A

Type 1 diabetes immunologic history

  1. Innate immune cells enter pancreatic islets (priming)
  2. Antigens in pancreatic lymph node trigger T cells
  3. T cells arrive from lymph nodes causing insulinitis
  4. Destructive insulinitis
  5. Disease onset w/o intervention
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11
Q

Type 1 diabetes is largely mediated by ___

A

Type 1 diabetes is largely mediated by T cells

(autoimmune destruction of pancreatic beta cells)

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12
Q

Patients with Type 1 diabetes are ___

A

Patients with Type 1 diabetes are insulinopenic

  • Depend on exogenous insulin for life
  • Ketosis prone under basal conditions
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13
Q

Type 1 diabetes has greatest incidence at age ____ and presents with ____, ____, and ____

A

Type 1 diabetes has greatest incidence at age 10-14 and presents with polyuria, weight loss, and fatigue

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14
Q

Type 1 diabetes is associated with ____ or ____ allele expression

A

Type 1 diabetes is associated with HLA DR3 or DR4 allele expression

  • HLA locus demonstrates strong association with T1DM consistent with autoimmune etiology
  • Variation in many genes
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15
Q

____, ____, and ____ are environmental risk factors for T1DM

A

Enteroviral infections, dietary factors, and beta cell stress secondary to insulin demand are environmental risk factors for T1DM

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16
Q

____ frequently present at diagnosis of Type 1 diabetes

A

Circulating islet cell antibodies frequently present at diagnosis of Type 1 diabetes

  • Marker of autoimmunity useful for predicting and diagnosing disease when presentation not classic for Type 1 diabetes
  • Presents years to months before onset of clinical type 1 diabetes
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17
Q

Islet specific antibodies that present with Type 1 diabetes are ____, ____, ____, ____, and ____

A

Islet specific antibodies that present with Type 1 diabetes are islet cell autoantibodies, glutamic acid decarboxylase autoantibodies, insulinoma associated 2 autoantibodies, insulin autoantibodies, and ZnT8 autoantibodies

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18
Q

Antibody ___ and age ___ lead to faster progression to T1DM

A

Antibody IA2A/GADA and age <12 lead to faster progression to T1DM

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19
Q

Stage 1 of T1DM involves ____, ____, and ____

A

Stage 1 of T1DM involves B cell autoimmunity, normoglycemia, and no symptoms

(secondary prevention)

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20
Q

Stage 2 of T1DM involves ____, ____, and ____

A

Stage 2 of T1DM involves B cell autoimmunity, dysglycemia, and no symptoms

(secondary prevention)

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21
Q

Stage 3 of T1DM involves ____, ____, and ____

A

Stage 3 of T1DM involves B cell autoimmunity, dysglycemia, and symptoms

(intervention)

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22
Q

Teplizumab acts by ____

A

Teplizumab acts by preventing effector T cells from acting on beta cells

(delays onset of diabetes)

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23
Q

Describe acute effect of lack of insulin

A

Acute effect of lack of insulin

  • Inhibits conversion of protein to amino acids
  • Promotes kidney excretion of glucose, water, and electrolytes
  • Prevents conversion of triglycerides to glycerol and FFA
  • Decreases pH
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24
Q

Describe pathogenesis of diabetic ketoacidosis

A

Pathogenesis of diabetic ketoacidosis

  • Insufficient insulin action -> hyperlipolysis -> ketoacidosis -> ketonuria
  • Ketoacidosis -> polyuria -> hyperosmolality -> dehydration
  • Ketoacidosis -> polyuria -> hypovolemia -> renal hypofunction
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25
Q

Describe therapeutic objectives for diabetic ketoacidosis

A

Therapeutic objectives for diabetic ketoacidosis

  • Immediate
    • Insulin therapy: catabolism -> anabolism
    • Fluid: replace losses
    • Electrolytes: Na, K, Cl
  • After recovery: continued anabolism, restore lost nitrogen and intracellular electrolytes
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26
Q

Describe fluid therapy for diabetic ketoacidosis

A

Fluid therapy for diabetic ketoacidosis

  • Loss of water > salt: replete vascular and extravascular volume first with isotonic fluid, then replete with hypotonic fluid
  • Acidosis: NaHCO3 therapy to correct
  • Blood glucose: use fluid with 5% glucose as glucose falls to 250-300 mg/dl
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27
Q

In diabetic ketoacidosis, there is a ___ K despite initial ___

A

In diabetic ketoacidosis, there is a deficiency of > 200 meq K despite initial hyperkalemia

  • Relief of acidosis and increased glucose utilization with insulin therapy will shift K from extracellular to intracellular space with resulting hypokalemia
  • Add K supplements to fluid when K enters normal range
  • Monitor EKG
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28
Q

Diabetic ketoacidosis ____ H+ levels so ____

A

Diabetic ketoacidosis increases H+ levels so K+ leaves the cell via the H+/K+ antiporter

(excreted in urine)

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29
Q

Insulin inhibits action of ____ so K+ ____

A

Insulin inhibits action of H+/K+ antiporter so K+ enters cell

30
Q
A
31
Q

Describe type 2 diabetes

A

Type 2 diabetes

  • Not absolutely dependent upon exogenous insulin
  • Not prone to ketoacidosis
  • Often obese
  • May be relatively free of classical symptoms
  • Strong FMHx of diabetes
  • Increasingly recognized in childhood due to childhood obesity
32
Q

Greater ____ score is associated with greater prevalence of Type 2 Diabetes

A

Greater polygenic risk score is associated with greater prevalence of Type 2 Diabetes

33
Q

Describe causes of hyperglycemia in type 2 diabetes

A

Causes of hyperglycemia in type 2 diabetes

  • Insulin resistance -> decreased glucose uptake by peripheral tissues
  • Pancreas: impaired insulin secretion
  • Liver: increased glucose production
34
Q

Insulin resistance is ____

A

Insulin resistance is decreased ability of insulin to lower circulating glucose concentrations

  • Impaired stimulation of glucose utilization by muscle and fat, impaired suppression of glucose production by the liver
  • Complex metabolic disorder: multiple factors contribute to insulin resistance
35
Q

Glucose disposal is ____ and hepatic glucose output is ____ in patients with type 2 diabetes

A

Glucose disposal is lower and hepatic glucose output is greater in patients with type 2 diabetes

(Hepatic glucose output greater in T2DM who are nonobese)

36
Q

Hepatic glucose output is ____ with fasting serum glucose levels

A

Hepatic glucose output is directly associated with fasting serum glucose levels

37
Q

Insulin resistance results from ___ and ___ factors

A

Insulin resistance results from inherited and acquired factors

  • Inherited: mutation in several genes (common), mutation in insulin receptor / glucose transporter / signaling proteins (rare)
  • Acquired: inactivity, overeating, aging, medications, hyperglycemia, and elevated FFAs
38
Q

Insulin sensitivity decreases with ____ BMI

A

Insulin sensitivity decreases with increasing BMI

39
Q

Most of diabetes risk is attributable to ____

A

Most of diabetes risk is attributable to excess weight

40
Q

Describe fat induced insulin resistance

A

Fat induced insulin resistance

  • Decreased lipid storage capacity in visceral adipose tissue -> portal circulation -> increased lipotoxicity and increased gluconeogenesis in lvier -> insulin resistance
  • Decreased lipid storage capacity in subcutaneous adipose tissue -> systemic circulation, increased lipotoxicity, decreased fat oxidation / insulin action / glucose uptake in skeletal muscle -> insulin resistance
41
Q
A
42
Q

There is ___ in insulin resistance

A

There is dysregulated glucose metabolism in insulin resistance

43
Q

Insulin resistance is associated with adipose tissue ____

A

Insulin resistance is associated with adipose tissue inflammation

44
Q

There is altered ____ receptor signaling in the setting of insulin resistance

A

There is altered insulin receptor signaling in the setting of insulin resistance

45
Q

Describe the pancreatic B cell response to insulin resistance

A

Pancreatic B cell response to insulin resistance

  • Normal B cells -> hyperinsulinemia (normal glucose)
  • Abnormal B cells -> hyperglycemia (relative insulin deficiency)
46
Q

Describe the feedback loop between pancreatic B-cells and insulin sensitive tissues

A

Feedback loop between pancreatic B-cells and insulin sensitive tissues

  • Insulin resistant with normal glucose tolerance -> impaired glucose tolerance -> type 2 diabetes
47
Q

Glucose trends ____ and insulin sensitivity and B cell function trend ____ before T2DM

A

Glucose trends up and insulin sensitivity and B cell function trend down before T2DM

48
Q

Insulin secretion ___ as insulin sensitivity increases

A

Insulin secretion decreases as insulin sensitivity increases

(failure of adequate B cell compensation with glucose intolerance and T2DM)

49
Q

Describe therapeutic approaches in Type 1 diabetes

A

Therapeutic approaches in Type 1 diabetes

  • Exogenous insulin mandatory
  • Conventional treatment: remain symptom free, minimal hypoglycemia, metabolic restoration incomplete
    • Tight control: frequent blood glucose monitoring, multiple doses subcutaneous injection or CSII, higher risk of hypoglycemia, near normal metabolic profiles
50
Q

Basal insulin secretion increases when ___

A

Basal insulin secretion increases when basal glucose increases

51
Q

Describe insulin preparations

A

Insulin preparations

  • Rapid-acting analog insulins: lispro, aspart, glulisine
  • Short-acting insulin: human regular insulin
  • Intermediate-acting human insulin: NPH
  • Long-acting analog insulin: detemir
  • Long-acting analog insulin: glargine
  • Long-acting analog insulins: U-300 glargine, degludec
52
Q

____ and ____ are common insulin regiments

A

Split-mixed (lispro/NPH) and glargine-lispro are common insulin regiments

53
Q

Describe options for insulin treatment and blood glucose monitoring

A

Insulin treatment and blood glucose monitoring

  • Treatment: insulin syringes, insulin pump, and insulin pen
  • Blood glucose monitoring: self monitoring, continuous glucose monitoring
54
Q

Describe lifestyle treatment of T2DM

A

Lifestyle treatment of T2DM

  • Nutrition therapy
  • Exercise (moderate intensity)
  • Reduce CV risk factors (smoking cessation)
  • Training in self-management and SMBG
55
Q

Describe therapeutic approaches in Type 2 diabetes

A

Type 2 diabetes therapeutic approaches

  • Decrease glucose absorption in intestine
  • Decrease hepatic glucose output
  • Increase renal glucose excretion
  • Increase insulin levels: stimulate insulin secretion
  • Enhance glucose uptake: increase insulin sensitivity
56
Q

Strategies to stimulate insulin secretion are ____ and ____

A

Strategies to stimulate insulin secretion are interacting with beta cell sulfonylurea receptor and enhance GLP-1 levels

  • Interact with B cell sulfonylurea receptor: sulfonylureas, meglitinides
  • Enhance GLP-1 levels: GLP-1 receptor agonists, DPP4 inhibitors
57
Q

Metformin ___ hepatic glucose output

A

Metformin decreases hepatic glucose output

58
Q

Thiazolidinediones activate ____ to enhance ____

A

Thiazolidinediones activate a nuclear receptor to enhance insulin sensitivity

59
Q

Alpha-glucosidase inhibitors inhibit ___

A

Alpha-glucosidase inhibitors inhibit glucose absorption

60
Q

SGLT2 is responsible for 90% of ____

A

SGLT2 is responsible for 90% of glucose reabsorbed in the renal tubules

61
Q

SGLT2 inhibitors act by ____ and ____

A

SGLT2 inhibitors act by shifting the glucose threshold for excretion to the left such that glucosuria occurs at physiologic glucose levels and appear to reduce the affinity of the transporter for glucose

(decreases A1c and decreases cardiovascular disease)

62
Q

Management of hyperglycemia in T2DM can be ___ or ___

A

Management of hyperglycemia in T2DM can be more or less stringent

63
Q

Vascular complications of diabetes are ____, ____, and ____

A

Vascular complications of diabetes are proliferative diabetic retinopathy, nephropathy, and neuropathy

64
Q

Diabetic neuropathy has ___

A

Diabetic neuropathy has a wide spectrum

65
Q

Intensive insulin treatment in Type 1 diabetes ____ risk of retinopathy, nephropathy, and neuropathy

A

Intensive insulin treatment in Type 1 diabetes decreases risk of retinopathy, nephropathy, and neuropathy

66
Q

As A1c increases, risk of microvascular complications ___

A

As A1c increases, risk of microvascular complications increases

67
Q

Intensive management ___ of microvascular complications

A

Intensive management reduces risk of microvascular complications

68
Q

Intracellular hyperglycemia occurs through the ____

A

Intracellular hyperglycemia occurs through the GLUT-1 transporter

69
Q

Microvascular complications result when ____

A

Microvascular complications result when increased oxidative stress from intracellular hypergluycemia leads to DNA strand breaks and activation of poly (ADP ribose) polymerase (PARP)

  • Increased flux through the polyol pathway
  • Increased advanced glycation end products (AGE formation)
  • Activation of protein kinase C isoforms
  • Increased flux through hexosamine
70
Q

Hyperglycemia causes tissue damage via ____ and ____

A

Hyperglycemia causes tissue damage via repeated acute changes in cellular metabolism and cumulative long-term changes in stable macromolecules

71
Q

Most people with diabetes die from ____

A

Most people with diabetes die from ischemic heart disease

72
Q

As weight decreases, waist circumference ____

A

As weight decreases, waist circumference decreases

  • Decreased HbA1c
  • Decreased SBP and DBP
  • Decreased TG
  • Increased HDL-c
  • No change in LDL-c

Endo (25 decks)

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