Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology II-Exam 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Endocrine secretes to…

A

Distant Sites

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

Paracrine secretes to…

A

Adjacent sites

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

Autocrine secretes to…

A

At origin

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

Intracrine secretes to…

A

Within origin

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

The pancreas controls what hormones?

A

Insulin, glucagon, & amylin

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

The pituitary gland controls what hormones?

A

GH, ACTH (adrenocorticotropic hormone), Oxytocin, ADH (vasopressin), Prolactin, LH, & FSH (follicle-stimulating hormone)

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

The hypothalamus controls what hormones?

A

GnRH (gonadotropin hormone-releasing hormone), Dopamine, CRH (corticotrophin-releasing hormone), GHRH (growth hormone-releasing hormone), & Somatostatin

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

The thyroid controls what hormones?

A

Thyroxine, Triiodothyronine, & calcitonin

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

The adrenal gland controls what hormones?

A

Epi, Norepi, aldosterone, cortisol, & sex steroids

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

The parathyroid controls what hormone?

A

PTH (parathyroid hormone)

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

What do endocrine hormones do when they initially bind to membrane receptors?

A
  1. Initiate signal transduction
  2. Activate cellular 2nd messengers
  3. Regulate gene expression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name 3 ways in which endocrine hormones can be dysfunctional

A
  1. Excess
  2. Deficiency
  3. Resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the main determinant of homeostasis?

A

Hypothalamus

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

What happens when hormones are released to a receptor?

A

They travel to pituitary gland and bind G-protein, which then activates adenyl cyclase, which then increases cAMP, then releases secretory hormones

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

The anterior of the pituitary releases what hormones?

A

Growth Hormone (bulk)

Adrenocorticotropic

Thyroid-Stimulating

Prolactin

LH &FSH

Beta-lipotropin

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

The posterior side of the pituitary gland releases what?

A

Vasopressin & Oxytocin

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

Which hormone is the most abundant?

A

GH

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

GH especially stimulates

A

Skeletal growth, but stimulates all tissues

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

How does GH enhance metabolic effects?

A
  1. Protein synthesis
  2. Lypolysis & mobilization of free fatty acids
  3. Na & H2O retention
  4. Antagonism of insulin & increased glucose availability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is GH stimulated?

A

Stress, sleep, hypoglycemia, & fasting

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

How is GH inhibited?

A

Pregnancy, hyperglycemia, cortisol, & obesity

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

Adrenocorticotropic Hormone (ACTH) regulates…

A

Secretion of cortisol & androgens

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

When is ACTH the highest & at its lowest?

A

AM
PM

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

What stimulates ACTH?

A

Stress

Sleep-wake transition

Hypoglycemia

Alpha agonist

Beta antagonist

CRH & decreased cortisol

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

What inhibits ACTH?

A

Increased cortisol

Opioids

Etomidate

Suppression of the HPA Axis

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

When is cortisol needed?

A

In times of physical stress, illness, or surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Decreased cortisol will cause the body to have…

A

Low BP, glucose, Na

High blood potassium

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

MOA of Alpha-2 agonist

A

Stimulate presynaptic α2-adrenergic receptors in the CNS → dilates peripheral blood vessels → lowers peripheral resistance → reduces blood pressure

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

MOA of Beta-adrenergic blockers/Beta antagonists

A

Block β receptors → prevent catecholamines (norepinephrine and epinephrine) from binding and activating them → decrease cardiac contractility, decrease conduction velocity through AV node, decrease heart rate, cardiac output, and blood pressure

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

Role of Thyroid Stimulating Hormone (TSH)

A

Accelerates thyroid hormone formation

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

When is TSH stimulated?

A

When there are low levels of T3, T4, & calcitonin

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

When is TSH inhibited?

A

Stress, surgery, SNS stimulation, or increased corticosteroids

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

Where is vasopressin produced & transported?

A

Produced in hypothalamus & transported in secretory granules

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

Where is the reservoir for vasopressin?

A

The posterior pituitary is the reservoir for release

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

What is the physiologic function of vasopressin?

A

Vasoconstriction
Water retention
Corticotropin secretion

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

When is vasopressin stimulated?

A

HOTN

Increased plasma osmolarity

Hyperthermia

N/V

Opioids

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

When is vasopressin inhibited?

A

Decreased Osmolarity

Cortisol

Hypothermia

Ethanol

Alpha agonists

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

Macroadrenomas often create a mass effect and cause functioning issues which is…

A

Overproduction of hormnoes

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

With macro adenomas, which hormone secretion is treated medically?

A

Prolactin

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

in acute surgery 9pituitary tumor removal), which glucocorticoid will the surgeon ask you to administer?

A

Hydrocortisone or methylprednisolone

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

What treats GH deficiency?

A

Recombinant growth hormone

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

What are the adverse effects of Recombinant growth hormone?

A

Edema, Myalgia, & arthalgias

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

Recombinant growth hormone interacts with

A

Corticosteroids & insulin, decreasing their effectiveness

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

Octreotide is what type of medication?

A

Somatostatin analogue

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

Octreotide inhibits…

A

GH release & treats acromegaly & acute upper GIB by decreasing blood floe and gastric acid secretion

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

Adverse effects of Octreotide

A

Edema, hyperglycemia, bradycardia, nausea, & increases QTc

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

What is the purpose of administering Cosyntropin?

A

Cosyntropin, a synthetic ACTH, is used to screen for adrenocortical insufficiency and increases cortisol release

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

Why isn’t cosyntropin given as a treatment?

A

Because it would increase release of ALL adrenal hormones

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

Where is melatonin secreted?

A

Pineal Gland

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

How is melatonin secreted and what does it regulate?

A

Stimulated by darkness & regulated circadian rhythm & sleep mood; may regulate reproduction, tumor growth, & aging; may improve delirium

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

Vasopressin can be used to treat…

A

Central DI in neurotrama, pituitary & hypothalamic surgery, cerebral malignancy, ischemia, excess water loss w/ hypernatremia, HOTN, shock, cardiac arrest, excessive blockade of RAAS

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

Vasopressin works on what receptors?

A

V1 & V2 receptor agonists

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

When are plasma vasopressin concentrations decreased?

A

In sepsis

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

What is a selective V2 agonist?

A

Desmopressin (DDAVP)

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

MOA of DDAVP (V2 agonist)

A

It activates Gs stimulatory protein, which activates adenyl cyclase, increasing cAMP in collecting ducts cells, increasing exocytosis of vesicles containing aquaporins (intense antidiuretic effect)

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

DDAVP can cause endothelial cells to release…

A

von Willebrand factor, which can treat hemophilia A, von Willebrand, & liver disease

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

What does can be given of DDAVP prior to surgery?

A

0.3mcg/kg IV 30min. prior to a patient who is deficient in von Willebrand factor & factor 8

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

MOA of Vasopressin (V1 receptor)

A

Activates stimulatory Gq protein, which activates phospholipase C, increasing IP3, which increases intracellular Ca+ release

All causing intense vasoconstriction, myocardial hypertrophy, platelet aggregation, & ACTH release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Dose of Vasopressin

A

1-4 units (bolus)

0.01-0.04 units/min infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Adverse effects of vasopressin

A

Coronary ischemia

Angina

Dysrhythmias

Splanchnic & peripheral ischemia

Increased GI peristalsis, leading to N/V & ABD pain

Uterine stimulation

Allergic reaction & anaphylaxis

Antibody formation w/long-term use

May decrease platelet count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

MOA of oxytocin

A

Increases intracellular calcium in uterine smooth muscle, which causes uterine muscle contraction

Causes contraction of the myoepithelial cells around milk-containing alveoli, resulting in milk ejection during lactation

Induces labor, reducing & preventing uterine atony

Reduces blood loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Labor dose of oxytocin

A

8-10mU/min IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Atony dose of oxytocin

A

1-5 International units IV bolus over 30sec

64
Q

Adverse Effects of Oxytocin

A

Direct vascular smooth muscle relaxation

Transient decrease in SBP/DBP, venous return & CO

Reflex Tachy & arrhythmia

Higher risk w/anesthetic-induced blunting or compensatory reflex mechanism

Higher risk in hypovolemia

65
Q

Adverse effects of Oxytocin in relation to fetus & neonate

A

Fetal hypoxia & hypercapnia

Variable decelerations of fetal HR

Neonatal jaundice & seizure

Low Apgar score

66
Q

What are the 3 pancreas cells

A

Alpha, beta, & delta

67
Q

What does the pancreas secrete?

A

Digestive substances into duodenum (exocrine)

Secrete insulin, glucagon, somatostatin & pancreatic polypeptide (Endocrine)

68
Q

Alpha cells & glucagon are what percent of islet cells and secrete what hormone?

A

25%

Catabolic hormone

69
Q

The catabolic hormone released in alpha cells do what?

A

Mobilizes glucose fatty acids & amino acids for use

Metabolized by liver w/ 1/2 time 3-6min

70
Q

In the alpha cells, catabolic hormone is stimulated by

A

Hypoglycemia

Stress, trauma

Beta Agonists

Acetylcholine

Cortisol

71
Q

In alpha cells, catabolic hormone is decreased by

A

Hyperglycemia

Free fatty acids

Insulin & somatostatin

Alpha agonists

72
Q

In Beta cells with glucagon, glucagon binds ______&_______ receptors

A

Glucagon & GLP-1

73
Q

In Beta cells with glucagon, binding of glucagon & GLP-1 receptors causes…

A
  1. Activation of adenyl cyclase
  2. Increases cAMP
  3. Modulates insulin release
74
Q

Beta cells & insulin account for what percentage of islet cells?

A

60%

75
Q

In Beta cells, Insulin is a ________hormone, which promotes________

A

Anabolic (builds up) hormone

Promotes storage of glucose, fatty acids & amino acids

Hepatic& renal metabolism with 1/2 time 5 min

76
Q

In Beta cells with insulin, the anabolic hormone is stimulated by…

A

Hyperglycemia

Beta Agonist

Acetylcholine

Glucagon

77
Q

In Beta cells, anabolic hormone is decreased by…

A

Hypoglycemia (inhibits K+ channels)

Beta Antagonoists

Alpha antagonists

Insulin & somatostatin

Volatile Anesthetics

Thiazide diuretics

78
Q

Glucose & Insulin relationship

A

Uptake & use promoted

Increases activity of glucokinase

Increases permeability of skeletal muscle

79
Q

Fat & insulin relationship

A

Increases storage in adipose

Inhibits lipase (lipolysis)

80
Q

Protein & Insulin relationship

A

Increases uptake & conservation of amino acids

Decreases degradation

81
Q

Delta cells & Somatostatins account for______of islet cells

A

5%

82
Q

Somatostatin, a ______hormone does the following:

A

Inhibitory hormone

Regulates islet cell secretion

Inhibits insulin & glucagon release

Inhibits gallbladder contraction, gastric motility & splanchnic blood flow

83
Q

Characteristics of Type I DM

A

Autoimmune

Destruction of pancreatic beta cells

Normal insulin sensitivity

84
Q

Characteristics of Type II DM

A

Pancreatic beta cell dysfunction

Failure to secrete insulin & insulin resistance

May/may not need insulin

85
Q

What causes the release of insulin

A

Released in response to increase in serum glucose

86
Q

Insulin promotes

A

Glucose uptake by fat & muscle

87
Q

Insulin inhibits

A

Gluconeogenesis

Glucogenolysis

88
Q

Insulin is a/an ________ hormone that promotes building of macromolecules and__________________________

A

Anabolic hormone

Storage & uptake of fats & glucose

89
Q

Patients with Type 2 DM will have issues with_________at the cellular level

A

Translocation

90
Q

At the cellular level, insulin is increased by

A

Beta-adrenergic or PSNS stimulation

91
Q

At the cellular level, insulin is decreased by

A

Alpha adrenergic stimulation

92
Q

How many units of insulin are secreted per day?

A

40

93
Q

What is the reservoir of insulin?

A

Skeletal muscle & adipose tissue

94
Q

How long does it take insulin to work

A

30-60 minutes

95
Q

Insulin relationship in liver & kidney

A

Enzymatic metabolism ini liver & kidney with an elimination 1/2 time of 5-10 min

Prolonged effects ini renal disease

96
Q

What happens in the absence of insulin?

A

Lipolysis & increase in fatty acids

Excess ketones

Acidosis

97
Q

What happens when insulin is low or when there is insulin resistance?

A

Hyperglycemia will cause:

Proinflammation

Prothrombotic

Proatherogenic

Impaired vasodilation

98
Q

DM on the macrovascular side will cause

A

Coronary issues like HF & death

Cerebrovascular effects like stroke

PVD

99
Q

DM on the microvascular side will cause

A

Neuropathy (issues w/conduction)

Nephropathy, leading to ESRD

Retinopathy (cause of blindness)

100
Q

The surgical stress response will causes_______& the release of _______

A

Neuroendocrine stress response

Release of epi, glucagon, cortisol, GH, & inflammatory cytokines

101
Q

Risks of Neuroendocrine stress response include

A

Acute insulin resistance & impaired secretion

Decreased peripheral glucose utilization

Lipolysis

Protein catabolism

Hyperglycemia

102
Q

What in crease your chances of having a surgical stress response?

A

GA, type of surgery, & additional factors such as sepsis, inflammation, or glucocorticoid use

103
Q

Which labs should the NAP student assess?

A

FSBS, renal, A1C

104
Q

Risks of neuropathy include

A

CV instability

Delayed Gastric emptying

OSA

Increased sensitivity to LA

105
Q

Increased sensitivity to LA can cause

A

Losses in sensation

Increased risk of nerve damage

Prolonged duration of action

106
Q

Slow, long acting insulin include

A

NPH, insulin glargine & insulin detemir

107
Q

Rapid, short acting insulin includes

A

Insulin aspart, Lispro, & Glulisine

108
Q

Insulin receptors are fully saturated at ______concentrations

A

Low (tight binding)

109
Q

Lispr o& insulin aspart are usually given

A

30-60 min before meals with a duration of 3-5 hours

110
Q

NPH is ________acting and is conjugated with_________

A

Intermediate acting

Protamine (developed sensitivity with long term use)

111
Q

Glargine & detemir are _____acting and are usually administered at _______

A

Long

Night (basal replacement for 24 hours)

112
Q

Which insulin therapy should be decreased by 50% before surgery?

A

NPH, glargine & detemir

113
Q

Regular insulin is used to treat

A

Abrupt onset of hyperglycemia & ketoacidosis

114
Q

IV onset of regular insulin?

SQ?

A

IV 10-15min

SQ 30-60min

115
Q

When should SQ insulin be avoided?

A

In hemodynamically unstable patients, hypothermia, & vasoconstriction

116
Q

What is the duration of IV & SQ insulin?

A

2-8 hours

117
Q

Does insulin bind to IV tubing?

A

Yes

118
Q

Goal of serum glucose

A

<180
>70

119
Q

Things to consider with SQ insulin correction

A

Surgery <4hours

They are hemodynamically stable w/minimal fluid shift

Not dosing more than Q2h

Monitor at leaast Q2h

Consider dose reduction in sensitive populations such as >70yrs, renal insufficiency, & no hx of DM

120
Q

Things to consider with continuous insulin infusion

A

Surgery >4hrs

Hemodynamic fluctuations

Use of inotropes

Massive fluid shift or temperature changes

Critically ill

Cardiac surgery

121
Q

Interventions when given Insulin continuously

A

Allows for rapid dose adjustments

Monitor BS hourly

Monitor K+ & HCO3-, Ca+

Do not abruptly stop

122
Q

Types of correctional insulin combinations that can be given

A

Insulin I& glucose t prevent hypoglycemia

Glucose-Insulin-Potassium (GIK) infused at 100ml/hr

123
Q

An insulin pump provides

A

Continued basal insulin, that should be monitored hourly & should be turned off is BS<110 and given additional insulin if BS<180

124
Q

Adverse effects of Insulin

A

Hypoglycemia

Hypokalemia

Allergic reaction/injection site reactions

Insulin resistance (acute)

125
Q

Signs of hypoglycemia

A

Tachycardia

Diaphoretic

HTN

Confusion

Seizures

126
Q

Hypoglycemia can be corrected with IV dextrose at

A

IV dextrose 5-25g

Onset <10min

127
Q

How should IV dextrose be given

A

Large PIV

Central Line

Administer slowly

Flush

128
Q

IV glucagon is a

A

Treatment for hypoglycemia

Insulin antagonist

Dose 0.5-1mg

Dilute w/sterile water

Also relaxes GI smooth muscle

129
Q

Insulin stimulates the _____pump and you should monitor for_______

A

NaK pump

Monitor for hypokalemia with insulin therapy

130
Q

How to treat hyperkalemia

A

Insulin + Dextrose (will temporarily shift K+ back into cell within 15min & lasts 2hrs

5-10 units IV insulin

25-50 g dextrose UNLESS hyperglycemia >200

131
Q

What is the first line treatment of Type II

A

Metformin, which is apart of the Biguanide class

132
Q

Does metformin cause hypoglycemia?

A

Rarely

133
Q

MOA of metformin

A

Suppression of hepatic glucose production

Decreases GI glucose absorption

Increases insulin sensitivity by peripheral tissues

Increases GLP-1 synthesis

134
Q

Adverse effects of Metformin

A

GI* (nausea, anorexia, diarrhea)

VIT B12 deficiency

Lactic Acidosis

High risk of hepatic or renal dysfunction

135
Q

When to give/hold metformin

A

Give in ambulatory surgery/minor cases, but hold for renal dysfunction, use of contrast/NSAIDS ACEI or ARBS

Hold day of for major surgery & restart w/in 24 hours

136
Q

MOA of sulfonylureas

A

Inhibit K+ ATP channels on beta cells (sulfonylurea receptor 1), causing Ca+ to enter cell and exocytosis of insulin

137
Q

Sulfonylureas require____& have a high risk of_____

A

Beta cell function

High risk of therapy failure

138
Q

Benefit of Sulfonylureas

A

Can drastically lower BS and decrease insulin resistance

Ineffective in Type I

139
Q

Examples of Sulfonylureas

A

Glyburide
Glipizide
Glimepiride
Chlorpropamide

140
Q

Adverse effects of Sulfonylureas

A

Hypoglycemia
CV risks (older drug)
GI issues
Abnorm liver function

141
Q

Hypoglycemia with Sulfonylureas is most common with what risks?

A

Drugs w/long half times

Malnutrition

> 60yrs

Impaired renal function

ETOH, warfarin, sulfonamide abx, or other drug interaction

More severe than insulin-induced hypoglycemia

142
Q

Examples of Thiazolidinediones (TZDs)

A

Rosiglitazone
Pioglitazone

143
Q

MOA of Thiazolidinediones (TZDs)

A

Increases insulin sensitivity at skeletal muscle, hepatic & adipose tissue, which decreases insulin resistance & hepatic glucose production

Increases glucose use by tissues

144
Q

Thiazolidinediones (TZDs) can also

A

Increase HDL, decrease triglycerides

Increase ECF (edema, wt gain)

Cause liver dysfunction

Should be continued preoperatively

145
Q

GLP-1 Receptor Agonists examples include

A

-glutides
Tirzepatide
Exenatide

146
Q

MOA for GLP-1 Receptor Agonists

A

Increase beta cell insulin secretion & satiety

Decreased alpha cell glucagon production & appetite

Slow gastric emptying

Wt loss

147
Q

Adverser effects of GLP-1 Receptor Agonists

A

GI issues (N/V/D)

Hypoglycemia risk when combined w/sulfonylurea & insulin

Acute pancreatitis

Gallbladder & biliary disease risk (cholecystitis)

Acute renal insufficiency

Injection site reaction

Delayed gastric emptying

148
Q

MOA for Sodium-Glucose Cotransporter 2 inhibitors

A

Inhibits SGLT2 in proximal tubule

Requires normal renal function

149
Q

Examples of Sodium-Glucose Cotransporter 2 inhibitors

A

-gliflozins

150
Q

Sodium-Glucose Cotransporter 2 inhibitors can cause

A

Wt loss
Reduce BP
Reduce CV events

151
Q

Adverse effects of Sodium-Glucose Cotransporter 2 inhibitors

A

Osmotic Diuresis due t trapping of glucose, causing hypovolemia, HOTN, AKI (higher risk in ACEI & ARBS

Euglycemia (norm BS) ketoacidosis

UTI & genital nifections

Reduced bone density

152
Q

Sodium-Glucose Cotransporter 2 inhibitors considerations

A

Risk for ketoacidosis & dehydration

Hold morning of-days

Restart w/adequate PO intake

153
Q

MOA of Dipeptidyl-Peptidase-4 inhibitors

A

Inhibits DPP-4 enzyme which breaks down incretini hormone (GLP-1), which increases insulin secretion & decreases glucagon secretion (increases GLP-1)

154
Q

Examples of Dipeptidyl-Peptidase-4 inhibitors

A

-gliptin

155
Q

Risks associated with Dipeptidyl-Peptidase-4 inhibitors

A

Musculoskeletal pain & pancreatitis

Hypoglycemia risk low

156
Q

Should Dipeptidyl-Peptidase-4 inhibitors be continued or held?

A

Continued perioperatively

Pharmacology II-Exam 2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions