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Endocrine - Summer 2019 > Pancreas > Flashcards

Pancreas Flashcards

1
Q

Pancreas characteristics

A

gladular organ with both digestive (exocrine) and endocrine function. It is about 6 inches longand rests behind the stomach

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2
Q

Two major hormones the pancreas secretes

A

insulin and glucagon

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3
Q

Islet of Langerhans - Alpha cells secrete ________

A

Gucagon

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4
Q

Islet of Langerhans - Beta cells secrete _______

A

insulin

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5
Q

Islet of Langerhans - Delta Cells secrete _________

A

somatostatin and pancreatic polypeptide

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6
Q

Glands secreting digestive juices into the abdomen

A

acini

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7
Q

Insulin is a hormone associated with _______ abundance and _______ or this excess energy

A

energy / storage

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8
Q

Insulin causes carbohydrates to be stored as __________ in muscle and liver

A

glycogen

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9
Q

Insulin causes fat storage in _______ tissue

A

adipose

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10
Q

Excess carbohydrates that cannont be converted to ______ are converted to ______ and are stored in adipose tissue

A

glygcogen / fats

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11
Q

_________ promotes upatake of amino acids and conversion to protein

A

insulin

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12
Q

**Insulin is stimulated by what?

A

High blood glucose, amino acids, beta-keto acids, glucagon, acteylcholine, intestinal hormones, sulfonyurea drugs (glyburide), insulin resistance (obesity)

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13
Q

**Insulin is inhibited by what?

A

Low blood glucose, Fasting, catecholamines (alpha-agonists), somatostatin

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14
Q

Insulin circulates almost entirely _______ with plasma half-life of ___ min

A

unbound / 6 min

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15
Q

_______ degrades unused insulin in liver, some degraded by kidney and muscles

A

insulinase

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16
Q

Highly specific ______ leads to endocytosis

A

receptor

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17
Q

Within seconds adipose and muscle cellls markedly _______ their _______ of glucose

A

increase / uptake

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18
Q

Do neurons in the brain respond to insulin in the same way as muscles and other cells?

A

No, because neurons are permeable to glucose. Normal blood glucose is required to prevent hypoglycemic shock

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19
Q

The cell membrane increases intake of amino acids, potassium and _____

A

phosphate

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20
Q

Anabolic effects of inuslin is basically what?

A

storing glucose for later use

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21
Q

Anabolic effects of insulin - Insulin ________ glycogenesis (glycogen is storage form of glucose)

A

increases

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22
Q

Anabolics effects of insulin - Insulin _______ glycogenolysis

A

inhibits

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23
Q

Insulin ________ gluconeogenesis

A

inhibits

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24
Q

Inuslin ________ glucose (traps) for use in glycolysis, glycogenesis

A

phosphorylates

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25
Q

Insulin fascilitates entry of ________ into cells of all tissues except _______, _______, _____, _____

A

gluose / brain, kidney tubules, intestinal mucosa, and RBCs

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26
Q

Insulin ________ hepatic upatake, storage and use of glucose

A

increases

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27
Q

The liver releases glucose between ______

A

meals

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28
Q

Insulin increases ____ and protein ______ in the liver

A

lipogenesis / synthesis

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29
Q

Insulin increases protein synthesis by stimulating amino acid _________ and inhibits protein ________ and depresses ________

A

transport / catabolism / gluconeogenesis

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30
Q

Insulin will increase ______ synthesis and storage

A

fat

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31
Q

Insulin increases formation of glycerol and fatty acids and the resulting ___________

A

triglycerides

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32
Q

Insulin promotes transport of glucose as well as conversion of excess glucose into _____ _____

A

fatty acids

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33
Q

T/F Insulin inhibits lipolysis enzymes

A

TRUE

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34
Q

Insulin will increase protein _____ and ______

A

synthesis and storage

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35
Q

Insulin increases amino acid _____ as welll as glucose ______

A

uptake / entry

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36
Q

Normally cells only slightly permeable to glucose, what increases permeability and uptake

A

exercise and insulin

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37
Q

Inuslin can increase glycogenesis and protein synthesis which can be used for energy if _______

A

exercising

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38
Q

_______ is secreted by alpha cells of the islets of Langerhans when glood glucose levels FALL

A

glucagon

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39
Q

Glucagon has effects that _______ the effects of insulin

A

oppose

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40
Q

Glucagon increases blood glucose concentration and can cause _______

A

hyperglycemia

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41
Q

Glucagon has a catabolic effect, generally OPPOSES inuslin but stimulates ______ release

A

insulin

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42
Q

Activates enzymes for glycogenolysis

A

glucagon

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43
Q

Increases gluconeogenesis

A

glucagon

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44
Q

Increases lipolysis and ketogenesis which inhibits triglyceride storage in liver

A

glucagon

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45
Q

T/F Glucagon increases proteolysis and flow of amino acids from muscle to liver for gluconeogenesis

A

TRUE

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46
Q

Enhances heart strength, increase blood flow in some tissues, enhances bile secretion, and inhibits gastric acid secretion

A

glucagon

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47
Q

Glucagon is stimulated by

A

fasting hypoglycemia, amino acids (protein meal), Beta-adrenergic stimulation, exercise, cholecystokinin, gastrin, cortisol

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48
Q

T/F Exercise is not associated with hypoglycemia, but may be a response to increased circulating amino acids

A

TRUE

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49
Q

Glucagon is INHIBITED by

A

high glucose levels, somatostatin, free fatty acids, ketones, insulin

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50
Q

Carbohydrate metabolism Anabolic (synthesis) Phase: Postprandial -If energy intake exceeds usage requirements energy is stored as what?

A

glycogen, structural proteins and fat

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51
Q

Carbohydrate metabolism Anabolic (synthesis) Phase is mediated by _________. Release begins at 100 mg/dl glucose, peaks at 400-600 mg/dl.

A

insulin

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52
Q

After eating, plasma insulin concentration increases almost ___ fold in 3-5 minutes due to dumping of performed, stored insulin. Level decreases in 5-10 minutes

A

10

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53
Q

At 15 minutes postprandial, new insulin plateau is reached due to more ______ and _____

A

release and synthesis

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54
Q

Insulin is shut off in 3-5 min after level under ____ mg/dL

A

80 mg/dL

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55
Q

Carbohydrate metabolism: Catabolic phase (fasting) - Needs met only by ________(Internal) sources and is mediated by _______

A

endogenous / glucoagon

56
Q

During the catabolic phase you have breakdown of glycogen, protein, triglyceride stores for energy supply which produces ____ and ____

A

glucose and ketones

57
Q

T/F The brain can function on glucose and ketones

A

TRUE

58
Q

Fasting 12-24 hrs

A

liver glycogen is sufficient for brain

59
Q

Fasting >24 hrs

A

Gluconeogenesis uses amino acids, glycerol and lactate to make glucose

60
Q

Amino acids from breakdown of muscle protein are a good source of _______ formation

A

glucose

61
Q

______ _______ significant in first few days of fasting

A

muscle wasting

62
Q

Gluconeogenesis is primarily in the ______ but also some happens in the _______

A

liver / kidney

63
Q

Days 2-4 fasting: Fat stores broken down to free fatty acids for tissues, some glucose, but primarily _____ for the brain

A

ketones

64
Q

Ketones are formed in the ______. At this point, most glucose used by CNS and protein loss is minimized by _____ loss. After weeks, brain uses primarily ______ which are measurable in the urine.

A

liver / fat / ketones

65
Q

Diabetes greek meas what?

A

to pass through, a siphon

66
Q

Diabetes is a disorder of __________ causing excessive thirst and the production of large quantities of ________

A

metabolism / urine

67
Q

Mellitus is latin for

A

honey sweet

68
Q

In diabetes insipidus the urine is dilute and has no _____. Whereas in mellitus the urine is _____

A

taste / sweet

69
Q

Thomas Willis in 1675 added mellitus to the word diabetes to coin the term

A

diabets mellitus

70
Q

DM is a syndrome of impaired carbohydrate, fat, and protein metabolism caused by what?

A

Either a lack of inuslin or a decreased sensitivity of the tissues to insulin

71
Q

Type I DM

A

caused by lack of insulin secretion and is less prevalent

72
Q

Type II DM

A

caused by a decreased sensitivity of target tissues to the metabolic effects of insulin (insulin resistance)

73
Q

Insulin _______ leads to hyperglycemia from decreased cell entry, increased gluconeogenesis, and glucose release from the ________

A

insufficiency / liver

74
Q

Glucose is reabsorbed by kidney until about ____ mg/dL. High blood glucose leads to _____ diuresis, loss of Na, loss of K, and glucosuria

A

180 / osmotic

75
Q

T/ F High blood sugar can lead to hypovolemic hypotension, dehydration, POLYURIA, POLYDIPSIA, POLYPHAGIA

A

TRUE

76
Q

Polyphagia is an increased appetite from _______

A

hypothalamus ventral nucleus

77
Q

Low insulin leads to muscle ________ and increased fat _________

A

catabolism / catabolism

78
Q

Low insulin increases the release of _____ acids which causes an ____ ____ metabolic acidosis

A

keto / anion gap

79
Q

Diabetes acute symptoms

A

Polyuria, polydipsia, polyphagia

80
Q

Polyuria results in

A

osmotic diuresis

81
Q

Polydipsia occurs from

A

intravascular volume depletion

82
Q

Polyphagia and weight loss occurs from

A

protein catabolism

83
Q

CNS irritability/confusion in diabetes is related to _______ ECF that leads to cell ______

A

hypertonic / shrinkage

84
Q

Visual disturbances from diabetes occurs from _____ formation in lens that causes osmotic swelling and glycation leads to opacification

A

sorbitol

85
Q

Microvascular dz affects perfusion to ______, and this often is present in 10-15 years

A

retina

86
Q

Chronic symptoms of DM

A

infection, macrovascular dz, microvascualr dz

87
Q

Chronic symptoms of DM - Infection: Why are diabetics more prone to infection

A

decreased PMN phagocytosis

88
Q

Chronic symptoms of DM - Why does macrovascular dz happen?

A

accelerated atherosclerosis / Think CAD, PAD, AMI, CHF, CVA

89
Q

Chronic symptoms of DM - Microvascular dz: Nephropathy

A

1/3 of transplants, 50% develop CRF

90
Q

Chronic symptoms of DM - Microvascular dz: Retinopathy

A

leading cause of blindess in US ages 20-65

91
Q

Chronic symptoms of DM - Microvascular dz: Neuropathy

A

symmetric, sensory, stocking glove. Autonomic issues include orthostatic hypotension and delayed gastric emptying

92
Q

Destruction of beta cells results in loss of insulin release. Caused by viral infections or autoimmune disorders. Heredity plays a role in determining susceptibility of beta cells to insults. Receptor and cellular mechanisms usually preserved

A

Type I DM

93
Q

Caused by greatly diminished sensitivity of target tissues to metabolic effects of insulin. High levels of keto acids are not usually present. Far more common than Type I. Formerly known as adult onset DM but obese children can develop as well.

A

Type II DM

94
Q

Plasma insulin is _______ in type II DM. However, levels still insufficient for regulation, beta-cells become ______ in some patients

A

elevated / exhausted

95
Q

Most patients with Type II DM are ____

A

obese

96
Q

Read slide 24

A

historical DM diagnosis

97
Q

HgbA1c is used to diagnose ___ and how well it’s managed

A

DM

98
Q

Normal HgbA1C

A

4-5.6%

99
Q

The higher the HgbA1C, the higher the risks of developing complications related to ____

A

diabetes

100
Q

T/F DM patients are at increased risk of CAD, HTN, CHF, perioperative MI (often silent), CVA

A

TRUE

101
Q

Increased risks with DM patients

A

increased risk for all of this: positioning injuries, autonomic neuropathy, hemodynamic instability, inability to compensate for changes in volume and vascular tone, post-induction hypotension and sudden death, gastroparesis, pulmonary aspiration, stiff joints (TMJ, AA, c-spine) resulting in difficulty with intubation

102
Q

Hyperglycemia causes increased:

A

CHF, 18x mortality, 2x LOS, increased risk of infection, sepsis, ARF, illness related to neuropathy, positioning injuries, CVA, poor fetal outcomes

103
Q

TKA infection rate for diabetics

A

7% infection / 12% wound complication / 15% UTI

104
Q

CVA and abdominal ssurgery infection rate is 2.7x higher if BG >

A

200

105
Q

Mortality for ICU patients with DM is at 8% if BG is between ____ and ___

A

180-200

106
Q

3 Distinct effects of gluose control: Inhibits lipolysis and elevated FFAs which are associated with ______ ______

A

cardiac arrhythmias

107
Q

3 Distinct effects of gluose control: Insulin inhibits ________ growth factors important in acute MI, and general inflammatory responses

A

inflammatory

108
Q

3 Distinct effects of gluose control: Decreased insulin leads to _________, while insulin infusions lead to favorable alterations in myocardial and skeletal muscle metabolism

A

proteolysis

109
Q

Perioperative stress may increase serum glucose concentrations due to _____ and _____ release

A

cortisol and catecholamine

110
Q

BS greater than _______ should be treated

A

200

111
Q

Perioperative glucose control guidelines

A

Plan surgery in diabetics as 1st case of the day to prevent prolonged fasting. Oral hypoglycemics are held day of surgery to prevent hypoglycemia until oral intake is restarted. Insulin therapy should balance adequate glucose control with the avoidance of hypoglycemia. Type I diabetics should continue basal insulin admnistration to avoid ketoacidosis. Patients on insulin pumps may be managed by continuing pump for short operations or changing over to IV insulin infusions.

112
Q

DKA can happen in Type I diabetics with profoundly low ____ levels. Elevated counterregulatory hormones (glucagon, cortisol, GH, catechols) render insulin _______

A

insulin / ineffective

113
Q

Primary features of DKA

A

dehydration, acidosis, electrolyte depletion

114
Q

In DKA, blood glucose rises without effective insulin leading to _____ diuresis and ______ losses

A

osmotic / electrolyte

115
Q

Dehydration in DKA can result in ___ to __ L fluid loss and loss of up to ____ body K+

A

4-6 / 10%

116
Q

T/F In DKA, accelerated protein breakdown leads to liver gluconeogenesis which worsens hyperglycemia

A

TRUE

117
Q

Activation of B-oxidation of fatty acids in DKA leads to what?

A

ketogenesis results, which overwhelms body’s buffer and results in ketoacidosis

118
Q

DKA symptoms

A

N/V, polyuria, polydipsia, polyphagia, anorexia, orthostatic changes, Kussmaul breathing, acetone, halitosis, altered LOC

119
Q

T/F LOC in DKA is related to patient’s OSMOLALITY not ACIDOSIS

A

TRUE

120
Q

Precipitating events for DKA

A

MI, Trauma, infectioin, non-compliance

121
Q

Treatment for DKA

A

Massive fluid resuscitation, electrolyte replacement, insulin therapy

122
Q

T/F DKA will often present with severe hyperkalemia in face of total body K depletion

A

TRUE

123
Q

Mortality for DKA

A

3-10%

124
Q

Nonketotic hyperosmolar state has same precipitating events as _____ with a very high _____

A

DKA / blood glucose

125
Q

Primary features of Nonketotic Hyperosmolar State

A

severe hyperglycemia, dehydration, severe hyperosmolar state and lack of ketoacidosis

126
Q

Symptoms of Nonketotic hyperosmolar state

A

thrombosis from hyperviscosity, focal neuro/reflex signs, global neuro signs, confusion, seizures, coma

127
Q

Treatment for Nonketotic hyperosmolar state

A

fluid resuscitation. Dextrose should be added to IVF when BG is 250 to avoid precipitous drop and cerebral edema. Provide K+, phos and insulin if needed.

128
Q

Mortality for nonketotic hyperosmolar state

A

10-20%

129
Q

Osmolarity formula

A

2[Na] + Glucose/18 + [BUN]/2.8

130
Q

Hypoglycemia (inuslin excess) has profound CNS effects including

A

confusion, convulsions, coma

131
Q

Early response to hypoglycemia is liver ______ breakdown. The ________ response is less important early and becomes increasingly important progressively

A

glycogen / glucagon

132
Q

Late response to hypolglycemia is sympathetic stimulation with _______ release

A

epi

133
Q

Very late response to hypoglycemia is ____ and ______ are secreted

A

GH and cortisol

134
Q

An insulinoma is a _____ cell adenoma. This can result in insulin shock (coma under 20 mg/dL). This is treated with ______

A

beta / glucose, glucagon, epi

135
Q

Hypoglycemic chock develops in range of __ to ___. It is characterized by progressive nervous irritiability that leads to fainting, seizures and coma. Brain uses only glucose available but can use fats/ketones with difficulty in times of stress. Treat hypoglycemic shock with _____.

A

20-50 / D50 + infusion of D5

136
Q

Prolonged hypoglycemia leads to brain cell ___ and ____

A

death and apoptosis

Endocrine - Summer 2019 (7 decks)

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