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N935 Pathophysiology > Endocrine Disorder 1/ Pancreatic Disorders > Flashcards

Endocrine Disorder 1/ Pancreatic Disorders Flashcards

1
Q

What are is the pancreas composed of?

A

two anatomically discrete sets of cells and functions

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2
Q

What two types of cells make up the pancreas?

A

exocrine

endocrine

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3
Q

What is the source of insulin and glucagon in the pancreas?

A

endocrine pancreas

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4
Q

What cells make up the bulk of the pancreas?

A

exocrine

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5
Q

What is the role of the exocrine pancreas?

A

secrete digestive enzymes into ducts that drain via the pancreatic duct and the common bile duct into the duodenum

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6
Q

What is the exocrine pancreas?

A

glands lined with epithelial (acinar) cells

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7
Q

What is in the endocrine pancreas?

A

islet of langerhans

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8
Q

What is the purpose of endocrine pancreas?

A

insulin and glucagon

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9
Q

What other hormones are excreted by the endocrine pancreas?

A

amylin, somatostatin, pancreatic polypeptide

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10
Q

Where can tumors occur in the pancreas?

A

head of the pancreas

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11
Q

What are the three major types of cells in the islet of langerhans?

A

alpha cells
beta cells
delta

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12
Q

Why is the blood supply near the islet of langerhans?

A

since the islet of langerhans secrete insulin and glucagon the vasculature allows for immediate secretion into the blood stream

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13
Q

What is the size of the islet of langerhans?

A

0.3mm in diameter

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14
Q

How many islets of langerhans are in the human pnacreas?

A

1-2 million

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15
Q

What do alpha cells secrete?

A

glucagon

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16
Q

What do beta cells secrete?

A

insulin

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17
Q

What do delta cells secrete?

A

somatostatin

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18
Q

Why are the cells within the islet of langerhans located close together?

A

Their close proximity allows for a close negative feedback loop
insulin inhibits glucagon secretion, amylin inhibits insulin secretion, and somatostatin inhibits the secretion of both insulin and glucagon

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19
Q

What is an example of a positive feedback loop?

A

oxytoxin during birth

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20
Q

What results in insulin release?

A

carbohydrate ingestion

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21
Q

What does insulin do when excess amounts of carbohydrates are consumed?

A

increases to store carbohydrates as glycogen in the liver

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22
Q

What happens with the excess carbohydrates that can not be stored as glycogen?

A

They are converted under the stimulus of insulin into fats and stored in adipose tissue

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23
Q

Define glycogenolysis

A

breaking down glycogen to glucose in the liver

glycogen breaks down into glucose 1 phosphate and glucose with hepatocytes

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24
Q

Define Gluconeogenesis

A

utilizing fructose and galactose to glucose

glucose is synthesized from non-carbohydrate metabolites

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25
Q

What form does insulin circulate into the blood?

A

unbound

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26
Q

What is the plasma 1/2 life of insulin?

A

6 minutes

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27
Q

What enzyme degrades insulin and where?

A

insulinase in the liver

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28
Q

How does insulin facilitate glucose uptake?

A

enzyme linked receptor on target cells in varying tissues

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29
Q

When is glucagon secreted?

A

In response to decreased blood glucose levels

opposite of insulin

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30
Q

What is the function of glucagon?

A

increase blood glucose concentration

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31
Q

Examples of hyperglycemic hormones

A

cortisol
growth hormone
epinephrine
glucagon (stimulates glycogenolysis/ glyconeogenesis and inhibits glycolysis)

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32
Q

How much does glucagon increase the blood glucose in the blood in what amount of time?

A

1mcg/kg of glucagon can elevate the blood glucose concentration approximately 20mg/100ml of blood (25% increase) in about 20 minutes

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33
Q

What affects does glucagon have on the liver (2)?

A

breakdown of liver glycogen (glycogenolysis)

increased gluconeogenesis in the liver

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34
Q

What are four OTHER functions of glucagon?

A

enhances the strength of the heart (contractility)
increases BF to some tissues (esp. kidneys)
enhances bile secretion
inhibits gastric acid secretion

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35
Q

What is the half life of somatostatin?

A

3 minutes

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36
Q

Somatostatin has the same chemical substance as

A

growth hormone inhibitory hormone

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37
Q

What is is somatostain designed to do?

A

delay the time the body can absorb the nutrients in the stomach
extend the period over which the food nutrients are assimilated into the blood

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38
Q

What does somatostatin do in a variceal bleed?

A

it inhibits the secretions to decrease motility in the GI tract

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39
Q

When is somatostatin normally secreted?

A

ingestion of food stimulate secretion

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40
Q

What are 3 inhibitory effects of somatostatin?

A

depresses secretion of both insulin and gallbladder

decreases motility of stomach, duodenum and gallbladder

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41
Q

What are majority of pancreatitis cases associated with?

A

gallstones or alcoholism

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42
Q

What does pancreatitis result from?

A

autodigestion and inflammation of the pancreas caused by inappropriate activated pancreatic enzymes

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43
Q

What is diabetes mellitus?

A

group of disorders with relative or absolute insulin deficiency

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44
Q

What does diabetes mellitus result from?

A

inadequate supply of insulin and/or inadequate tissue response to insulin

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45
Q

What lab levels will be increase in pancreatits?

A

amylase

lipase

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46
Q

what does diabetes mellitus result in?

A

hormone induced metabolic abnormalities
microvascular and macrovascular lesions
long-term end organ complications

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47
Q

Describe the type 1 diabetes mellitus

A

autoimmune destruction of the pancreatic beta islet cells

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48
Q

Describe the type 2 diabetes mellitus

A

peripheral insulin resistance through multiple defects with insulin action and secretion

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49
Q

What is associated with type 1 DM?

A

15% associated with other autoimmune diseases (graves disease, hashimoto thyriditis, addison disease and myasthenia gravis)

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50
Q

How are plasma insulin levels in type 1 DM?

A

relatively low for the level of blood glucose (absence or minimal circulating levels)

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51
Q

What type of DM requires insulin therapy?

A

Type 1 DM

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52
Q

How does Type 1 DM result?

A

autoimmune related

results from T cell mediated destruction of beta cells within pancreatic islets

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53
Q

What type of DM is 90% of cases?

A

Type 2

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54
Q

What is associated with type 2 DM?

A

associated with excessive weight gain in adults and pediatrics

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55
Q

How are plasma insulin levels in type 2 DM?

A

plasma insulin levels are normal or increased

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56
Q

What is type 2 DM prone to?

A

susceptible to hyperglycemic-hyperosmolar nonketotic state

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57
Q

How does Type 2 DM result?

A

not immune related

results from defects in insulin receptors and postreceptor intracellular signaling pathways

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58
Q

What is type 1 DM susceptible to?

A

ketoacidosis

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59
Q

What are the common medications for diabetes?

A 
acarbose
biguinades
dipeptidyl peptidase 4 inhibitors
glucagon like peptide 1 receptor agonists
meglitinide
sodium-glucose transport protein 2 inhibitors
sulfonylureas
thiazolidinediones
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60
Q

What is acarbose?

A

delay GI glucose absorption

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61
Q

What is an example of biguanides?

A

metaformin

62
Q

What do biguanides?

A

suppresses excessive hepatic glucose release

63
Q

What are examples of dipeptidyl peptidase 4 inhibitors?

A

sitagliptin
saxagliptin
vildagliptin

64
Q

What are examples of glucagon-like peptide 1 receptor agonist?

A

albiglutide
dulagutide
exenatide

65
Q

What are examples of meglitinides?

A

repaglinide or nateglinide

66
Q

What is the MOA of sulfonylureas?

A

increases insulin availability (by stimulating insulin secretion from pancreatic beta cells; enhance insulin-stimulated peripheral tissue utilization of glucose

67
Q

What is the MOA thiazolidinediones?

A

improves insulin sensitivity

68
Q

What is the MOA of meglitinides?

A

increases insulin availability

69
Q

What are examples of sodium-glucose transport protein 2 inhibitors?

A

canagliflozin or empagliflozin

70
Q

What are are examples of sulfonylureas

A

glibenclamide
glipizide
glimepiride

71
Q

When do insulin dependent patients experience an increase in insulin requirements? Why?

A

during the post midnight hours

accelerated glucose production and impaired glucose use due to noctural surges in secretion of growth hormone

72
Q

What is the BS of an insulin dependent patient in the early mornings?

A

hyperglycemia

73
Q

What is the absorption of insulin dependent on?

A

highly variable and dependent on type of insulin, the site of administration, and subcutaneous blood flow

74
Q

What are the 5 major risk factors for diabetic patients undergoing surgery?

A

cardiovascular
renal
joint collagen tissue abnormalities (limited neck extension)
neuropathies
infections complications and poor wound healing

75
Q

What is more important with a patient with long standing diabetes perioperative?

A

degree of glucose control

end-organ dysfunction that exists

76
Q

What is glucotoxicity?

A

long term exposure to high blood glucose
nonenzymatic glycosylation reactions that lead to the formation of abnormal proteins which weaking endothelial junctions and decrease elastances

77
Q

What are signs and symptoms of glucotoxicity

A

difficult intubations, decreased wound healing, tensile strength
glucose-induced vasodilation

78
Q

What does glucose-induced vasodilation from glucotoxicity cause?

A

prevents target organs from protecting against increase in systemic blood pressure
renal failure in time

79
Q

What varies in vascular beds?

A

the threshold for glycemic toxicity

retinopathy vs coronary arteries

80
Q

According to the WHO surgical safety checklist, what is the target BS ?

A

100-180mg/dL

81
Q

How do you initiate insulin therapy for hyperglycemia?

A

bolus 5-10units IV

divide the last serum glucose value by 150

82
Q

What is the primary site of endogenous glucose production?

A

lvier

83
Q

What are the precursors for gluconeogenesis?

A

pyruvate and lactate

certain gluconeogenic amino acids and glycerol (from fat metabolism)

84
Q

Discuss normal glucose physiology

A

eating
increased blood glucose
stimulate insulin secretion
stimulates glucose utilization in tissues

85
Q

What occurs postprandial with glucose?

A

glucose utilization exceeds glucose production
transition from exogenous glucose delivery to endogenous production + decreased insulin secretion
= maintenance of a normal plasma glucose

86
Q

Where is 70-80% of the glucose released by the liver metabolized?

A

insulin-insensitive tissues

brain, GI tract, RBCs

87
Q

What age does Type 1 diabetes present?

A

before age 40 in genetically susceptible individuals

88
Q

what causes onset of type 1 diabetes?

A

sudden onset due to critical mass of loss of beta cells

89
Q

How much beta cell function must be lost prior to hyperglycemia occurs?

A

80-90%

90
Q

What are signs and symptoms of hyperglycemia?

A 
fatigue
weight loss
polyuria
polydipsia
blurry vision
intravascular volume depletion
91
Q

What is diagnoses of Type 1 DM based on

A

presence of random blood glucose >200mg/dL and a hemoglobin A1c >7%

92
Q

If insulin is withheld in a DM1, what can occur?

A

diabetic ketoacidosis

93
Q

What are characteristics of Type 2 diabetes?

A

relative beta cell insufficiency and insulin resistance
inherited insulin resistance
obesity and sedentary lifestyle are contributing factors

94
Q

Describe the initial pathological insult in type 2 DM

A

peripheral tissues (skeletal muscle, adipose tissue, liver) become insensitive to insulin leads to an increase in pancreatic insulin secretion (hyperinsulinemia) to maintain normal plasma glucose

95
Q

Describe the progression of DM2

A

pancreatic cell function decreases, and insulin levels are unable to compensate and hyperglycemia occurs

96
Q

What are the three main defects of DM2

A

increased rate of hepatic glucose release
impaired basal and stimulated insulin secretion
inefficient use of glucose by peripheral tissues

97
Q

What syndrome is seen with DM2 patients?

A

metabolic syndrome

98
Q

What does metabolic combine insulin resistance with

A 
hypertension
dyslipidemia
procoagulant states
obesity
premature atherosclerosis/ cardiovascular disease
99
Q

Diagnosis of DM according to the American diabetes association,

A

fasting (no caloric intake for > 8hrs) plasma glucose .126mg/dl
random plasma glucose concentration >200mg/dL
2-hour plasma glucose level > 200mg/dL during an oral glucose tolerance test

100
Q

What is an impaired fasting glucose?

A

101-125mg/dL

101
Q

What does an hemoglobin A1c provide?

A

valuable measure of long term glycemic control

102
Q

What is a normal HbA1c?

A

4-6%

103
Q

What does glucose do to a hemoglobin molecule?

A

nonenzymatically glycosylated

104
Q

What is the importance of glycosylated hemoglobin?

A

freely crosses the RBC membrane and is directly proportional to average plasma glucose concentration during the preceding 60-90 days

105
Q

What is the first line treatment of DM2?

A

weight loss and exercise therapy

106
Q

How does weight loss and exercise therapy help with DM2

A

decreases adiposity improves hepatic and peripheral tissues insulin sensitivity, enhances post-receptor insulin action and may possibly increase insulin secretion

107
Q

How is pharmacologic therapy of DM2 managed?

A

titrated to achieve fasting and peak postprandial glucose levels recommended by the ADA

108
Q

What are the common pharmacologic therapies for DM2?

A

sulfonylurea or biguanide

109
Q

What is added to a DM2 regimen if combination oral therapy is unsuccessful?

A

a bed time dose of intermediate-acting insulin

110
Q

Why is an intermediate acting insulin added at night for DM2?

A

hepatic glucose overproduction is typically highest at night

111
Q

When is a DM2 patient switched to insulin therapy alone?

A

if oral agents plus single dose insulin therapy isn’t effective

112
Q

What are the 4 kinds of insulin?

A 
basal insulin (intermediate acting and administered twice daily)
long acting (administered once daily)
short acting (regular) (provide glycemic control at meal times)
rapid acting (provide glycemic control at meal times)
113
Q

What is a typical insulin requirement/ regimen for a DM1?

A

0.5-1u/kg/day divided into multiple doses with 50% given as basal insulin

114
Q

What is diabetic ketoacidosis?

A

high glucose levels exceed the threshold for renal tubular absorption causing significant osmotic diuresis with marked hypovolemia

115
Q

When does ketosis occur?

A

when the carbohydrate intake is low

116
Q

How are ketones produced?

A

When the body breaks down fat it produces an acid, ketones or ketone bones

117
Q

What becomes the body’s main source of energy in hyperglycemia/DKA?

A

ketones

118
Q

What does the increase in ketoacids create?

A

anion-gap metabolic acidosis

119
Q

Hepatic ketogenesis leads to

A

overproduction of ketocaids in the liver

120
Q

What labs are seen in DKA

A

hypokalemia
hyponatremia
hypophosphatemia

121
Q

How does hyponatremia occur in DKA

A

results from the effect of hyperglycemia and hyperosmolality on water distribution (dilutional)

122
Q

How does hypokalemia occur in DKA

A 
usually substantial (3-5meq/l) as moves into the intracellular space with insulin as the acidosis is correct
K also excreted in urine b/c of the increased delivery of sodium to the distal renal tubules that accompanies volume expanison
123
Q

How does hypophosphatemia occur in DKA

A

result of tissue catabolism, impaired cellular uptake and increased urinary losses and can lead to diaphragmatic and skeletal muscle dysfunction and impaired myocardial contractility

124
Q

What is the treatment for DKA?

A

normal saline
IV loading dose of 0.1u/kg of regular insulin plus a low dose insulin infusion of 0.1 u/kg/h
caution with correction of hyperglycemia without simutaneous correction of serum sodium-> can lead to cerebral edema and seizures
correct electrolytes

125
Q

What is hyperglycemic hyperosmolar syndrome?

A

severe hyperglycemia, hyperosmolarity and dehydration

126
Q

S/S of HHS

A 
polyuria
polydipsia
hypovolemia
hypotension
tachycardia
organ hypoperfusion
127
Q

What is responsible for mental obtundation or coma in HHS?

A

hyperosmolality

>340mOsm/L

128
Q

If a DM patient presents with metabolic acidosis what is a difference between DKA and HHS?

A

ketoacidosis (only in DKA)

129
Q

What is the treatment of HHS?

A

large volumes of hypotonic saline (1000-1500ml/h) should be administered until the osmolarity is <320mOsm/L then isotonic saline (1000-1500ml/h)
IV bolus of 15 U of regular insulin followed by a 0.1u/kg/hr infusion
less severe electrolyte deficits then DKA

130
Q

What are complications of diabetes?

A 
nephropathy
peripheral neuropathy
retinopathy
autonomic neuropathy (tachycardia/ST elevation)
cardiovascular disease
131
Q

What can reduce the development ad progression of additional comorbidities in DM

A

strict glycemic control and blood pressure control

132
Q

What are 3 newer treatments of DM

A

implanted (like a pacemaker) glucose analyzer with electronic transmission to a surface (watch) monitor
new islet transplantation medication
INGAP (islet neogenesis-associated protein) peptide

133
Q

What does INGAP do?

A

may cause regrowth of normally functioning islet cells

134
Q

What does the islet transplantation medications do:?

A

make islet cell transplants more successful and rejection medication less hazardous

135
Q

How is hypoglycemia caused in a non-diabetic patient?

A 
pancreatic islet cell adenoma or carcinoma
large hepatoma
large sarcoma
alcohol ingestion
use of various medications
136
Q

What is hypoglycemia

A

plasma glucose level <50mg/dl

137
Q

What are symptoms of hypoglycemia?

A

adrenergic (sweating, tachycardia, palpitations, restlessnes, pallor) and neuroglycopenic (fatigue, confusion, headache, somnolence, convulsions, coma)

138
Q

What is the treatment for hypoglycemia?

A

dextrose 0.5-1g/kg IV/IO

139
Q

What % dextrose for adults?

A

50

140
Q

What % dextrose for pediatrics

A

25

141
Q

What % dextrose for neonates

A

5-10

142
Q

What is an insulinoma?

A

rare benign insulin secreting pancreatic islet cell tumors

143
Q

What can an insulinoma present as

A

multiple endocrine neoplasia syndrome tpye 1

144
Q

What is the triad for MEN 1?

A

insulinoma
hyperparathyroidism
pituitary tumor

145
Q

Diagnosis of insulinoma

A

whipple’s triad
symptoms of hypoglycemia with fasting
a glucose level below 50 with symptoms
relief of symptoms with administration of glucose

146
Q

What confirms an insulinoma?

A

inappropriately high insulin level (>5-10mu/ml) during a 48 to 72 hour fast confirms the diagnosis

147
Q

What medication will a patient with an insulinoma be taking preoperatively?

A

diazoxide

directly inhibits insulin release from beta cells

148
Q

Does the surgical treatment for insulinoma curative?

A

yes

149
Q

How frequently are you checking BS during an insulinoma removal?

A

q15minutes

150
Q

What will BG levels be intraoperatively with an insulinoma?

A

hypoglycemia with tumor manipulation

hyperglycemia following tumor removal

151
Q

What medications can be used intraoperatively with an insulinoma?

A

somatostatin analogue octreotide

suppress insulin release from such tumors

152
Q

What needs to be in fluids after insulinoma removal?

A

glucose to MIVF

N935 Pathophysiology (6 decks)

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