Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

.Pharmacology > Part 18: Diabetes > Flashcards

Part 18: Diabetes Flashcards

1
Q

the regulation of insulin and glucagon secretion is controlled by circulating blood ____ levels

A

glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

under normal conditions, there is a ____ (low/high) level of basal insulin release

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

large secretions of insulin from the pancreas happens in response to ____

A

elevations in blood glucose, like after meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

insulin secretion closely mirrors blood ___ spikes

A

glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

glucose from food sources is absorbed in the GI tract into the blood, then stimulating the ____ to release insulin

A

pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

insulin is made by ___ cells in the pancreas

A

B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

____ and ____ nerve stimulation also promote insulin release

A

incretins & vagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

insulin circulates in the blood and stimulates insulin receptors on tissues like the ____, ___ and _____ cells

A

liver, adipose, muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the effect of activating insulin receptors in target tissue cells?

A

these cells with start taking up glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the 2 possible fates of the glucose that is taken up by cells that were stimulated by insulin?

A
  1. used immediately in glycolysis for energy production

2. stored for later metabolic use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

insulin promotes the making and storage of ___, ___ and ____

A

glycogen, triglycerides, and protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the primary job of the pancreatic B cells?

A

insulin production and secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

glucose is able to enter beta cells via the ____ transporters on the surface of the cells

A

GLUT 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

t/f glucose must be transported across cell membranes

A

t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when glucose levels rise after a meal, the level of ___ also rises

A

ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ATP made by B cells binds to ____ channels and causes them to ____ (open/close)

A

ATP-dependent K; close

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

the closing of the ATP-dependent K channels results in membrane ____ which causes the _____ (opening/closing) of voltage gated Ca channels

A

depolarization; opening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Ca influx into beta cells results in Ca-mediated exocytosis of _____ into the blood

A

insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the steps of B cells making insulin?

A
  1. glucose comes in by GLUT-2
  2. glucose metabolized to make ATP, which activates ATP-dependent K channels and closes them, which depolarizes the membrane
  3. depolarization opens voltage-gated Ca channels
  4. Ca influx causes Ca-mediated exocytosis of insulin into the blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

insulin receptors are ____ type receptors

A

tyrosine kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

insulin receptors have ___transmembrane portions and ligand binding causes ___ of the 2 subunits

A

2; dimerization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

when the insulin receptor dimerizes, the intracelllar portions come togther and the _____ domains phosphorylate each other, this is called ___

A

intrinsic kinase; autophosphorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

the key process involved in glucose homeostasis involves the activation of the ___ kinase, which causes an increase in the trafficking of _____ to the cell membrane

A

pi3; GLUT-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

____ transporters are critical, as they are the primary way to get glucose into target cells

A

GLUT-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MAP kinase pathways are also activated and promote ___ and ___

A

cellular growth and proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the 5 main steps of the cellular mechanism of insulin?

A
  1. insulin binds to insulin receptors of target tissue cells
  2. the kinase domains of the receptor undergo autophoshporylation, starting intracellular signalling cascades
  3. insulin response substrates (IRS) activate phosphatidylinositol-3kinase (PI3-K) and the mitogen-activated protein kinase (MAPK) signalling cascades
  4. GLUT-4 glucose transporters are trafficked to the cell membrane, which allows glucose to enter the target tissue cells
  5. MAPK pathways promote cellular growth and proliferation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

glucagon is a counter hormone to ____

A

insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

where is glucagon made?

A

pancreatic a cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

glucagon is secreted when blood glucose levels are _____(high/low)

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

glucagon stimulates the release of ____ from hepatocytes

A

glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

glucagon binds to a ____ receptors

A

glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what type of receptors are glucagon receptors?

A

gpcr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

glucagon receptors are located on ____ cells

A

hepatocytes in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

glucagon receptors are ____ coupled

A

Gs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

activated glucagon receptors activate adenyl cyclase and increase levels of ___ which activates ___, which mediates cellular processes aimed to increase blood glucose levels

A

cAMP; PKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

when glucagon receptors are activated, glycogen stores are broken down in a process called ____ and new glucose is made in cells from other biochem building blocks in a process called ____

A

glycogenolysis; gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

glucagon receptor activation causes a ____ 9decrease or increase) in glycolysis and glycogenesis

A

decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

when is the typical onset of type 1 diabetes?

A

juvenile (early onset)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Type 1 diabetes is characterized by a destruction of _____ cells in the pancreas

A

beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

type 1 diabetes presents as a ____ disease early in life

A

autoimmune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

in type 1 diabetic patients, do they have some ability to make insulin?

A

no, no ability to make insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the onset of type 2 diabetes?

A

late onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

type 2 diabetes is usually secondary to other health problems like ____

A

obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

type 2 diabetes is usually a multi-factorial ____ disease

A

metabolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the issue with the B cells in type 2 diabetes?

A

beta cells in the pancreas are less responsive to glucose and insulin secretion after a meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

there is often insulin ____ of target cells in type 2 diabetes

A

resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

are there non-pharm treatments for type 1 diabetes?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what are the non-pharm treatments for type 2 diabetes?

A

diet, exercise, smoking cessation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is the pharm treatment for type 1 diabetes?

A

SC insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is the pharm treatment for type 2 diabetes?

A

antihyperglycemic agents, insulin (late in disease), control systemic complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the primary common feature between type 1 and type 2 diabetes?

A

hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

elevated blood glucose levels can have what clinical presentation?

A

fatigue, increased thirst (polydipsia), frequent urination (polyuria), exercise intolerance and dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

why does diabetes make people tired?

A

glucose cant enter cells to be used as energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what can happen in extreme and prolonged cases of diabetes due to glucose getting trapped in the blood?

A

ketoacidosis, cognitic impairments, visual impairment, renal dysfunction, CVD, circulatory problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is the 1st line treatment for type 2 diabetes?

A

lifestyle: reducing weight, increasing exercise, reducing sugar intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what are 2nd line & adjunct pharm treatments for type 2 diabetes?

A

metformin, insulin secretagogues, incretin agents or gliflozins (all anti-hyperglycemics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

as type 2 diabetes progresses, insulin-producing ability of the pancreas often ____ (increases or decreases)

A

decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what are the 3 main goals of insulin replacement therapy?

A
  1. closely mimic physiologic secretion of insulin
  2. regulate blood glucose levels, prevent hyperglycemia
  3. minimize risks of hypoglycemia
59
Q

t/f insulin therapy mimics the physiologic release of insulin to prevent hypoglycemia between meals

A

t

60
Q

why does insulin need to be given SC and cant be given PO?

A

it is a peptide hormone that is too big and would be broken down in the stomach

61
Q

t/f IV insulin can be given in hospital

A

t

62
Q

t/f protein/peptide therapeutics must be carefully stored to prevent degradation

A

t

63
Q

what is the MOA of insulin replacement therapy?

A

insulin gets absorbed into the systemic circulation and activates insulin receptors on target cells, which increases the presence of GLUT-4 transporters, allowing glucose uptake into these cells for metabolism (just like how endogenous insulin would work)

64
Q

there are many different types of insulin and their key differences are related to ______ variations between formulas

A

PK

65
Q

what is the effect of the PK variations between formulas of insulin?

A

affects the rate of absorption at the site of administration

66
Q

when is rapid acting insulin given?

A

just before a meal

67
Q

what is the onset of action of rapid onset insulin?

A

5-15 min

68
Q

what is the duration of action of rapid acting insulin?

A

3-4 hrs

69
Q

when does regular insulin need to be given ?

A

30 min before a meal

70
Q

what is the onset of action for regular insulin?

A

30-60 minutes

71
Q

what s the duration of action for regular insulin?

A

6-8 hours

72
Q

intermediate and long acting insulin provide ____ insulin levels between meals and between bolus insulin doses

A

low, basal

73
Q

what is the onset time for intermediate insulin?

A

2-4 hours

74
Q

what is the duration of action for the intermediate insulin>

A

10-20 HRS

75
Q

what is the onset time of long acting insulin?

A

~1 hour, but there is no peak

76
Q

what is the duration of action of long acting insulin?

A

~17-24 hours

77
Q

what can happen if insulin administration and glucose intake are mismatched?

A

hyper or hypo glycemia

78
Q

what experimental treatments for type 1 diabetes are being trialed?

A

beta cell transplats, stem cell and gene therapy

79
Q

what is A1C?

A

a parameter that can be measured in routine blood tests which provides a more longitudinal picture of how well a patient’s blood glucose is controlled

80
Q

A1C is the abbreviated term used to describe ____

A

the glycosylated form of hemoglobin

81
Q

when glucose levels are elevated for a long time, proteins in the blood, such as hemoglobin in RBCs can become ______

A

glycosylated

82
Q

the % of RBC that have been glycosylated is indicated by the %____

A

A1C

83
Q

the %A1C is used to indicate the extent and duration of ____ in patients

A

blood glucose elevations

84
Q

an RBC typically circulates in the blood for about 3 months, so the % A1C value can be seen as ____

A

a 3 month running avg of blood glucose control

85
Q

in most cases, the desirable % A1C is below ___ %

A

7

86
Q

what is typically the first pharm choice for type 2 diabetes>

A

metformin

87
Q

why is metformin the 1st pharm choice for type 2 diabetes?

A

acts by several mechanisms to reduce blood glucose levels and improve glucose utilazation by cells

88
Q

the most significant pharm effect of metformin involves the stimulation of ____ pathways in the liver to reduce de novo synthesis of ___

A

AMP kinase; glucose

89
Q

by metformin blocking AMP kinase pathways to make new glucose, what does it force the body to do?

A

use stored glucose (such as fat)

90
Q

metformin improves ____ of target cells so that glucose can be taken up and metaboliszed more effectively

A

insulin sensitivity

91
Q

metformin reduces the absorption of ____ from dietary sources in the GI tract, forcing the body to use up its stores

A

glucose

92
Q

t/f patients typically experience weight loss when starting metformin

A

t

93
Q

what happens if metformin alone is not enough to llower A1C to the target range?

A

additional antihyperglycemic agents ae considerd based on patient factprs

94
Q

t/f some anti-hyperglycemics also have CV benefits, so if a patient has CV concerns on top of diabetes, these are typically chosen

A

t

95
Q

____ and ____ (anti-hyperglycemics) have been shown to have clinical benefit in patients with type 2 diabetes

A

empagliflozin and liraglutide

96
Q

the gliflozin drug class is relatively new, with the fist agent approved in Canada in the year ____

A

2014

97
Q

what is teh MOA of the gliflozin class such as empagliflozin?

A

inhibit the SGLUT2 glucose transporter in the kidney, which reduces the reabsorption of glucose from the urine, lowering blood glucose

98
Q

normally, ____% of glucose is reabsorbed at the proximal convoluted tuble

A

98

99
Q

gliflozins target SGLT2 trnasporters in which part of the renal system?

A

the proximal convoluted tubule

100
Q

why does empagliflozin help with CVD?

A

reduces BP by getting rid of more solute (glucose) through urination

101
Q

t/f bc empagliflozin causes more glucose excretion in the urine, it also causes more water excretion, lowering BP

A

t

102
Q

t/f the BP lowering effect of empagliflozin can be bad for normotensive patients

A

t

103
Q

why can empagliflozin lead to more UTIs?

A

more glucose in the urine allows bacteria to multiply rapidly in the bladder

104
Q

liraglutide is a ____ receptor agonist

A

GLP-1

105
Q

liraglutide belongs to which class of drugs?

A

incretin agents (class of antihyperglycemic)

106
Q

what is the MOA of incretins like liraglutide?

A

naturally secreted in the GI tract when food is consumed, bind to GLP-1 on B cells and increase insulin secretion and when on GLP-1 on A cells, signals that glucose is on the wasy , so there is no need to secrete glucogon or make new glucose

107
Q

do incretins like liraglutide increase or decrease gluconeogenesis?

A

decrease

108
Q

GLP-1 activation enhances the closing of K channels and opening of Ca channels through a ____mediated pathway

A

cAMP

109
Q

the GLP-1 receptor is a ___ coupled G protein receptor

A

Gs

110
Q

activation of the GLP-1 receptor causes an increase in ___, which activates ___, which phosphorylates _____ in the cell, allowing more ____entry, which enhances the release of ___

A

cAMP, PKA, ion channels, Ca, insulin

111
Q

normally, GLP-1 is broken down quickly ny an enzyme called ____

A

DPP4

112
Q

the half life of endogenous GLP-1 is only ____, so the boose in insulin secretion is only trnasient

A

a few min

113
Q

can the GLP-1 pathway cause insulin secretion on its own?

A

no, glucose needs to be present to initiate the closing of the K channels and cause depolarization

114
Q

why is using liraglutide on GLP-1R more efficient that the endogenous hormone?

A

it has a much longer half-life

115
Q

what is the MOA of DPP4 inhibitors like sitagliptin?

A

prolong the presence of endogenous GLP-1, causeing more insulin release

116
Q

t/f sitagliptan has good oral F and T1/2 that only needs to be dose once daily

A

t

117
Q

what is the oral f of sitagliptan?

A

85%

118
Q

what is the t1/2 of sitagliptan?

A

12 hours

119
Q

how is liraglutide administered?

A

Sc injection

120
Q

t/f sitagliptide relies on the body’s production of GLP-1 in the GI tract

A

t

121
Q

does sitagliptaide have any addded benefit for CVD?

A

no

122
Q

what is a down fall of the gliflozins and liraglutide?

A

very $$$

123
Q

t/f older agents like glyburide are less $$

A

t

124
Q

glyburide belongs to what class of AHGs?

A

insulin secretagogues

125
Q

what is the MOA of insulin secretagogues like glyburide?

A

bind to receptors on the beta cells and stimulate them to release insulin from the pancreas

126
Q

secretagogues are only effective if ____ and ____

A

the pacreas is able to make insulin and the process is independennt of glucose

127
Q

glyburide blocks ____

A

ATP K channels

128
Q

when glyburide binds to the K channels, this results in beta cells becoming ____

A

depolarized

129
Q

the depolarization of b cells caused by glyburide causes an influx of ___ ions and a release of ___

A

Ca; insulin

130
Q

how can glyburide cause insulin release independent of glucose?

A

removes the need for ATP to open the K channels, which would have needed the breakdown of glucose

131
Q

what is a clinical downfall of glyburide?

A

can cause high levels of circulating insulin without the influx of glucose from a meal can cause hypogylcemia

132
Q

what are the presenting symptoms of hypoglycemia?

A

sudden onset of hunger, weakness, increased HR, which can result in dizziness, falls

133
Q

reversal of hypoglycemia can be achieved by administering __

A

glucose

134
Q

what is the ideal formulatiion to give glucose to a patient who is hypoglycemic?

A

something that dissolves readily or fruit juice bc they can be quickly absorbed by the GI tract

135
Q

prolonged periods of hypoglycemia can result in ___

A

ketoacidosis

136
Q

why can prolonged periods of hypoglycemia result in ketoacidosis?

A

cells begin to breakdown ketones for energy

137
Q

can ketoacidosis be life-threatening>

A

yes

138
Q

which AHG agents are notorious for causing hypoglycemia?

A

secretagogues

139
Q

diabetic ___ can lead to vision loss

A

retinopathy

140
Q

diabetic renal dysfuction can become so severe that pts require ___

A

dialysis

141
Q

t/f diabetic pts are at higher risk for CVD and MI

A

t

142
Q

t/f there is an increased risk of infection in diabetes

A

t

143
Q

why is peridontal disease higher in diabetic patients

A

dry mouth (?)

144
Q

t/f diabetic pts can experience peripheral neurpathies

A

t

.Pharmacology (55 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions