Pancreas Flashcards

1
Q

The primary issue in T2D is _

A

The primary issue in T2D is insulin resistance

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2
Q

As T2D progresses, we move from a problem of just insulin resistance to more of an _

A

As T2D progresses, we move from a problem of just insulin resistance to more of an insulin deficiency

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3
Q

What is the general trend in C-peptide as T2D progresses?

A

C-peptide may decrease as we progress to more of an insulin deficiency

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4
Q

The primary issue related to T1D is _

A

The primary issue related to T1D is insulin deficiency

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5
Q

(T1D/T2D) has a stronger genetic link

A

T2D has a stronger genetic link

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6
Q

The mechanism for insulin deficiency in T1D is _

A

The mechanism for insulin deficiency in T1D is autoimmune islet cell destruction

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7
Q

Name the key antibodies in T1D

A

Key antibodies in T1D:
* Anti-glutamic acid decarboxylase (GAD)
* Zinc transporer
* Islet cell antibodies

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8
Q

Insulin and C-peptide will be _ in T2D

A

Insulin and C-peptide will be high/ normal in T2D (later can both be low as T2D progresses)

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9
Q

Insulin and C-peptide will be _ in T1D

A

Insulin and C-peptide will be low in T1D

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10
Q

_ is a characteristic skin finding that indicates insulin resistance in patients with T2D

A

Acanthosis nigricans is a characteristic skin finding that indicates insulin resistance in patients with T2D

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11
Q

First line therapy for patients with T1D is _

A

First line therapy for patients with T1D is insulin replacement
* Amylin can be added as conjunct therapy

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12
Q

T1D is associated with HLA _ and _

A

T1D is associated with HLA-DR3 and HLA-DR4

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13
Q

(T1D/T2D) has more severe glucose intolerance

A

T1D has more severe glucose intolerance

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14
Q

4 ways to diagnose diabetes mellitus

A

4 ways to diagnose diabetes mellitus:
1. Hemoglobin A1C > 6.5%
2. Fasting glucose > 126
3. Symptomatic individual with a glucose > 200
4. Oral glucose tolerance test with glucose > 200

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15
Q

A1C represents_

A

A1C represents glycated hemoglobin
* Represents what the blood sugar has been over past 2-3 months

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16
Q

List the onset, peak, and duration of lispro

A
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17
Q

List the onset, peak, and duration of regular human insulin

A
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18
Q

List the onset, peak, and duration of NPH

A
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19
Q

List the onset, peak, and duration of glargine

A
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20
Q

Three rapid acting insulin options for meal time include _ , _ , _

A

Three rapid acting insulin options for meal time include lispro , aspart , glulisine

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21
Q

Two long acting options for basal insulin coverage are _ and _

A

Two long acting options for basal insulin coverage are detemir and glargine
* These can last for up to 24 hours

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22
Q

_ is another insulin option for basal control that needs to be dosed every 12 hours (intermediate acting)

A

NPH is another insulin option for basal control that needs to be dosed every 12 hours (intermediate acting)

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23
Q

_ and _ are two T2D drugs that can cause weight loss

A

GLP-1 RA and SGLT-2 inhibitors are two T2D drugs that can cause weight loss

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24
Q

4 drugs that can cause weight gain in T2D are:

A

4 drugs that can cause weight gain in T2D are:
* Insulin
* Sulfonylureas
* Meglitinides
* TZDs

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25
Q

Name three categories of drugs that have a risk of hypoglycemia

A

Name three categories of drugs that have a risk of hypoglycemia:
1. Insulin
2. Sulfonylureas
3. Meglitinides

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26
Q

Metformin and DDP-4 inhibitors are T2D drugs that are weight _

A

Metformin and DDP-4 inhibitors are T2D drugs that are weight neutral

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27
Q

_ and _ are two cardioprotective diabetes drugs

A

GLP-1 RA and SGLT-2i are two cardioprotective diabetes drugs

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28
Q

Which drugs increase insulin release from the pancreas?

A
  • Sulfonylurea
  • Meglitinides
  • GLP-1 RA
  • DPP4 inhibitors
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29
Q

_ and _ are two T2D drugs that decrease insulin resistance

A

Metformin (Biguanides) and TZDs are two T2D drugs that decrease insulin resistance

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30
Q

SGLT-2 inhibitors work by _

A

SGLT-2 inhibitors work by decreasing glucose reabsorption at the kidneys (increasing glucose secretion in the urine)

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31
Q

Alpha glucosidase inhibitors work by _

A

Alpha glucosidase inhibitors work by decreasing carbohydrate absorption

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32
Q

Amylin analogues work by _

A

Amylin analogues work by increasing satiety, decreasing glucagon secretion, decreasing gastric emptying

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33
Q

Clinical symptoms of DKA might include:

A

Clinical symptoms of DKA might include:
* Polyuria, dehydration
* Dizziness, tachycardia
* Abdominal pain, nausea, vomiting

34
Q

Lab findings associated with DKA:

A

Lab findings associated with DKA:
* Hyperglycemia
* Elevated anion gap metabolic acidosis
* Hyperkalemia
* Low total body K+
* Hyponatremia
* Elevated ketones
* Low phosphorus and magnesium
* High Cr and BUN (dehydration)

35
Q

Elevated beta-hydroxybutyrate and acetoacetate may indicate (DKA/HHS)

A

Elevated beta-hydroxybutyrate and acetoacetate may indicate DKA

36
Q

Stress can elevate insulin’s counterregulatory hormones such as _

A

Stress can elevate insulin’s counterregulatory hormones such as cortisol, GH, glucagon, catecholamines

37
Q

Insulin is a _ type hormone and its counterregulatory hormones are _

A

Insulin is a anabolic type hormone and its counterregulatory hormones are catabolic
* Cortisol, GH, glucagon, catecholamines want to increase hepatic gluconeogenesis and proteolysis

38
Q

Explain the pathogenesis of DKA

A

Insulin is deficient –> hyperglycemia –> despite the hyperglycemia, the low insulin signals that we are in starvation mode –> ketone formation –> metabolic acidosis

39
Q

Hyperglycemia isn’t enough to trigger DKA; another inciting event is required that increases _ hormones

A

Hyperglycemia isn’t enough to trigger DKA; another inciting event is required that increases catabolic hormones and additional hyperglycemia
* Infection
* Infarction
* Insulinopenia (missing insulin doses)
* Iatrogenic (glucocorticoids)
* Pregnancy

40
Q

Patients with (HHS/DKA) will have high serum osmolarity (> 320 mOsm/L)

A

Patients with HHS will have high serum osmolarity (> 320 mOsm/L)

41
Q

Patients with HHS tend to have (higher/lower) glucose levels than in DKA and (higher/lower) potassium

A

Patients with HHS tend to have higher glucose levels than in DKA and lower potassium

42
Q

(DKA/HHS) is associated with more severe kidney injury

A

HHS is associated with more severe kidney injury (due to the amount of dehydration)

43
Q

The most common population for HHS is _

A

The most common population for HHS is older, Type II

44
Q

The most common population for DKA is _

A

The most common population for DKA is younger, Type I

45
Q

Pathogenesis of HHS

A
46
Q

Dehydraton in HHS and DKA should be addressed with _

A

Dehydraton in HHS and DKA should be addressed with aggressive IV fluids with isotonic saline
* Patients with DKA are often 5-10 L down
* Patients with HHS are often > 10 L down
* Don’t replace more than 4L over the first 4 hrs (electrolyte shifts)

47
Q

Hyperglycemia in DKA and HHS should be addressed with _

A

Hyperglycemia in DKA and HHS should be addressed with IV insulin
* In DKA this also decreases ketone production

48
Q

Insulin needs to be continued in DKA/HHS treatment even when the glucose level falls to target level; we will just need to supplement _

A

Insulin needs to be continued in DKA/HHS treatment even when the glucose level falls to target level; we will just need to supplement dextrose

49
Q

During DKA treatment, when the glucose falls below _ , dextrose should be added to the fluids to prevent hypoglycemia

A

During DKA treatment, when the glucose falls below 200 , dextrose should be added to the fluids to prevent hypoglycemia

50
Q

During HHS treatment, when the glucose falls below _ , dextrose should be added to the fluids to prevent hypoglycemia

A

During HHS treatment, when the glucose falls below 300, dextrose should be added to the fluids to prevent hypoglycemia

51
Q

Patients with DKA and HHS have _ total body potassium and sodium

A

Patients with DKA and HHS have low total body potassium and sodium

52
Q

Isotonic saline is most often used in DKA and HHS treatment; _ electrolyte may need to be added even if levels are higher than normal

A

Isotonic saline is most often used in DKA and HHS treatment; potassium (if < 5.3) may need to be added even if levels are higher than normal (5-5.2)

53
Q

Insulin has _ effect on potassium

A

Insulin shifts potassium into cells
* Admistration of insulin during DKA/ HHS can cause severe drops in K+ which is why we replete K+ if < 5.3

54
Q

Hyperkalemia may present with _ on EKG

A

Hyperkalemia may present with peaked T waves on EKG
* Also PR prolongation, QRS prolongation

55
Q

Hypokalemia may present with _ on EKG

A

Hypokalemia may present with U waves on EKG

56
Q

Cross linking of _ to _ occurs via the nonenzymatic glycation of proteins, nucleotides, and lipids

A

Cross linking of collagen to plasma occurs via the nonenzymatic glycation of proteins, nucleotides, and lipids –> produces advanced glycation end products

57
Q

Nonenzymatic glycation has _ effect on vasculature

A

Nonenzymatic glycation increases vascular permeability and stiffness
* Also increases inflammation and tissue ischemia

58
Q

Protein glycation increases the risk of _ microvascular events

A

Protein glycation increases the risk of nephropathy, retinopathy, and peripheral nervous system damage

59
Q

Elevated sorbitol concentrations have _ effect

A

Elevated sorbital concentrations cause oxidative and osmotic damage to tissue

60
Q

Certain tissues like _ , _ and _ are vulnerable to sorbital damage due to their lack of _

A

Certain tissues like lens , retina and peripheral nerves are vulnerable to sorbital damage due to their lack of sorbitol dehydrogenase
* High glucose –> lots of sorbitol
* Without sorbitol dehydrogenase we cannot convert sorbitol –> fructose

61
Q

Advanced glycation end products cause _ effects

A

Advanced glycation end products cause receptor mediated cytokine effects

62
Q

Macrovascular disease associated wtih diabetes include _

A

Macrovascular disease associated wtih diabetes include CAD, peripheral vascular disease, stroke

63
Q

Microvascular disease associated wtih diabetes include

A

Microvascular disease associated wtih diabetes include nephropathy, peripheral neuropathy, and retinopathy

64
Q

How can we prevent diabetics’ risk of CAD

A
  • Low dose aspirin
  • Statins
  • Target BP < 130/80
  • ACEi and ARBs for nephropathy
65
Q

Poorly controlled diabetes and high glucose levels can cause blood vessels around the eye to swell and leak, causing _

A

Poorly controlled diabetes and high glucose levels can cause blood vessels around the eye to swell and leak, causing macular edema
* This leads to ischemia and floaters from tiny blood clots

66
Q

_ is a condition that can happen in diabetes in which new vessels form in the eye due to ischemia; the new vessels are fragile and bleed easily

A

Neovascularization is a condition that can happen in diabetes in which new vessels form in the eye due to ischemia; the new vessels are fragile and bleed easily

67
Q

The pancreas comes from the _ embryologic structure

A

The pancreas comes from the foregut endoderm

68
Q

The pancreatic tail and duct arise from the _ embryologic structure

A

The pancreatic tail and duct arise from the ventral bud (to the right of the duodenum)

69
Q

The pancreatic body, tail, and duct arise from the _ embryologic structure

A

The pancreatic body, tail, and duct arise from the dorsal bud (left of the duodenum)

70
Q

The head of the pancreas is in close proximity to the duodenum; it is the most common site for _

A

The head of the pancreas is in close proximity to the duodenum; it is the most common site for pancreatic cancer (pancreatic adenoma)

71
Q

Insulin has _ effect on glycolysis

A

Insulin increases glycolysis
* Also increases intracellular glucose and glycogenesis

72
Q

Somatostatin has _ effect on GI, pancreatic, and pituitary secretions

A

Somatostatin has an inhibitory effect on GI, pancreatic, and pituitary secretions

73
Q

Effects of insulin on:
Glycogenesis
Lipogenesis
Gluconeogenesis

A

Effects of insulin on:
Glycogenesis- increased
Lipogenesis- increased
Gluconeogenesis- decreased

74
Q

Type I Diabetes is most commonly associated with _ antibodies

A

Type I Diabetes is most commonly associated with antiglutamic acid decarboxylase antibodies

75
Q

T1D is associated with _ complications

A

T1D is associated with DKA, retinopathy, cataracts, and neuropathy

76
Q

T1D diagnostics:
_ insulin
_ C-peptide
_ HbA1C

A

T1D diagnostics:
Low insulin
Low C-peptide
HbA1C > 6.5%

77
Q

Advanced glycation end products (AGE) from non-enzymatic glycation end up trapping proteins in the ECM causing _

A

Advanced glycation end products (AGE) from non-enzymatic glycation end up trapping proteins in the ECM causing diffuse thickening of the basement membrane
* Results in coronary, cerebral, peripheral circulation arterial narrowing
* Also capillary closure in the retina and glomerulus

78
Q

(Diabetic retinopathy/ glaucoma) is associated with an increased intraocular pressure

A

Glaucoma is associated with an increased intraocular pressure

79
Q

Describe the pathogenesis of diabetic nephropathy

A

non-enzymatic glycation –> thickening of the GBM –> glomerular sclerosis –> afferent and efferent arteriolar hyalinosis –> albuminuria, low GFR, high creatinine

80
Q

Large vessel disease like CAD in diabetics is due to atherosclerosis from the increase in _

A

Large vessel disease like CAD in diabetics is due to atherosclerosis from the increase in triglycerides

81
Q

The pathogenesis of diabetic neuropathy involves (glycation/ sorbitol)

A

The pathogenesis of diabetic neuropathy involves sorbitol
1. Increased sorbitol
2. Osmosis
3. Cell-swelling/lysis and oxidative damage
4. Demyelination of peripheral nerves

82
Q

Ketones are made in the _

A

Ketones are made in the liver