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Pathophysiology > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

exocrine cells of pancreas secrete?

-secreted into?

A

digestive enzymes
bicarb
***into duodenum

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2
Q

what digestive enxymes does pancreas secrete

A

trypsin
chymotrypsin
lipase
amylase

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3
Q

endocrine cells secrete?

A

insulin

glucagon

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4
Q

role of insulin

A

drive glucose into cell

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5
Q

role of glucagon

A

causes release of glucose into the blood for the tissues that need it

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6
Q

name the hormones that raise blood [glucose[

A

glucagon
cortisol
GH
norepi/epi

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7
Q

what cells secrete insulin

A

beta cells of pancreas

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8
Q

what organ produces glucagon

what organ stores it

A

liver produces as GLYCOGEN

pancreas stores

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9
Q

high blood gluc levels stimulates insulin to promote_____ (2)

A

glycolysis—b/d of glucose–ATP
AND
glyocogenesis–production of glycogen (glucose storage)

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10
Q

when glucose levels are low… glucagon decreases____(1) and increases _____ (2)

A
  • decreases glycolysis (glucose b/d)
  • increases gluconeogenesis (glucose formation)
  • increases glycogenolysis–b/d of glycogen to release glucose
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11
Q

define the following:

  1. Glycolysis
  2. Gluconeogenesis
  3. Glycogenolysis
  4. glycogenesis
A
  1. b/d glucose
  2. making of glucose– in the LIVER
  3. b/d of glycogen to release glucose
  4. synthesis of glycogen–aka storing glucose
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12
Q

where does gluconeogenesis occur

A

the liver

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13
Q

what is the storage form of glucose

A

glycogen–liver

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14
Q

what is the real goal of glucagon

A

mobilize glucose stores from the liver so that it can be sent to the brain and heart– for energy

its goal is not directed to breaking down glucose for energy

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15
Q

after insulin takes up glucose into the celll– it is stored as?

A

glycogen
fat
protein

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16
Q

what cells produce glucagon

A

alpha cells

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17
Q

what cells produce insulin

A

beta cells

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18
Q

what cells produce somatostatin

A

delta cells

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19
Q

where are the endocrine cells of the pancreas located?

A

islets of Langerham

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20
Q

which cell (A B or D) composes most of the mass?

A

beta

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21
Q

arterial blood supply to pancreas

A

splenic artery

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22
Q

which organ is exposed to most of the endocrine hormones?

why

A

LIVER

because of the venous drainage of pancreas drains into hepatic portal vein

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23
Q

do pancreatic hormones go through first pass metabolism?

A

yes

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24
Q

what does vagal nerve stimulation do to pancreas>

A

stimulates insulin release

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25
Q

things that simulate insulin release: 2

A
  • high blood glucose levels

- vagal nerve stimulation

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26
Q

vagal nerve stimulation activates secretion of?

A

insulin
glucagon
somatostatin
pancreatic polypeptide

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27
Q

which cells in the islets is generally spared from auto immune destruction

A

pancreatic poylpeptide cells

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28
Q

hyperglucagonemia?

A

hypersecretion of glucagon–>excess glucagon in blood

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29
Q

alpha cell dysfunction is reflected by?

A

hyperglucagonemia

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30
Q

sympathetic nerve stimualtion inhibits___ and activates secretions of?

A

inhibits insulin and somatostatin secretion

activates glucagon and pancreatic polypeptide secretion

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31
Q

insulin is what kind of homrone

A

polypeptide

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32
Q

active form of insulin is produced by modification of?

A

proinsulin

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33
Q

principle stimulus for insulin release?

A

glucose

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34
Q

how does glucose enter the Beta cells?

A

via GLUT 2

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35
Q

what happens to glucose after entering beta cells?

A

undergoes glycolysis–ATP production

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36
Q

glucose levels higher than _______ mg/dl will stimulate insulin synthesis

A

70

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37
Q

what neurotransmitter will amplify the glucose induce release of insulin

A

acteylcholine

*binds to cell membrane of beta cells and stimulates the insulin release

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38
Q

release of insulin is ___ and ___ in nature

A

rhythmic and pulsatile

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39
Q

pulsatile release of insulin is imp for?

A

reaching maximal physiologic effects

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40
Q

ex of the physiologic effects that the pulsatile release of insulin do?

A

-supresses liver gluocse production

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41
Q

physiologic effects of insulin:

  • immediate
  • early (witin mins)
  • moderate (hours)
  • delayed (within days)
A

immediate: glucose and K+ transport into cells
early: regulation of metabolic enzyme activity
moderate: modulation of enzyme sythnesis
delayed: effects on growth and cell diffferentiation

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42
Q

insulins actions on target tissue promote sythnesis of?

A

carbohydrates
fat
protein

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43
Q

insulin and effect on carb metabolism

  • stimulates
  • inhibits
A

stimulates:
- glucose transport into adipose and muscle tissue
- glycolysis
- glycogen storage

inhibits:
- glycogen b/d
- glycogenolysis and gluconeogenesis in liver

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44
Q

insulin affets on lipid metabolism

  • stims
  • inhibs
A

stims

  • synthesis of FAs
  • uptake of trigs from blood–>tissue
  • cholesterol synthesis liver

inhibs:
- lipolysis in tissue–lowering plasma FA level
- ketogenesis

45
Q

insulin affects on protein metabolism

  • stims
  • inhibs
A

stims

  • AA transp into tissue
  • protein synthesis

inhibs

  • protein b/d
  • urea formation
46
Q

specific effects of insulin on____ _____ is the dominant action of insulin

A

skeletal muscle glucose

47
Q

what is one of the main target organs of insulin

A

skeletal muscles

48
Q

insulin levels are High/Low during early DM2?

A

HIGH

hence the insulin resistance

49
Q

high levels of insulin are called?

A

hyperinsulinemia

50
Q

hyperinsulinemia has been linked to?

A

certain types of CA:

  • endometrium
  • breast
  • colon
  • kidney
51
Q

list conditions that cause elevated insulin

A 
high waist circumference 
excess visceral fat 
high waist-to-hip ratio 
-high BMI 
-sedetary lifestle 
-high energy intake
52
Q

cells do what when exposed to hyperinsulinemia?

A

excessive proliferation

53
Q

hyperinsulinemia and insulin resistance closely linked with what pathologic conditions

A

HTN
atherosclerosis
CVD
dyslipidemia

54
Q

glucagon is what kind of hormone

A

polypeptide

55
Q

antagonist homrone to insulin?

A

glucagon

56
Q

two main products of proglucagon?

A

glucagon–alpha cells pancreas

glucagon-like-peptide 1 (GLP-1) in the intestinal cells

57
Q

GLP-1 is produced in resonse to?

A

high [ ] of glucose in intestinal lumen

58
Q

another name for GLP-1

A

incretin

59
Q

what is an endocrine mediator that amplifies insulin release from beta cells in response to a glucose load?

A

GLP-1 or incretin

60
Q

what inhibits and stimulates glucagon release

A

hyperglycemia–inhibits

hypoglycemia–stims

61
Q

a meal high in carbs will stimulate and inhibit release of?

A

stim–insulin thru beta cells via release of GLP-1

inhib–glucaogn

62
Q

epinephrine stims/inhibis glucagon release

A

stimulates

63
Q

epinpehrine stims/inhibis insulin rel

A

inhibits

64
Q

somatostain inhibs/stims glucagon release?

A

inhibits

65
Q

vagal stimulation increase/decreasses glucagon rel?

A

increases

66
Q

principle target tisssue for glucagon?

A

liver

67
Q

how does glucagon increase plasma glucose concentrations

A

stimulates de novo hepatic glucose production through gluconeogenesis and glycogen b/d—–bc these actions counter act insulin

68
Q

glucagon receptor is found where in body

A 
liver********* 
pancreatic beta cells
kidney 
adipos tissue
heart
vascular tissues
brain
stomach
adrenal glands
69
Q

what does pro-insulin make after proteolytic processing

A

c-peptide

mature insulin

70
Q

how and where are C-peptide and mature insulin sotred

A

together

in beta cell

71
Q

how are c-pep and mature insulin secreted

A

co-secreted from secretory granules in beta cells

72
Q

which is cleared slower–c pep or mature insulin

A

c-peptide cleared slower in the body

73
Q

which is a more useful marker of insulin secretion—c peptide or insuin

A

c-peptide bc it is cleard slower vs inisulin

74
Q

elevated levels of ____ can be used to indicate early beta dyfsunction

A

pro-insulin

75
Q

high levels of pro inslin help indicate early?

A

beta cell destruction

76
Q

c peptides travel to?

A

portal circulation

77
Q

which hormone is the best to differentiate b/w DM 1 and 2

A

c-peptides

78
Q

whcih hormone is a better accurate reading of islet cell functions?

A

c peptides

79
Q

DM1:
c-peptides high or low?
insulin high or low?

A

c-peptides: low

insulin: low

80
Q

DM2:
c-peptides high or low?
insulin high or low?

A

normal or high level c-peptide

81
Q

insulinoma?

A

insulin secreting tumor on pancreas

82
Q

insulinoma can be assoc with?

A

MEN 1

83
Q

PTs with insulinoma have what kind of blood gluc levels

A

low low low

*AMS

84
Q

glucagonomas

A

rare
can produce s/s of DM
can produce catabolic effects on fat and muscle

85
Q

type 1 DM

A

beta cell DESTRUCTION
5% of cases
younger people–also called juvenille DM
higher risk to develop DKA w/o insulin tx

86
Q

type 2 DM

A

insulin resistance–part of syndrome X
loss of normal regulation of insulin secretion
accounts for more than 90% of cases
*obesity in adults
*mild hyperglycemia–rarely leads to ketoacidosis

87
Q

which DM is part of syndrome x

A

DM 2

88
Q

basic patho for DM overall

A

impaired entry of glucose into cells–>glucose accumulates in blood–>increase in plasma osmolarity—->urinary loss of glucose–>excess loss of water and sodium–>POLYURIA

resulting dehydration triggers compensatory thirst–>POLYDIPSIA

inability of the cells to utilize glucose resembles a state of starvation–>stimulates hunger–>POLYPHAGIA

89
Q

patho for DM2

A

results from decr responsiveness of peripheral tissues to insulin action
also
inadequate responsvienss to B cells to glucose
so—>leads to decrease release of insulin in response to glucose
*also affects the pulsatile release of insulin–becomes sluggish, smaller bursts and erratic

90
Q

do patients with type 2 DM secrete normal amounts of insulin during fasting?

A

YES

91
Q

do patient with type 2 DM secrete normal amount of insulin in response to glucose load?

A

no—- they secrete less insulin (70% less)

**beta cells over time become less responsive to glucose–leads to less insulin secretion

92
Q

earliest physiologic indication of B cell destruction is?

A

delay in acute insulin response to glucose

93
Q

three main pathologic defects in DM

A
  1. excessive hepatic glucose production–seen with high fasting glucose
  2. defective beta cell secretory function
  3. peripheral insulin resistance
94
Q

what is pancreas’ compensatory mechanism to insulin resistance

A

to release more insulin–only temporary tho

95
Q

as insulin resistance increases…. ___ ___ develops

A

glucose tolerance

96
Q

what three patholigc processes characterize DM 2

A

impaired insulin secretion
insulin resistance
excessive hepatic glucose production

97
Q

complications of DM

  • acute
  • chronic
A

acute:
- hypoglycemia
- DKA
- hyperglycemic-hyperosmolar nonketoic coma

chronic:
- peripheral nerve damage
- skin damage
- lens damange

98
Q

end state renal disease, blidness and neuropathy are MC in DM 1 or 2?

A

DM 1

99
Q

MI and stroke are MC in DM 1 or 2? why?

A

DM 2

* macrovascular disease

100
Q

main s/s of hypoglycemia

A

tachycardia
palps
sweating
tremors

gets lowr: 
irritability 
confusion 
blurry vision 
triedness 
HA
diff speaking

super low:
LOC
seizures

101
Q

main characteristics of DKA?

*patho behind DKA

A

characterisitcs: hyperglycemia, metabolic acidosis and incr ketone bodies

PATHO:

  1. gluconeogenesis continues in liver (w/o opposition of insulin
  2. incr [glucose]= incr osmolarity
  3. lack of insulin + high levels of counterregulatory hormones (gucagon, cortison, epi) cause LIPASE hormone to b/d fat for fuel and release ketones
102
Q

main characerisitcs of hyperglycemic hyperosmolar coma

A

severe hyperglycemia
hyperosmolarity
dehydration
*ABSENCE of ketosis

103
Q

underlying medication conditions (2) associ with HHC

A

CHF

renal insuff`

104
Q

patho for DM 1

A
  1. islet cell autoantibody destruction (islets are sensitive to inflammation)
  2. activated lymphocytes in islets–peripancreatic lymph nodes and systemic circulation
  3. t lymphocytes that proliferate when stimulated with islet proteins
  4. release cytokines inside islets
105
Q

what mediates beta cell death in DM1? and not so much?

A

T lymphocytes*****

not so much mediated by islet autoantibodies

106
Q

explain insulin resistance *what does pancreas do as compensatory mech:?

A

cells in muscle, fat and liver do not respond well to insulin—- so they cannot use glucose from blood as energy
*to compensate— pancreas makes MORE INSULIN—–

107
Q

a high insulin level without a correspondingly high c-peptide suggests?

A

exogenous insulin administration

108
Q

normal or elevated levels of insulin despite hypoglycemia can indicate what pathogenic cause?

A

insulinoma–insulin producing tumor on pancreas

109
Q

what are the corresponding levels of c-epptide with an insulinoma

A

elevated too because the extra insulin is endoengous

Pathophysiology (13 decks)

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