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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
Name three categories of drugs that have a risk of hypoglycemia
Name three categories of drugs that have a risk of hypoglycemia: 1. Insulin 2. Sulfonylureas 3. Meglitinides
26
Metformin and DDP-4 inhibitors are T2D drugs that are weight _
Metformin and DDP-4 inhibitors are T2D drugs that are **weight neutral**
27
_ and _ are two cardioprotective diabetes drugs
**GLP-1 RA** and **SGLT-2i** are two cardioprotective diabetes drugs
28
Which drugs increase insulin release from the pancreas?
* Sulfonylurea * Meglitinides * GLP-1 RA * DPP4 inhibitors
29
_ and _ are two T2D drugs that decrease insulin resistance
**Metformin (Biguanides)** and **TZDs** are two T2D drugs that decrease insulin resistance
30
SGLT-2 inhibitors work by _
SGLT-2 inhibitors work by **decreasing glucose reabsorption at the kidneys** (increasing glucose secretion in the urine)
31
Alpha glucosidase inhibitors work by _
Alpha glucosidase inhibitors work by **decreasing carbohydrate absorption**
32
Amylin analogues work by _
Amylin analogues work by **increasing satiety, decreasing glucagon secretion, decreasing gastric emptying**
33
Clinical symptoms of DKA might include:
Clinical symptoms of DKA might include: * Polyuria, dehydration * Dizziness, tachycardia * Abdominal pain, nausea, vomiting
34
Lab findings associated with DKA:
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
Elevated beta-hydroxybutyrate and acetoacetate may indicate (DKA/HHS)
Elevated beta-hydroxybutyrate and acetoacetate may indicate **DKA**
36
Stress can elevate insulin's counterregulatory hormones such as _
Stress can elevate insulin's counterregulatory hormones such as **cortisol, GH, glucagon, catecholamines**
37
Insulin is a _ type hormone and its counterregulatory hormones are _
Insulin is a **anabolic** type hormone and its counterregulatory hormones are **catabolic** * Cortisol, GH, glucagon, catecholamines want to increase hepatic gluconeogenesis and proteolysis
38
Explain the pathogenesis of DKA
Insulin is deficient --> hyperglycemia --> despite the hyperglycemia, the low insulin signals that we are in starvation mode --> ketone formation --> metabolic acidosis
39
Hyperglycemia isn't enough to trigger DKA; another inciting event is required that increases _ hormones
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
Patients with (HHS/DKA) will have high serum osmolarity (> 320 mOsm/L)
Patients with **HHS** will have high serum osmolarity (> 320 mOsm/L)
41
Patients with HHS tend to have (higher/lower) glucose levels than in DKA and (higher/lower) potassium
Patients with HHS tend to have **higher** glucose levels than in DKA and **lower** potassium
42
(DKA/HHS) is associated with more severe kidney injury
**HHS** is associated with more severe kidney injury (*due to the amount of dehydration)*
43
The most common population for HHS is _
The most common population for HHS is **older, Type II**
44
The most common population for DKA is _
The most common population for DKA is **younger, Type I**
45
Pathogenesis of HHS
46
Dehydraton in HHS and DKA should be addressed with _
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
Hyperglycemia in DKA and HHS should be addressed with _
Hyperglycemia in DKA and HHS should be addressed with **IV insulin** * In DKA this also decreases ketone production
48
Insulin needs to be continued in DKA/HHS treatment even when the glucose level falls to target level; we will just need to supplement _
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
During DKA treatment, when the glucose falls below _ , dextrose should be added to the fluids to prevent hypoglycemia
During **DKA treatment**, when the glucose falls **below 200** , dextrose should be added to the fluids to prevent hypoglycemia
50
During HHS treatment, when the glucose falls below _ , dextrose should be added to the fluids to prevent hypoglycemia
During **HHS treatment**, when the glucose falls **below 300**, dextrose should be added to the fluids to prevent hypoglycemia
51
Patients with DKA and HHS have _ total body potassium and sodium
Patients with DKA and HHS have **low** total body potassium and sodium
52
Isotonic saline is most often used in DKA and HHS treatment; _ electrolyte may need to be added even if levels are higher than normal
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
Insulin has _ effect on potassium
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
Hyperkalemia may present with _ on EKG
Hyperkalemia may present with **peaked T waves** on EKG * Also PR prolongation, QRS prolongation
55
Hypokalemia may present with _ on EKG
Hypokalemia may present with **U waves** on EKG
56
Cross linking of _ to _ occurs via the nonenzymatic glycation of proteins, nucleotides, and lipids
Cross linking of **collagen** to **plasma** occurs via the nonenzymatic glycation of proteins, nucleotides, and lipids --> produces advanced glycation end products
57
Nonenzymatic glycation has _ effect on vasculature
Nonenzymatic glycation **increases vascular permeability and stiffness** * Also increases inflammation and tissue ischemia
58
Protein glycation increases the risk of _ microvascular events
Protein glycation increases the risk of **nephropathy, retinopathy, and peripheral nervous system damage**
59
Elevated sorbitol concentrations have _ effect
Elevated sorbital concentrations cause **oxidative and osmotic damage to tissue**
60
Certain tissues like _ , _ and _ are vulnerable to sorbital damage due to their lack of _
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
Advanced glycation end products cause _ effects
Advanced glycation end products cause **receptor mediated cytokine** effects
62
Macrovascular disease associated wtih diabetes include _
Macrovascular disease associated wtih diabetes include **CAD, peripheral vascular disease, stroke**
63
Microvascular disease associated wtih diabetes include
Microvascular disease associated wtih diabetes include **nephropathy, peripheral neuropathy, and retinopathy**
64
How can we prevent diabetics' risk of CAD
* Low dose aspirin * Statins * Target BP < 130/80 * ACEi and ARBs for nephropathy
65
Poorly controlled diabetes and high glucose levels can cause blood vessels around the eye to swell and leak, causing _
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
_ 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
**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
The pancreas comes from the _ embryologic structure
The pancreas comes from the **foregut endoderm**
68
The pancreatic tail and duct arise from the _ embryologic structure
The pancreatic tail and duct arise from the **ventral bud** (to the right of the duodenum)
69
The pancreatic body, tail, and duct arise from the _ embryologic structure
The pancreatic body, tail, and duct arise from the **dorsal bud** (left of the duodenum)
70
The head of the pancreas is in close proximity to the duodenum; it is the most common site for _
The head of the pancreas is in close proximity to the duodenum; it is the most common site for **pancreatic cancer (pancreatic adenoma)**
71
Insulin has _ effect on glycolysis
Insulin **increases glycolysis** * Also increases intracellular glucose and glycogenesis
72
Somatostatin has _ effect on GI, pancreatic, and pituitary secretions
Somatostatin has an **inhibitory** effect on GI, pancreatic, and pituitary secretions
73
Effects of insulin on: Glycogenesis Lipogenesis Gluconeogenesis
Effects of insulin on: Glycogenesis- **increased** Lipogenesis- **increased** Gluconeogenesis- **decreased**
74
Type I Diabetes is most commonly associated with _ antibodies
Type I Diabetes is most commonly associated with **antiglutamic acid decarboxylase** antibodies
75
T1D is associated with _ complications
T1D is associated with **DKA, retinopathy, cataracts, and neuropathy**
76
T1D diagnostics: _ insulin _ C-peptide _ HbA1C
T1D diagnostics: **Low** insulin **Low** C-peptide HbA1C **> 6.5%**
77
Advanced glycation end products (AGE) from non-enzymatic glycation end up trapping proteins in the ECM causing _
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
(Diabetic retinopathy/ glaucoma) is associated with an increased intraocular pressure
**Glaucoma** is associated with an increased intraocular pressure
79
Describe the pathogenesis of diabetic nephropathy
non-enzymatic glycation --> thickening of the GBM --> glomerular sclerosis --> afferent and efferent arteriolar hyalinosis --> albuminuria, low GFR, high creatinine
80
Large vessel disease like CAD in diabetics is due to atherosclerosis from the increase in _
Large vessel disease like CAD in diabetics is due to atherosclerosis from the increase in **triglycerides**
81
The pathogenesis of diabetic neuropathy involves (glycation/ sorbitol)
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
Ketones are made in the _
Ketones are made in the **liver**

Endocrine (8 decks)

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