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Endocrine > Section 6 - Pancreas > Flashcards

Section 6 - Pancreas Flashcards

1
Q

Location of pancreas?

A

Near stomach and small intestine

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2
Q

head of the pancreas

A

touches the duodenum

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3
Q

uncinate process

A

wraps around superior mesenteric artery and vein

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4
Q

neck of the pancreas

A

in front of the superior mesenteric artery and vein

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5
Q

body of the pancreas

A

before the tail

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6
Q

tail of pancreas

A

tip

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7
Q

main pancreatic duct

A

joins common bile duct to drain in the duodenum via the major duodenal papilla

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8
Q

accessory pancreatic duct

A

duct that can be functional or non-functional. varies from person to person

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9
Q

pancreatic acinar cells (exocrine pancreas)

A

secretes juice. consists of a majority of the cells.

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10
Q

pancreatic islets of islets of Langerhans (endocrine pancreas)

A

secretes into alpha, beta, and delta cells

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11
Q

alpha cells

A

consist of 20% of cells

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12
Q

beta cells

A

consists of 65% of cells

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13
Q

what is the chemistry of insulin?

A

it’s a peptide hormone. A and B chains are linked together with 2 disulfide bridges

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14
Q

what stimulates insulin?

A

increases in blood glucose concentration
increased amino acid concentration
increased fatty acid concentration
parasympathetic NS

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15
Q

what inhibits insulin?

A

decreased blood glucose
fasting
exercise

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16
Q

when and where and how is insulin synthesized?

A

synthesized in beta cells of the pancreas

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17
Q

what are the physiological effects of insulin?

A
  • promote glucose storage as glycogen in liver
  • promote uptake of glucose and storage as glycogen and amino acids and storage as protein
  • promote uptake of glucose and storage as fat in adipose tissue; and uptake in most cells in general
  • causes increase in uptake of ion especially potassium and phosphate
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18
Q

what is the chemistry of the glucagon hormone?

A

it is a peptide hormone

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19
Q

what stimulates glucagon?

A
  • decrease in blood glucose concentration

- fasting

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20
Q

when, where and how is glucagon synthesized?

A

synthesized in alpha cells of pancreas

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21
Q

physiological effects of glucagon?

A
  • mobilize nutrients by breaking down glycogen and fat
  • stimulates glycogen breakdown in liver
  • stimulates formation of glucose from amino acids in liver
  • stimulates glycogen breakdown in skeletal muscles
  • stimulates lipolysis
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22
Q

what inhibits glycogen?

A

insulin

somatostatin

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23
Q

pathophysiology of pre-diabetes

A

high glucose levels

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24
Q

etiology of pre-diabetes

A

lifestyle and diet

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25
Q

clinical manifestations of pre-diabetes

A

nothing yet since this stage is irreversible. However there is an increased risk of type-2 diabetes, heart disease, and strokes

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26
Q

treatment of pre-diabetes

A

lifestyle changes and diet

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27
Q

pathophysiology of type 1 diabetes mellitus

A

high glucose levels in blood

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28
Q

etiology of type 1 diabetes mellitus

A

immune mediated - cellular-mediated autoimmune destruction of beta cells. Antibodies can be for islet cells, insulin, decarboxylase

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29
Q

clinical manifestations of type 1 diabetes mellitus

A
  • diabetic ketoacidosis
  • diabetic retinopathy (non-proliferative, proliferative)
  • diabetic nephropathy
  • diabetic neuropathy (peripheral diabetic neuropathy, autonomic neruopathy)
  • coronary heart disease/cerebrovascular disease/peripheral vascular disease
  • infections
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30
Q

treatment of type 1 diabetes mellitus

A

lifestyle modifications with regular checkups and insulin

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31
Q

type 2 diabetes mellitus pathophysiology?

A

high levels of glucose in blood

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32
Q

etiology of type 2 diabetes mellitus?

A

cells have insulin resistance and cannot take up glucose from blood

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33
Q

clinical manifestations of type 2 diabetes mellitus?

A
  • hyperosmolar hyperglycemic state
  • diabetic retinopathy (non-proliferative, proliferative)
  • diabetic nephropathy
  • diabetic neuropathy (peripheral diabetic neuropathy, autonomic neuropathy)
  • coronary heart disease/cerebrovascular disease/peripheral vascular disease
  • infections
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34
Q

treatment of type 2 diabetes mellitus

A

lifestyle changes with regular check-ups. oral medications and insulin

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35
Q

diabetic retinopathy

A

glaucoma, cataracts, and other disorders of the eye

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36
Q

non-proliferative (diabetic retinopathy)

A

cotton wool spots, microaneurysms, venous dilation, exudates, and small hemorrhages

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37
Q

proliferative (diabetic retinopathy)

A

same as non-proliferative with neurovascularization. new blood vessels are fragile and easily break open -> vision becomes more clouded as the amount of the bleeding increases

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38
Q

diabetic nephropathy

A

progressive damage to glomerular basement membranes of the kidneys -> lose ability to filter. measure microalbuminauria - clinical evidence of nephropathy

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39
Q

diabetic neuropathy

A

nerve cells are vulnerable to damage from chronic hyperglycemia

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40
Q

peripheral diabetic neuropathy

A

results in sharp, stabbing, or burning pain in toes, feet, legs, and hands. discomfort when skin is touched and a heaviness/clumsiness in their feet and legs.

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41
Q

Charcot’s joints

A

nerve damage that impairs the patient’s ability to perceive pain from a joint

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42
Q

autonomic diabetic neuropathy leads to

A
  • erectile dysfunction
  • chronic diarrhea/constipation
  • orthostatic hypotension (low bp when you stand up, sit down, etc)
  • neurogenic bladder
43
Q

coronary heart defect/cerebrovascular disease/peripheral vascular disease

A
  • CHD accounts for majority of diabetic deaths
  • strokes are 3x higher mortality rate
  • PVD in lower extremities can lead to gangrene
44
Q

-hyperglycemic crisis

A

Diabetic ketoacidosis (DKA

45
Q

-happens more in type 1 diabetes

A

Diabetic ketoacidosis (DKA)

46
Q

-happens in a 24 hour period

A

Diabetic ketoacidosis (DKA)

47
Q

-not enough insulin so fat gets metabolized into fatty acids and made into ketones

A

Diabetic ketoacidosis (DKA)

48
Q

-leads to osmotic diuresis -> reduction of intravascular volume -> diminished renal blood flow -> decreased gluocose excretion -> exacerabation of hyperglycemia & hyperosmolality -> polydipsia

A

Diabetic ketoacidosis (DKA)

49
Q

-can cause neuronal hydration which will lead to severe mental status changes and potential coma

A

Diabetic ketoacidosis (DKA)

50
Q

-acidosis can lead to diminished cardiac output and vascular tone which leads to potential development of shock

A

Diabetic ketoacidosis (DKA)

51
Q

-hyperglycemic crisis

A

Hyperosmolar hyperglycemic state (HHS or non-ketotic hyperglycemia)

52
Q

-happens more in type 2 diabetes

A

Hyperosmolar hyperglycemic state (HHS or non-ketotic hyperglycemia)

53
Q

-develops over several days

A

Hyperosmolar hyperglycemic state (HHS or non-ketotic hyperglycemia)

54
Q

-leads to glycosuria and osmotic diuresis. there is no ketone production because of presence of insulin in blood

A

Hyperosmolar hyperglycemic state (HHS or non-ketotic hyperglycemia)

55
Q

-neurologic abnormalities/mental state changes are more likely in HHS because it is easier to reach severe hyperosmolality

A

Hyperosmolar hyperglycemic state (HHS or non-ketotic hyperglycemia)

56
Q

Dental aspects of diabetes

A
  • increase in periodontal disease
  • xerostomia
  • thrush
  • burning mouth syndrome
  • impaired/delayed wound healing
  • length of time of DM goes uncontrolled impacts periodontal disease
57
Q

rapid-acting insulin

A

use if need insulin immediately

58
Q

short-acting insulin

A

use after eating a large meal

59
Q

intermediate-acting insulin

A

use for a long period such as all day or all evening

60
Q

long-acting insulin

A

used for all day or all evening

61
Q

pre-mixed insulin combinations

A

mixture of different types of insulin so it lasts throughout the dsay

62
Q

what can insulin therapy cause if there is a meal that is skipped?

A

hypoglycemia

63
Q

mechanism of action of insulin?

A

decrease glucose levels

64
Q

explain how insulin pumps, continuous glucose monitoring and ketone monitoring work in the care of the diabetic patient

A

insulin pumps help apply insulin without having to much to worry about giving shots. refillable and more or less easy, and can last several days before refill.

Use A1c to monitor glucose over the previous couple of months, usually up to 3 months. use fasting glucose test which measures amount of glucose after 8 hours of fasting - this can be used to test results right away.

combination of both can indicate if patient has been properly managing diabetes

65
Q

medication used to treat type 2 diabetes mellitus?

A

insulin secretagogues (sulfonylureas, meglitinides)

66
Q

how much does sulfonylureas reduce A1c by?

A

1-1.5%

67
Q

method of action of sulfonylureas?

A

inhibit ATP-sensitive K+ channels, increasing secretion of pancreatic insulin

68
Q

major adverse and toxic effects of sulfonylureas?

A 
hypoglycemia
weight gain
skin rash
nausea
vomiting
cholestasis
leukopenia
thrombocytopenia
69
Q

what are the different types of sulfonylureas (3)

A

glimepiride
glipizide
glyburide

70
Q

insulin sensitizers?

A

biguides, thiazolidinediones or glitazones

71
Q

biguanides reduce A1C by how much?

A

1.0-1.5%

72
Q

method of action of biguanides?

A

increases number or affinity of insulin receptors at target tissues which promotes glucose uptake. it decreases intestinal absorption of glucose.

DOES NOT CAUSE hypogyclemia or weight gain.

73
Q

major adverse and toxic effects of biguanides?

A

GI-related (metallic taste, nausea, diarrhea, abdominal pain)

74
Q

special consideration of biguanides?

A

NOT RECOMMENDED for patients with renal or liver impairment

75
Q

what is an example of a specific biguanide?

A

metformin

76
Q

thiazolidinediones/glitazones reduce A1C by how much?

A

1.0-1.5%

77
Q

method of action of thiazolidinediones/glitazones?

A

agonists at peroxisome proliferator - activated receptor g which regulates expression of genes coding for GLUT 4 in cell membranes of skeletal muscle, liver and adipose. Makes insulin sensitivity of these tissues and more glucose leaves the blood.

78
Q

major adverse and toxic effects of thiazolidinediones/glitazones

A

weight gain
peripheral edema
increased risk of heart failure

79
Q

different types of thiazolidinediones? (2)

A

rosiglitazone

pioglitazone

80
Q

rosiglitazone

A

full agonist. use it as a LAST resort. increased risk of MI

81
Q

pioglitazone

A

partial agonist. slight increased risk of bladder cancer with higher doses and long-term use.

82
Q

alpha-glucosidase inhibitors reduce A1C by?

A

0.5-1%

83
Q

method of action of alpha-glucosidase inhibitors?

A

inhibits “relatively minor” brush border enzyme a-glucosidase, delaying digestion of carbohydrates so it passes out into feces

84
Q

major adverse and toxic effects of alpha-glucosidase?

A

can cause GI-related problems (abdominal pain, flatulence, diarrhea)

85
Q

different types of a-glucosidase inhibitors?

A

acarbose

miglitol

86
Q

SGLT-2 inhibitors reduce A1C by?

A

0.5-1.0%

87
Q

method of action of SGLT-2?

A

in proximal convoluted tubules of nephrons, inhibiting glucose reabsorption and stimulating glucose secretion.

88
Q

major toxic and adverse effects of SGLT-2?

A

volume depletion

increased risk of UTI’s

89
Q

different types of SGLT-2 ihibitors? (3)

A

canagliflozin
dapaglifozin (increased risk of bladder cancer)
empaglifilozin

90
Q

incretin mimetics/enhancers (GLP-1 mimetics, DPP-4 inhibitors) reduce A1C by?

A

1.0-1.5%

91
Q

method of action of incretin mimetics/enhancers (GLP-1 mimetics, DPP-4 inhibitors)?

A

based on incretins (peptide hormone). GLP-1 is the most important which stimulates insulin release, increase uptake of glucose by skeletal muscle & adipose tissue; slow gastric emptying; increase sateity, and decreased food intake.

92
Q

major adverse and toxic effects of incretin mimetics/enhancers (GLP-1 mimetics, DPP-4 inhibitors)?

A 
nauesa
vomiting
renal insufficiency
pancreatitis
interfere with absorption of other drugs
93
Q

examples of GLP-1 mimetics

A

byetta, bydureon, liraglutide, albiglutide

94
Q

DPP-4 inhibitors - reduces A1C by?

What does it do?

A

0.5-1.0%

prevents the breakdown of GLP-1 from DPP-4

95
Q

major adverse and toxic effects of DPP-4?

A

acute pancreatitis

hypersensitivity reactions

96
Q

DPP-4 inhibitors

A

alogliptin
linagliptin
saxagliptin
sitagliptin

97
Q

fixed combination medications

A

combination of medications to help reduce % of glucose in blood

98
Q

common overall management approaches of the diabetic patient

A

combination of change in lifestyle; frequent check-ups; insulin medication; and oral medication that helps reduce overall glucose levels.

99
Q

dental aspect of handling a diabetic patient

A
  • schedule early morning dental appointments since blood sugar is stable in the morning
  • reduce stress whenever possible
  • knowing blood sugar levels prior to and during stressful or invasive procedures
  • need to keep in mind of a acute raises/drops in blood sugar levels during appointment.
100
Q

what is symptoms of hypoglycemia

A

shakiness, sweating, fast or irregular heartbeat, dizziness or lightheadedness, hunger, nervousness

101
Q

what causes hypoglycemia?

A

due to taking too much insulin, disruption in food intake; unexpected or unplanned increase in physical activity

102
Q

hyperglycemia/hyperglycemic crisis

A

most common events are medical or catabolic stress. discontinuation of inadequate insulation therapy can affect this. low insulin levels, higher consuption of food + less exercise, stress can cause this. High levels of sugar in urine, frequent urination, increased thirst, fatigue, and blurred vision are symptoms

103
Q

Signs of depletion are common in both DKA and HHS, including

A

decreased skin turgor, dry axillae and oral mucosa, low jugular venous pressure and hypotension.

Endocrine (6 decks)

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