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Endocrine Flashcards

1
Q

Anterior pituitary gland releases

A

Growth Hormone (GH)

Adrenocorticotropic (ACTH)

Thyroid-stimulating (TSH)

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2
Q

Posterior pituitary releases

A

Arginine Vasopressin

Oxytocin

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3
Q

Growth hormone stimulates

A

All tissues, especially skeletal growth & cell proliferation

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4
Q

Growth hormone enhances what metabolic effects?

A

Protein synthesis

Lipolysis

Mobilization

Na+ & H2O retention

Antagonism of insulin & increased glucose availability

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5
Q

What stimulates GH?

A

Stress

Sleep

HYPOglycemia

Fasting

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6
Q

What inhibits GH?

A

Pregnancy

HYPERglycemia

Cortisol

Obesity

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7
Q

Recombinant GH is used to treat

A

GH deficiency

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8
Q

What are the side effects of recombinant GH?

A

Edema

Myalgia

Arthalgias

Interacts w/corticosteroids & insulin, decreasing its effectiveness

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9
Q

Octreotide is a

A

Somatostatin (inhibitory)

Inhibits GH release

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10
Q

Octreotide is the treatment choice for

A

Acromegaly & Acute upper GIB by decreasing sphintic blood flow & gastric acid secretion

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11
Q

What are the side effects of Octreotide?

A

Edema

HYPERglycemia

Nausea

QT increased

Bradycardia

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12
Q

ACTH regulates

A

The secretion of cortisol & androgens via cAMP

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13
Q

ACTH is stimulated by

A

CRH & decreased Cortisol

Stress

Sleep-wake transition

HYPOglycemia

Alpha agonist

Beta antagonist

Emergence/pain

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14
Q

ACTH is inhibited by

A

Increased cortisol

Opioids

Etomidate

Suppression of HPA

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15
Q

What is the use of Cosyntropin?

A

Synthetic ACTH used to screen for adrenocortical insufficiency & increases cortisol release

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16
Q

What are the side effects of Cosyntropin?

A

Hypersensitivity

Anaphylaxis

HYPOkalemic metabolic alkalosis

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17
Q

Cosyntropin has what effects?

A

Mineralocorticoid

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18
Q

What stimulates the Thyroid hormone?

A

Low T3, T4 & Calcitonin

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19
Q

What inhibits TSH?

A

Surgery

Stress

SNS stimulation

Corticosteroids

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20
Q

Where is arginine vasopressin reserved? Produced?

A

Pituitary is reservoir

Produced in hypothalamus

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21
Q

Arginine vasopressin will cause

A

Vasoconstriction

Water retention

Increase in Corticotropin Secretion

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22
Q

What stimulates Arginine vasopressin?

A

Increase in plasma osmolarity

Hypovolemia

HOTN

Pain/Stress

HYPERthermia

N/V

Opioids

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23
Q

How is Arginine vasopressin Inhibited?

A

Decrease in osmolarity

Cortisol

HYPOthermia

Ethanol

Alpha agonists

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24
Q

Which V receptor treats HOTN related to shock/cardiac arrest?

A

V1

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25
Q

Vasopressin concentrations are

A

Low in sepsis

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26
Q

What can reverse refractory HOTN?

A

Supraphysiologic concentrations

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27
Q

Which V receptor treats central DI?

A

V2

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28
Q

Desmopressin (DDAVP) is a selective _____agonist with this dose

A

V2

0.3mcg/kg over 30 min

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29
Q

DDAVP can treat

A

Central DI

Hemophilia A

vWF

Liver disease

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30
Q

MOA of DDAVP

A

Gs–>adenyl cyclase–> increased cAMP, causing vesicles to release aquaporins

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31
Q

Vasopressin works on which receptor?

A

V1

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32
Q

How is vasopressin activated (same for oxytoin)?

A

Gq–>Phospholipase C–> increased IP3–> increases intracellular Ca+ release

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33
Q

Vasopressin can be given to

A

Patients with pulmonary HTN, due to its effects on SVR

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34
Q

What is the dose of Vasopressin?

A

1-4 units (bolus)

0.01-0.04 units/min infusion

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35
Q

Activation of the Gq cascade will lead to

A

Intense vasoconstriction (SVR> PVR)

Myocardial hypertrophy

PLT aggregation

ACTH release

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36
Q

What are the adverse effects of Vasopressin?

A

Ischemia

Angina

Increased GI peristalsis leading to N/V & ABD pain

Uterine stimulation

Decreased PLT count

Allergic reaction

Antibody formation

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37
Q

Dose of Oxytocin

A

Labor 8-10mU/min IV

Atony 1-5 international units IV bolus (up to 40; over 30 seconds)

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38
Q

What are the fetal adverse effects of oxytocin?

A

Fetal hypoxia/hypercapnia

Neonatal jaundice & seizure

Low APGAR

variable decelerations of fetal HR

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39
Q

Adverse effects of Oxytocin?

A

Direct Vascular smooth muscle relaxation, leading to transient decrease in BP, venous return & CO

Reflex tachycardia

Arrhythmia

Higher risk w/general & hypovolemic patient

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40
Q

Which glucocorticoids are often given for pituitary adenoma?

A

Hydrocortisone

Methylprednisolone

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41
Q

Glucagon is

A

Catabolic, meaning it breaks down complex molecules for energy

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42
Q

Glucagon stimulates

A

Gluconeogenesis

Glucogenolysis

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43
Q

Glucagon helps

A

Mobilize glucose, fatty acids & amino acids

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44
Q

Glucagon’s release is stimulated by

A

HYPOglycemia

Stress/trauma

Beta Agonists

ACh

Cortisol

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45
Q

Glucagon’s release is inhibited by

A

HYPERglycemia

free fatty acids

Insulin & somatostatin

Alpha agonists

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46
Q

Glucagon binds glucagon & GLP-1 receptors which

A

Activates adenyl cyclase, increases cAMP & modulates insulin release

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47
Q

Insulin is

A

Anabolic, meaning it builds up & promotes storage

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48
Q

Insulin’s release is stimulated by

A

HYPERglycemia

Beta Agonists

ACh

Glucagon

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49
Q

Insulin’s release is inhibited by

A

HYPOglycemia

Beta Antagonists

Alpha Agonists

Insulin & somatostatin

Volatile Anesthetics

Thiazide diuretics

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50
Q

Anesthetics inhibit

A

K+ channels on Beta cells, causing a decrease release of insulin

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51
Q

Insulin increases the activity of

A

Na/K pump, causing hypokalemia (K+ moves from blood stream to inside the cell)

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52
Q

Insulin can treat

A

Hyperkalemia

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53
Q

Insulin increases the activity of

A

Glucokinase, which helps promote glucose storage

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54
Q

Insulin inhibits

A

Lipase (Lipolysis)

Gluconeogenesis/lysis

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55
Q

Insulin decreases

A

Protein degradation

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56
Q

Insulin increases

A

Permeability of Skeletal muscle

Uptake of protein & conversion of amino acids

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57
Q

Insulin’s effects are prolonged in

A

Renal disease

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58
Q

GLUT4=

A

Translocation

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59
Q

Insulin is increased by _____adrenergic

Decreased by _______ adrenergic

A

Beta adrenergic (PSNS stimulation)

Alpha adrenergic stimulation

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60
Q

Insulin is absent in

A

Type 1

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61
Q

Absent insulin will cause

A

Lipolysis

Increase in free fatty acids

Excess Ketones

Acidosis

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62
Q

Low or insulin resistance can cause

A

Pro-inflammation

Pro-thrombotic

Pro-atherogenic

Impaired vasodilation

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63
Q

In type 1 DM, there is an increase risk of

A

Breaking down fat & increased fatty acids

Excess Ketones

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64
Q

Type 1 DM is classified as being

A

Autoimmune

Pancreatic cell destruction

Normal insulin sensitivity

Little insulin production

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65
Q

Type 2 DM is characterized as having

A

Pancreatic cell dysfunction

failure to secrete insulin & has insulin resistance

Problem with Translocation

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66
Q

The surgical stress response will cause an increase release of

A

Epi

Glucagon

Cortisol

GH

Inflammatory Cytokines

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67
Q

The surgical stress response will place the patient at a higher risk of

A

Acute insulin resistance

Impaired secretion

Decrease peripheral glucose utilization

Lipolysis

Protein Catabolism

Hyperglycemia

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68
Q

Neuropathy will cause

A

CV instability (resting tachy; post-induction HOTN; lability)

Delayed gastric emptying

Increased sensitivity to LA (prolonged duration)

OSA

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69
Q

Insulin receptors are ___________ at ___________ leading to a tight bond

A

Fully saturated

Low concentration

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70
Q

What are the slow & long acting insulin?

A

NPH (intermit acting)
Glargine
Insulin Detemir

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71
Q

What are the rapid & short acting insulin?

A

Insulin Aspart
Lispro
Glulisine

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72
Q

Rapid & short acting insulin have the duration of

A

3-5hrs

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73
Q

What is special about NPH?

A

There is a delay in SUBQ absorption d/t conjugation with protamine (which is used for heparin reversal)

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74
Q

What is the IV onset of regular insulin?

A

10-15 min

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75
Q

What is the SQ onset of regular insulin?

A

30-60min

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76
Q

What is the duration of regular insulin?

A

2-8 hrs

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77
Q

Regular insulin can

A

Bind to IV tubing

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78
Q

Administration should be reduced in what populations?

A

> 70

Renal insufficiency

No hx of DM

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79
Q

In a major surgery, what should be monitored?

A

BS Q1hr

K

HCO3

Ca

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80
Q

When should SUBQ insulin be avoided?

A

Hemodynamic instability

Hypothermia

Vasoconstriction

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81
Q

What are the s/s of hypoglycemia?

A

Tachycardia

Diaphoretic

HTN

Confusion

Seizure

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82
Q

Administration of insulin can cause an

A

Allergic reaction

Acute insulin resistance

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83
Q

What can go unrecognized?

A

Hypoglycemia when a patient is under general

84
Q

What is the solution & gram for IV dextrose?

A

2.5-70%

5-25g

85
Q

What is the onset of IV dextrose

86
Q

IV glucagon is an insulin

A

Antagonist

87
Q

What is the dose of IV Glucagon?

A

0.5-1mg

Dilute w/sterile water

88
Q

IV glucagon also

A

Relaxes GI muscle

89
Q

Insulin will decrease K by

90
Q

Which drug is the first line treatment for DM2?

A

Metformin (rare to cause hypoglycemia)

91
Q

Metformin can improve

A

Lipid profile

92
Q

What is the MOA of Metformin?

A

Suppression of hepatic glucose production

Decreases GI glucose absorption

Increases insulin sensitivity & GLP-1 synthesis

93
Q

What are the adverse effects of Metformin?

A

Gi disturbances

Vit B12 deficiency

LACTIC ACIDOSIS (due to inhibition of converting lactate to pyruvate)

94
Q

When should MEtformin be held?

A

Contrast

Renal dysfunction

NSAIDs

ACEI

ARBs

95
Q

What are examples of Sulfonylureas?

A

Glyburide

Glipizide

Glimepiride

Chlorpropamide

96
Q

Sulfonylureas drastically

A

Lower BS

Decrease insulin resistance

97
Q

Sulfonylureas require

A

Beta Cell function, so they are ineffective in Type 1 Dm

98
Q

What are the adverse effects of Sulfonylureas?

A

Therapy failure CV risks

GI

Abnormal liver function

99
Q

What should receive special attention with
Sulfonylureas?

A

HYPOGLYCEMIA, which is more severe than insulin induced hypoglycemia

100
Q

With a patient taking Sulfonylureas, the risk of hypoglycemia is elevated by

A

Malnutrition

> 60

Impaired renal function

ETOH

Warfarin

Sulfonamide ABX

101
Q

What is the MOA of Sulfonylureas?

A

Inhibits K ATP on beta cells

Ca+ enters cell

Insulin leaves the cell

102
Q

Sulfonylureas should be held

A

Morning of

103
Q

What are examples of Thiazolidinediones (TZDs)?

A

Rosiglitazone

Pioglitazone

104
Q

What is the MOA of Thiazolidinediones (TZDs)?

A

Increases insulin sensitivity & glucose use

Decreases insulin resistance & hepatic glucose production

105
Q

TZDs also increase__________ & decreases_______

A

HDL & ECF

Triglycerides

106
Q

TZDs should be continued

A

In peri-op

107
Q

TZDs can cause

A

Liver dysfunction

108
Q

What are examples of GLP-1 receptor agonists?

A

Liraglutide

Semaglutide

Dulaglutide

Tirzepatide

Exenatide

109
Q

What is the MOA of GLP-1 receptor agonists?

A

Increases beta cell insulin secretion & satiety

Decreases alpha cell glucagon production and appetite

110
Q

GLP-1 receptor agonists can cause

A

Wt loss

Slowed gastric emptying

111
Q

What are the adverse effects of GLP-1 receptor agonists?

A

Gi disturbances

Hypoglycemia (when combined w/sulfonylureas & insulin)

Acute pancreatitis & renal insufficiency

Gallbladder & biliary disease risk

Injection site reaction

112
Q

What are examples of sodium glucose cotransporter inhibitors? (SGLT2)?

A

Canagliflozin

Dapagliglozin

Empagliflozin

113
Q

What is the MOA of sodium glucose cotransporter inhibitors (SGLT2)?

A

Inhibits SGLT2 in the proximal tubule

114
Q

Sodium glucose cotransporter inhibitors (SGLT2) require

A

Normal renal function

115
Q

Sodium glucose cotransporter inhibitors (SGLT2) can cause

A

Wt loss

Decreased BP & CV events

116
Q

What are the adverse effects of Sodium glucose cotransporter inhibitors (SGLT2)?

A

Osmotic diuresis due to glucose trapping (hypovolemia, HOTN, AKI; higher risk with ACEI & ARBs)

Euglycemic ketoacidosis

UTI & genital infections

Decreased bone density

117
Q

What is the anesthetic consideration with Sodium glucose cotransporter inhibitors (SGLT2)?

A

Risk for ketoacidosis & dehydration

118
Q

What are examples of Dipeptidyl- peptidase 4 inhibitors?

A

Saxagliptin

Sitagliptin

Linagliptin

Alogliptin

119
Q

What is the MOA of Dipeptidyl- peptidase 4 inhibitors?

A

Inhibits DPP4 enxyme, which breaks down incretin hormones

Increases insulin secretion

Decreases glucagon secretion

120
Q

DDP4 inhibitors have a very low risk of

A

Hypoglycemia

121
Q

DPP4 inhibitors have a risk of

A

Musculoskeletal pain

122
Q

Metformin

A

Decreases endogenous glucose production

123
Q

TZDs

A

Increase glucose uptake

124
Q

DPP4 inhibitors

A

Increase incretins

125
Q

Sulfonylureas

A

Increase insulin

Decrease glucagon

126
Q

SGLT2 inhibitors

A

Decrease tubular glucose reabsorption

127
Q

The thyroid maintains

A

Optimal metabolism for tissue function

128
Q

T3 is also known as

A

Triiodothyronine

Active form

129
Q

T3 comes from

A

T4 synthesis

130
Q

T3 increases

A

O2 consumption & metabolism

131
Q

T3 is involved in

A

Protein catabolism

132
Q

T4 is known as

A

Thyroxine & is synthesized from tyrosine

133
Q

Calcitonin will decrease

A

Concentration of Ca in the plasma

134
Q

Calcitonin on osteocytes

A

Weakens osteoclasts

Strengthens osteoblasts

135
Q

Calcitonin will cause a decrease in

A

Renal reabsorption of Ca+ & phosphates

136
Q

What causes Hypothyroidism?

A

Deficient thyroid production

Iodine Deficiency

Autoimmune disease

137
Q

Which 2 drugs are used for hypothyroidism?

A

Levothyroxine (synthroid)

Liothyronine (T3)

138
Q

Levothyroxine is synthetic

139
Q

Synthroid will increase

A

metabolism

SNS activity

Growth & development

(DNA transcription)

140
Q

Levothyroxine affects

A

Protein synthesis

141
Q

T3 binds

A

Thyroid hormone receptors

142
Q

Liothyronine is

A

More potent but less effective & has no effect on hypothyroid symptoms

143
Q

Does hypothyroidism affect MAC?

144
Q

Levothyroxine may cause

A

Synergism with anticoagulants & epi

(lead to bleeding & exaggerated effect with epi)

145
Q

Non-euthyroid patients may experience

A

Sedation

Delayed emergence

Respiratory depression

Respiratory muscle weakness

Vasopressor resistant HOTN

Bradycardia

Diastolic dysfunction

Diminished response to alpha & beta adrenergic

Decreases BS

Anemia

Hypothermia

146
Q

What disease is characterized as hyperthyroidism?

A

Grave’s (autoimmune disorder of TSH receptor antibodies)

147
Q

What are risk factors of thyroid storm?

A

Surgery

trauma

Acute illness

Pregnancy

148
Q

What are s/s of thyroid storm?

A

Hyperthermia

Agitation

Delirium

Seizures

tachycardia

Afib

HF

Diarrhea

Jaundice

149
Q

What are examples of Thionamides?

A

Methimazole

Propylthiouracil (PTU)

Carbimazole

150
Q

What is the MOA of Thionamides?

A

Inhibits thyroid peroxidase & formation of TH

Decreases concentration of antithyrotropin receptor antibodies

PTU inhibits deiodination of T4–>T3

151
Q

What are the adverse effects of Thionamides?

A

Urticaria

Skin rash

Arthralgia

GI discomfort

Agranulocytosis & granulocytopenia (monitor WBC)

Hepatic toxicity

152
Q

What are examples of Potassium Iodides?

A

Potassium Iodide

Potassium Iodid-iodine (Lugol’s)

153
Q

What is the MOA of Potassium Iodides?

A

Decreases iodine uptake by thyroid, TH synthesis & release, thyroid size & thyroid vascularity

154
Q

What are the adverse effects of Potassium Iodides?

A

Allergic reaction (rare)

Angioedema

Laryngeal edema

Bleeding disorders

155
Q

What is the definitive treatment for Graves?

A

Radioactive Iodine

156
Q

What is the MOA of radioactive iodine?

A

Uptake by thyroid cells

Iodine isotopes trapped in thyroid

Beta rays destroy cells with minimal to no damage to surrounding tissues

157
Q

What are the risks of radioactive iodine?

A

Hypothyroidism risks

Contraindicated in pregnancy

Radiation toxicity

Infertility

158
Q

What should be considered when taking radiation iodine?

A

It can cause arrhythmias, ischemia & HF, so it is best to treat with a long acting beta blocker like PROPRANOLOL, which inhibits T4–>T3 conversion

This will control HR, HTN & fever

Dose 0.5-1mg over 10min

159
Q

The main mineralocorticoid is

A

Aldosterone

160
Q

Aldosterone will cause a

A

Increase in Na reabsorption

Ca, K & Mg excretion

161
Q

Aldosterone will increase

A

Na/K ATPase activity

162
Q

Aldosterone will cause

A

Muscle weakness due to a K+ & Ca+ excretion

163
Q

The main glucocorticoid is

164
Q

Cortisol can cause

A

Diuresis

Increases HGB & RBCs

Muscle wasting

Bone loss

Decreased bone remodeling

Increase IOP

165
Q

How is cortisol released?

166
Q

Cortisol influence with surgery

A

Minor- x2

Mod-3-4x

Major-5-10x

167
Q

Primary adrenal insufficiency is due to

A

A local problem

Autoimmune

Carcinoma

TB

168
Q

What is chronic AI called?

169
Q

What is secondary adrenal insufficiency?

A

Pituitary gland not stimulated enough

170
Q

What is the MOA of corticosteroid?

A

Bind cytoplasmic receptors

DNA transcription

Regulates protein synthesis

Glucocorticoids are widely distributed

171
Q

Which glucocorticoids have mineralocorticoid activity?

A

Fludrocortisone

Aldosterone

172
Q

Which glucocorticoids have no mineralcorticoid activity?

A

Betameth

Triaminolone

173
Q

Adrenal insufficiency has what effect on blood vessels?

A

Vasodilation

174
Q

Glucocorticoids effect on SVR

A

Can increase it

175
Q

When should dexamethasone be avoided?

A

In severe head injury/hemorrhage

176
Q

Dexamethasone is often given with

A

Zofran & Droperidol for nausea

177
Q

What is the action of glucocorticoid use for analgesia?

A

peripheral inhibition along COX & lipoxygenase

(dex & Betameth)

178
Q

Long term use of glucocorticoids can cause

A

HPA suppression

Decrease in cortisol stress response

Risk of acute adrenal crisis

179
Q

Glucocorticoids can have these effects

A

Fluid resistant HOTN

Change in consciousness & cognitive decline

N/V?ABD pain

Hypoglycemia

Decrease Na

Increase K

Persistent fever

180
Q

Replace cortisol therapy is

A

> 20mg/day or >3 weeks of therapy

or

S/s of Cushing (cortisol excess)

181
Q

Unknown HPA suppression?

A

5-20/day or prolonged therapy

Variable suppression

182
Q

How can you assess cortisol levels

A

Serum cortisol
>10mcg/dL-no suppression

5-10=some suppression

183
Q

Why is a stress dose steroid given?

A

Enhances vascular reactivity

Inhibits Prostacyclin PGI1

184
Q

Cortisol is involved in

A

Catecholamine synthesis

185
Q

Hydrocortisone (solu-cortef) has

A

Both glucocorticoid & mineralocorticoid activity

186
Q

What is the treatment choice of HPA suppression?

A

Hydrocortisone (Solu-cortef) or methylpred

187
Q

Which medication is first line for stress dose?

A

Hydrocortisone (solu-cortef)

188
Q

Hydrocortisone (Solu-cortef) can treat

A

Acute adrenal crisis

Chronic AI

Inflammation

Status Asthmatics

189
Q

What is the dose of Hydrocortisone for surgery types?

A

Min- 25mg

Mod-50-75mg

Major-100mg

190
Q

What is the duration of Hydrocortisone?

A

8-12 hours (short-acting)

191
Q

When should hydrocortisone be administered?

A

Prior to incision

Give every 8 hours

192
Q

For normal mineralocorticoid activity, consider using

A

Methylprednisolone

193
Q

Duration of dexamethasone (decadron)

A

Long acting

3-5 days

194
Q

Decadron is not compatible with

195
Q

Dose of Decadron as an antiemetic, analgesia, post intubation & for neuro cases

A

Antiemetic- 4-12

Analgesia-4-10

Post-intubation-10-16

Neuro-10

196
Q

Decadron is a potent

A

Glucocorticoid with minimal to no mineralocorticoid activity

197
Q

Decadron can help prolong

A

Regional anesthesia

198
Q

What are the adverse effects of corticosteroids?

A

HPA suppression

Decrease K+ (skeletal muscle myopathy)

Alkalosis

Edema/wt gain

Increased BS

CNS effects

Increased HCT

Osteoporosis

Inhibits growth

199
Q

Large doses of opioids can

A

Alter cortisol

200
Q

Etomidate can

A

Inhibit cortisol synthesis, leading to adrenal insufficiency

201
Q

Volatile anesthetics have

A

Minimal suppression

202
Q

Regional anesthesia decreases

A

Cortisol release

203
Q

What is the standard tx for COPD?
Asthma?

A

Inhaled anticholinergics

204
Q

What effects PAP?

A

CO

FiO2

Positive pressure ventilation

Left arterial pressure

CO2

205
Q

Nitrous Oxide can cause

A

Pulmonary vasoconstriction

206
Q

Epidural can cause

A

HOTN & RV dysfunction

pharm 4 (4 decks)

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