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Pharm > Diuretics, Histamine, Asthma (Exam 3) > Flashcards

Diuretics, Histamine, Asthma (Exam 3) Flashcards

Exam 3

1
Q

What does a diuretic do?

A

increase urine volume

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2
Q

Another name for diuretic?

A

Naturietic

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3
Q

What does a naturietic do?

A

increase sodium ion secretion

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4
Q

Does water follow sodium?

A

yes, osmosis

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5
Q

Overall results of diuretics

A

Decrease blood volume, decrease HTN

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6
Q

main targets for diuretics

A

Membrane transport proteins
Water permeable segments of nephron
Enzyme inhibition
Interference w hormone receptors

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7
Q

Classes of diuretics (6)

A

Carbonic anhydrase inhibitors
loop diuretics
thiazides
potassium sparing diuretics
agents that alter water excretion
SGLT2 inhibitors

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8
Q

What else is SGLT2 inhibitor used for?

A

Antidiabetic

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9
Q

___ is filtered and ____ is produced by the nephron

A

Blood, urine

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10
Q

What is ammonia converted into?

A

Urea

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11
Q

What is the glomerulus responsible for?

A

Filtration

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12
Q

What is typically reabsorbed?

A

water, electrolytes, glucose, amino acids

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13
Q

What is typically secreted?

A

H+, NH3, K+

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14
Q

Is there a different osmolality in the medulla compared to the cortex?

A

Yes

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15
Q

How many nephrons total in one kidney?

A

800,000 to 1,000,000 nephrons

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16
Q

What does a nephron consist of?

A

Renal corpuscle and associated tubules (NOT THE COLLECTING DUCTS)

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17
Q

Where is the blood plasma filtered?

A

Renal corpuscle ->glomerulus

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18
Q

What surrounds the glomerulus?

A

Bowman’s capsule

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19
Q

How many arteries associated with one glomerulus?

A

2 arteries

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20
Q

What are the arteries called

A

Afferent and Efferent

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21
Q

How many tubules associated with one glomerulus?

A

2

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22
Q

What are the names of the tubulues associated with the glomerulus?

A

Proximal convoluted tubule
Distal convoluted tubule

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23
Q

Where is the loop of Henle?

A

Between the proximal and distal convoluted tubules

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24
Q

What part of the nephron is in the medulla?

A

Lower portions of convoluted tubules in the cortex->thin tubules

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25
Q

Where does the distal convoluted tubule empty into?

A

The collecting duct

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26
Q

Are there any glomeruli in the medulla?

A

No

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27
Q

Where are glomeruli found

A

in the cortex

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28
Q

what do podocytes sit on?

A

The glomerular network

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29
Q

What are between podocytes and what happens there?

A

filtration slits where filtration can occur

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30
Q

Should we see protein in urine?

A

No

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31
Q

What is protein in the urine called?

A

Proteinuria

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32
Q

What are the macula densa cells responsible for?

A

Sensing Na delivery and fluid pressure/ volume, can affect the afferent arteriole

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33
Q

Who synthesizes renin?

A

Juxtaglomerular cells

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34
Q

How would you describe juxtaglomerular cells?

A

Modified endothelium cells, they can contract and limit amount of blood coming into capillaries

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35
Q

Can the macula densa trigger the RAAS?

A

Yes

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36
Q

What is osmolality?

A

The number of dissolved substances in a solution. Determines osmotic pressure

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37
Q

Where are the maculla densa cells located?

A

Directly outside of the arteries

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38
Q

Who do the maculla densa send information to?

A

juxtaglomerular cells

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39
Q

What are the peritubular capillaries responsible for?

A

Secretion and reabsorption

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40
Q

What is the renal corpuscle responsible for?

A

Filtration

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41
Q

What molecule do we not want to lose?

A

HCO3

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42
Q

What is reabsorbed in the loop of henle?

A

H2O and salt

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43
Q

How much filtrate is reabsorbed in the proximal tubule?

A

80%`

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44
Q

How much filtrate is reabsorbed in the distal tubule?

A

9%

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45
Q

How much filtrate is reabsorbed in the collecting tubule?

A

4%

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46
Q

What is involved in the juxtaglomerular apparatus?

A

Macula densa and juxtaglomerular cells

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47
Q

Rate of excretion =

A

filtration rate + secretion rate - reabsorption rate

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48
Q

what is involved in neural regulation

A

SNS

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49
Q

How can we regulate GFR

A

Adjust blood flow
Alter capillary surface area
Control arteriole diameter

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50
Q

Types of autoregulation

A

Renal, neural and hormonal

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51
Q

Whats involved in hormonal regulation? (2 mentioned)

A

Epi and endocrine

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52
Q

What is reabsorbed in the proximal tubule?

A

NaCl, sodium bicarb, glucose, amino acids, potassium, water

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53
Q

Where do carbonic anhydrase inhibitors work?

A

Proximal convoluted tubules

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54
Q

What does a carbonic anhydrase inhibitor do?

A

Block NaHCO3 reabsorption

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55
Q

what does caffeine do?

A

weakly blocks adenosine receptors in PCT -> pee a lot

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56
Q

What effect does carbonic anhydrase inhibitors have on the NHE3 pump?

A

Blocks the pump, traps hydrogen in cell, keeps sodium in urine and water follows sodium.

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57
Q

What are the effects on the urinary electrolytes due to carbonic anhydrase inhibitors?

A

Wasted K, drop in body pH, high amount of NaHCO3 lost

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58
Q

___ binds to ___ to form carbonic acid

A

H+ and bicarbonate

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59
Q

What does carbonic anhydrase do in the urinary membrane?

A

Traps hydrogen ions to form carbonic acid, and is then converted into CO2 and H2O

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60
Q

Where does CO2 diffuse from?

A

Urine to epithelium

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61
Q

What does carbonic anhydrase do in the epithelial cell?

A

Reattches CO2 and H2O to make H2CO3 and then make bicarb.

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62
Q

Where does bicarb move after becoming remade again?

A

bloodstream via a transporter

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63
Q

How does sodium get pumped back into the blood stream?

A

Na K ATPase Pump

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64
Q

What tubule is juxtaglomerular apparatus a part of?

A

The distal convoluted tubule

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65
Q

What is the osmolality of the cortex?

A

300

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66
Q

In PCT water does what with sodium

A

Follows Na to keep osmolality constant

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67
Q

Where does the countercurrent mechanism take place?

A

in the medulla

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68
Q

A high Na sodium blood is what kind of osmolality?

A

high osmolality

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69
Q

what is the osmolality in the medulla?

A

1200

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70
Q

Water reabsorption must equal ____ to keep osmotic gradient equal

A

Na reabsorption

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71
Q

Is mannitol an impermeable solute?

A

Yes

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72
Q

Where does mannitol work?

A

in the PCT

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73
Q

If we increase mannitol _____ increases also

A

osmolality

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74
Q

What effect does mannitol have on water?

A

Prevents further reabsorption of water

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75
Q

Where is the straight segment located?

A

in the proximal tubulue

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76
Q

what is the descending loop of henle responsible for?

A

water reabsorption

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77
Q

what is the ascending loop of henle responsible for?

A

impermeable to water, active transport of NaCl via the NKCC2, reabsorption of mag and calcium due to positive urine, removal of K

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78
Q

What do loop diuretics do to NaCl reabsorption?

A

Selectively inhibit in the thick ascending limb

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79
Q

Do loop diuretics cause acidosis or alkalosis?

A

alkalosis

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80
Q

Are loop diuretics the most efficacious?

A

yes

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81
Q

an example of a loop diuretic

A

furosemide (lasix)

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82
Q

are loop diuretics the strongest or weakest diuretic?

A

strongest

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83
Q

What ions do we see excreted with loop diuretics? (5)

A

Na, Cl, K, Mg, Ca

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84
Q

What does NKCC2 stand for?

A

Na K 2-Cl

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85
Q

what allergic reactions do we need to worry about with loop diuretics?

A

sulfa allergy

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86
Q

What are loop diuretics made of?

A

sulfonamide

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87
Q

what can be used if allergic to loop diuretic?

A

ethacrynic acid

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88
Q

Is there a lot of water movement in the DCT?

A

little water movement

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89
Q

How much sodium is reabsorbed in the DCT?

A

low amount

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90
Q

where is the DCT located?

A

in the cortex

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91
Q

What pump reabsorbs Na and Cl in the DCT?

A

NCC

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92
Q

what area do thiazides work on?

A

DCT

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93
Q

What transporter do thiazides work on?

A

NaCl (NCC)

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94
Q

Do thiazides work on carbonyl anhydrase activity too?

A

Yes

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95
Q

What is the prototype for Thiazides?

A

hydrochlorothiazide

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96
Q

Is there a sulfa allergy associated with thiazides?

A

Yes

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97
Q

Do thiazides cause acidosis or alkalosis?

A

alkalosis

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98
Q

What two diuretic groups produce the most water movement

A

loops and thiazides

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99
Q

Where is the final site of sodium reabsorption?

A

collecting tubule

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100
Q

What is the most important site for potassium secretion?

A

collecting tubule

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101
Q

What kind of transporter is in the prinicipal cells?

A

cotransporter, ENaC, only positive ions (cations)

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102
Q

What charge is in the urine lumen with the collecting tubule and why?

A

negative charge, more Na than K out

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103
Q

what kind of movement of Cl with the collecting tubule?

A

Cl into blood through paracellular route

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104
Q

Is aldosterone used in the collecting tubule for Na reabsorption?

A

Yes

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105
Q

Who is the worst potassium wasting diuretic?

A

Carbonic anhydrase inhibitor

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106
Q

Potassium sparing diuretics antagonize what hormone?

A

aldosterone

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107
Q

what potassium sparing diuretic blocks aldosterone receptors?

A

spironolactone?

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108
Q

What potassium sparing diuretic blocks the ENaC?

A

amiloride

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109
Q

If we block the ENaC, what do we see with potassium?

A

potassium moves into the principal cello

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110
Q

When are potassium sparing diuretics most useful?

A

in states of aldosterone excess

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111
Q

Primary reasons for potassium sparing diuretics?

A

conn’s syndrome, ectopic ACTH production

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112
Q

Secondary reasons for potassium sparing diuretics?

A

CHF, nephrotic syndrome

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113
Q

Contraindications for potassium sparing diuretics?

A

patients taking supplementary potassium

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114
Q

What does ADH do?

A

increases water reaborsption

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115
Q

Does ADH concentrate the urine?

A

yes

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116
Q

does adh add more AQP2 in the cell membrane?

A

yes

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117
Q

What is the antagonist to vasopressin?

A

conivaptan

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118
Q

Are the PCT and descending loop freely permeable to water?

A

yes

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119
Q

What drug class is mannitol?

A

osmotic diuretic

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120
Q

What is the primary reason for using mannitol?

A

decreasing ICP

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121
Q

Does mannitol remove renal toxins?

A

Yes

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122
Q

What effect does mannitol have on the GI tract?

A

Diarrhea

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123
Q

Overall result of osmotic diuretics?

A

Increase urine volume, decrease Na reabsorption

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124
Q

Biggest toxicities with osmotic diuretics?

A

Edema and dehydration

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125
Q

Why do we use an in filter set with mannitol?

A

Because it crystallizes

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126
Q

Most common use for diuretics?

A

Peripheral or pulmonary edemaN

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127
Q

Non edematous states (6)

A

HTN, renal stones, hypercalcemia, rhabdo, urinary casts, diabetes insipidus

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128
Q

Do we have sufficient ADH or insufficient ADH with Diabetes insipidus?

A

insufficient ADH

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129
Q

What side effects do we see with insufficient ADH

A

excessive thirst (polydipsia) and excessive urination (polyuria)

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130
Q

What drug class can we use to treat DI?

A

thiazides

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131
Q

how do thiazides work on DI? (6 steps)

A

decrease DCT na reabsorption, increase urinary excretion, lower extracellular volume, increase na and water reabsorption in the PCT, decrease distal delivery of Na and water, which will decrease urine output.

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132
Q

What is airway resistance dependent on?

A

airway diameter

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133
Q

Types of obstructive disorders?

A

asthma, chronic bronchitis, emphysema, copd

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134
Q

What is COPD made of?

A

chronic bronchitis and emphysema

135
Q

what is the most common chronic disease in children?

A

asthma

136
Q

How many children will show improvement with age?

A

30-70%

137
Q

Suspects for asthma increasing prevalence?

A

hygiene hypothesis, worsening air quality, infant second-hand smoke

138
Q

Asthma has what airway issues?

A

inflammation and obstruction

139
Q

What cells are involved with asthma?

A

WBCs and epithelial cells

140
Q

symptoms of asthma

A

wheezing, breathlessness, chest tightness, coughing, worse at night and early morning

141
Q

What is involved in the widespread narrowing of airways with asthma?

A

contraction of airway
mucosal thickening
mucous plugs

142
Q

What is FEV1

A

forced expiratory volume

143
Q

what tests for bronchial hyperreactivity?

A

FEV1

144
Q

What is a fall in expired volume in 1 second provoked by inhaling large concentration of histamine or methacholine?

A

FEV1

145
Q

What is PEF

A

Peak expiratory flow

146
Q

what is the maximal flow of forced expiration?

A

PEF

147
Q

What do we give to treat the contraction of smooth muscle?

A

beta agonists

148
Q

What do we give to treat edema and cellular infiltration?

A

anti-inflammatory agents

149
Q

Can asthma be intrinsic and extrinsic

A

yes

150
Q

What do you think when you hear atopic or extrinsic?

A

allergens

151
Q

what happens first when a dendritic cell comes into contact with an allergen?

A

It becomes an antigen presenting cell -> MHC2 and activates inflammatory cells

152
Q

What inflammatory cells are activated?

A

T helper 2 cells, B cells, B memory cells, plasma cells

153
Q

What does the T helper 2 cell produce to interact with B cells?

A

Interleukin 4

154
Q

What do plasma cells produce to bind with mast cells?

A

IgE

155
Q

Is IgE an antibody?

A

yes

156
Q

What do we see after sensitization of mast cells and basophils?

A

mast cell degranulation

157
Q

A fast response from the the degranulation produces what?

A

histamines

158
Q

A slow response from the mast cell degranulation produces what>

A

Leukotrienes

159
Q

What do we see with histamines and leukotrienes?

A

mucus secretion, hay fever, anaphylaxis, itching, capillary dilation

160
Q

what can we give to block IL4 from binding to B cells?

A

Dupilumab

161
Q

Do antihistamines work on asthma?

A

No

162
Q

What are antihistamines used for?

A

allergic reactions

163
Q

Can stimulating the vagus nerve cause an asthma attack?

A

yes

164
Q

Are prostaglandins proinflammatory?

A

yes

165
Q

what induces smooth muscle contraction and bronchospasms?

A

histamine

166
Q

what mediator is a potent bronchoconstrictor?

A

prostaglandins

167
Q

Do prostaglandins enhance histamine effect?

A

yes

168
Q

when are leukotrienes liberated from the lungs?

A

during inflammation

169
Q

Can we see more problematic inflammation hours after an asthma attack?

A

Yes

170
Q

Overall pathway of allergens effects on airway wall and mast cells

A

granulation of mast cells, releases histamine, PGD2, LTC, contraction of smooth muscle, cytokines released from t lymphocytes, Eosinophils and neutrophils release proteases

171
Q

what do proteases do to cell wall proteins?

A

break them down

172
Q

what happens when blood vessel wall proteins are broken down

A

fluid leaks out into surrounding tissues

173
Q

What is mucus produced by?

A

goblet cells and epithelial cells

174
Q

what is mucus primarily made of?

A

water

175
Q

if mucus dries out, what happens to the viscosity?

A

it increases

176
Q

What do B2 agonists do to airway?

A

produce bronchodilation

177
Q

what nerves innervate the airway?

A

PNS, SNS, and NANC

178
Q

What nerve is associated with the PNS

A

vagus nerve 10

179
Q

Major resistance airways have what receptor?

A

alpha agonists

180
Q

do alpha blockers have any effect on asthma?

A

minimal effect

181
Q

what can trigger an asthma attack?

A

allergens, resp infections, irritants, certain meds, exercise, GERD, anxiety/stress

182
Q

What do we treat croup with?

A

nebulized epi

183
Q

Loss of elastic recoil is associated with what disease?

A

emphysema

184
Q

What is primarily associated with chronic bronchitis?

A

mucus is thicker and hypersecreted, chronic productive cough that lasts longer than 3 months of the year

185
Q

what is associated with emphysema?

A

abnormal permanent enlargement of alveoli

186
Q

2 asthma treatment categories

A

short term and long term

187
Q

What makes up the short treat treatment for asthma>

A

sympathomimetics

188
Q

what makes up the long term treatment of asthma?

A

corticosteroids

189
Q

beta 2 agonist relax airway smooth muscle and _____

A

inhibit mast cell substances

190
Q

Best sympathomimetic drugs to treat asthma

A

terbutaline, albuterol, metaproterenol, pirbuterol, samleterol, epi, iso

191
Q

Can epi be given SB and inhaled?

A

yes

192
Q

why do we see tachycardia when taking epi?

A

bc its a B1 and B2 agonist

193
Q

Is isoproterenol a potent bronchodilator?

A

yes

194
Q

What does the UK study show for iso high doses?

A

increased mortality rate

195
Q

What does SAB2A mean?

A

short acting beta 2 agonist

196
Q

What does LAB2A mean?

A

Long acting beta 2 agonist

197
Q

Most widely used treatment for asthma?

A

albuterol

198
Q

What receptor does albuterol work on?

A

beta 2

199
Q

how long does albuterol last?

A

3-4 hours

200
Q

Is terbutaline available as parenteral?

A

yes

201
Q

Are salmeterol and formeterol Long acting or Short acting?

A

long acting, 12 hours.

202
Q

How much of oral inhalation reaches airway?

A

10-20%

203
Q

Are methylxanthines short term or long term?

A

short term

204
Q

Examples of methylxanthines?

A

caffeine, theophylline, theobromine

205
Q

What are the propose MOA of methylxanthines?

A

PDE inhibitors, keeps cAMP in cell, relaxation, inhibitor adenosine receptors

206
Q

Will methylxanthines increase cAMP in the heart too?

A

yes

207
Q

Will methylxanthines cause kidney diuresis?

A

yes

208
Q

where do we get theophylline from?

A

natural tea and purified extract

209
Q

What toxic effects do we see with methylxanthines?

A

headache, N/V, tremors, seizures, arrhythmias

210
Q

What organ metabolizes methylxanthines?

A

the liver

211
Q

who is more selective, ipra or atropine?

A

ipra

212
Q

Most common antimuscarinics?

A

atropine and ipratropium bromide

213
Q

We can combine ipra with ___ for synergistic treatment of COPD

A

beta agonists

214
Q

Who is longer acting ipra or tiotropium?

A

tiotropium

215
Q

do corticosteroids have an anti-inflammatory effect?

A

yes

216
Q

what is inhibited with corticosteroids>

A

cytokine production, lymphocytic and eosinophilic airway inflammation

217
Q

Is COPD more or less responsive to corticosteroids?

A

less responsive

218
Q

How do glucocorticoids work?

A

by inhibiting immune response by blocking transcription/translation

219
Q

corticosteroids may increase ___ with long term therapy and they may ____ the rate of growth in children

A

osteoporosis and slow

220
Q

What does GRE stand for with glucocorticoids?

A

glucocorticoid response element

221
Q

can GREs only be a silencer?

A

no they can be an enhancer too

222
Q

do glucocorticoids increase or suppress annexin 1

A

increase

223
Q

does annexin 1 suppress or increase phospholipase A2 and leukocytic response

A

suppress

224
Q

do glucocorticoids increase or decrease leuokoprotease inhibitor?

A

increase

225
Q

do glucocorticoids increase or decrease IL-10 immunosuppresive?

A

increase

226
Q

do glucocorticoids decrease or increase Inh-NFkB

A

decrease

227
Q

is INh-NFkB pro or anti inflammatory?

A

pro inflammatory

228
Q

What oral issue do corticosteroids cause?

A

candidiasis - thrush

229
Q

what method of administration of corticosteroids is most effective?

A

aerosolized/ inhaled

230
Q

What do Anti-IgE monoclonal antibodies target?

A

the portion of IgE that binds to mast cells

231
Q

Do the anti-IgE monoclonal antibodies provoke degranulation?

A

No

232
Q

Leukotrienes cause what?

A

bronchoconstriction, bronchial reactivity, mucosal edema, hypersecretion

233
Q

Xolair blocks what?

A

IgE receptors on mast cells

234
Q

What leukotriene pathway inhibitor blocks the lipoxygenase pathway?

A

zileuton

235
Q

what LPI inhibits the binding of leukotrienes to their receptor?

A

montelukast and zafirlukast

236
Q

Do we give LPIs by themselves or with other drugs too?

A

With other drugs too

237
Q

What to treat with mild asthma?

A

beta 2 receptor agonist

238
Q

Moderate asthma treatment?

A

anti-inflammatories: corticosteroids and oral leukotriene receptor antagonists

239
Q

what to give for Frequent symptoms of asthma treatment?

A

inhaled corticosteroids

240
Q

Symptoms less than 2x month, treat with what?

A

SAB2A, low dose ICS

241
Q

Step 2: symptoms >2x month, not daily, what treatment?

A

Low dose ICS, formoterol, alternate of LTRA, SAB2A

242
Q

Step 3: symptoms daily

A

low dose ICS and LABA, add LTRA, short acting: ICS/ formoterol

243
Q

Step 4: daily symptoms, low lung function treatment

A

medium dose ICS-LABA, add tiotropium or LTRA, short acting ICS/formoterol

244
Q

Step 5: uncontrolled symptoms

A

high dose ICS-LABA, OCS, add tiotropium and anti-IgE mab, short term: ICS/formoterol

245
Q

What are treatment standard drugs for COPD?

A

LABA and Long acting muscarinic antagonist.

246
Q

Treating asthma attacks

A

oxygen, nebulizer with beta 2 agonist, prednisone/methylprednisone, intubation

247
Q

What mediators are part of the autacoid group?

A

histamine, serotonin, prostaglandins, leukotrienes

248
Q

what does the autacoid group induce on the skin?

A

pruritis

249
Q

can pruritis be neuropathic and psychogenic?

A

yes

250
Q

____ is the mediator of allergic and inflammatory response

A

histamine

251
Q

where is histamine stored

A

in vesicles

252
Q

where is histamine found

A

stomach and brain (neurotransmitter)

253
Q

What can induce the mast cells with histamine?

A

trauma

254
Q

histamine can be released in response to what drugs?

A

morphine and tubocurarine

255
Q

What receptors are associated with pain and itching?

A

H1 and H3

256
Q

What histamine receptor is associated with the stomach?

A

H2

257
Q

What CV effects do we see with histamine?

A

vasodilation and reflex tachycardia

258
Q

Most common effect of antihistamine in CNS?

A

drowsiness

259
Q

Wheal and Flare is also known as

A

“triple response”

260
Q

What mediator are we testing with the allergen testing wheal and flare?

A

histamine response

261
Q

____ reverses effects of histamine

A

epinephrine

262
Q

Receptor antagonists
1st gen

A

sedation, blocks ANS

263
Q

Histamine receptor antagonists 2nd gen

A

less sedation

264
Q

What do we typically use histamine to treat?

A

allergic rhinitis

265
Q

what does histamine do in the lungs?

A

bronchoconstricts

266
Q

What does histamine do in the GI tract

A

contraction

267
Q

What types of drugs do H1 receptor antagonists mimic?

A

antimuscarinics

268
Q

Most common side effects of antihistamine H1

A

sedation and antinausea

269
Q

Dramamine treats

A

nausea

270
Q

dramamine is similar to

A

scopolamine

271
Q

toxic effects are similar to ____

A

antimuscarinics

272
Q

What toxicity do we see with H1 receptor antagonists

A

sedation, antimuscarinic - urinary retention, seizures

273
Q

H2 receptor antagonists

A

pepcid, cimetidine

274
Q

What effects do we see when platelets release serotonin?

A

vasoconstriction

275
Q

Serotonin is also known as

A

5HT: 5 hydroxytryptamine

276
Q

What cells are serotonin stored in?

A

enterochromaffin cells

277
Q

H2 receptor antagonists primarily treat

A

stomach acid

278
Q

Who produces serotonin?

A

raphe nuclei and enterochromaffin cells

279
Q

what amino acid does serotonin come from?

A

L-tryptophan

280
Q

what is serotonin a precursor to?

A

melatonin

281
Q

Can screen for 5HIIA to find what disease?

A

enterochromattin tumor

282
Q

5HT3 is what kind of receptor

A

ion channel

283
Q

what is 5HT3 responsible for

A

nausea, vomitting

284
Q

does serotonin have anything to do with pain and itch?

A

yes

285
Q

how strong is the chemoreceptor reflex with serotonin?

A

minor, bradycardia and hypotension

286
Q

what is the effect of serotonin on the lungs?

A

constriction, hyperventilation

287
Q

effects of 5HT on CV

A

contraction of vascular smooth muscle and platelet aggregation

288
Q

affects of serotonin on the gut

A

increases tone and persistalsis

289
Q

What is 5HT1A targeted for?

A

anxiety

290
Q

Are 5HT1D and 1B associated with migraine headaches?

A

yes

291
Q

What receptor does buspar target?

A

5HT1A agonist

292
Q

is buspar a benzo?

A

no

293
Q

what serotonin receptor does sumatriptan target?

A

5HT 1D 1B

294
Q

what does sumatriptan treat?

A

migraines

295
Q

is there a cause of migraines?

A

no

296
Q

two important signalling modifiers for migraines?

A

CGRP and Substance P

297
Q

5 treatments for migraines

A

pain relief
triptans
ergotamine
anti-nausea
glucocorticoids

298
Q

where do triptans work?

A

cranial blood vessels

299
Q

preventatives with migraines (5)

A

beta blockers
antidepressants
antiseizures
botox
MAbs

300
Q

toxicity of triptans

A

coronary vasospasm, serotonin syndrome

301
Q

what is serotonin syndrome?

A

HTN, tremors, hyperactive bowel sounds, mydriasis, agitation, hyperthermia

302
Q

BMI with obesity

A

> 30

303
Q

Phenoxybenzamine and cyproheptadine work on which serotonin receptor as antagonists

A

5-HT2

304
Q

Zofran targets what serotonin receptor?

A

5-HT3

305
Q

does st. johns wort affect serotonin concentration

A

yes

306
Q

treatment for neurolpetic malignant syndrome?

A

benadryl

307
Q

Treatment for malignant hyperthermia?

A

dantrolene

308
Q

Treatment for serotonin syndrome

A

benzos

309
Q

Tyrosine is the precursor for ____

A

dopamine

310
Q

how many receptors for dopamine

A

5

311
Q

has serotonin been used for weight loss?

A

yes

312
Q

semaglutides treat what?

A

diabetes and weight

313
Q

Orlistat inhibits what?

A

Gi lipase

314
Q

Is D1 post synaptic or pre?

A

post

315
Q

Is D2 pre or post synaptic>

A

postsynaptic

316
Q

nigrostriatal is responsible for which pathway in dopamine?

A

motor movement

317
Q

mesolimbic is responsible for what in dopamine pathways?

A

reinforcement and addiction

318
Q

mesocortical is responsible for what in the dopamine pathway?

A

working memory and planning

319
Q

Who is affected more by depression and anxiety?

A

women 2x as much as men

320
Q

What does a diuretic do?

A

increase urine volume

321
Q

what is the difference between depression and anxiety?

A

depression is lack of energy, anxiety is too much energy

322
Q

what does dysthymia mean?

A

overall depression

323
Q

antidepressant treatment drug classes (4)

A

SSRIs, SNRIs, TCAs, MAOIs

324
Q

SSRI drugs

A

prozac, citalopram, paroxetine (paxil), zoloft (sertraline), escitalopram (lexapro)

325
Q

SNRIs drugs

A

duloxetine, desvenlafaxine

326
Q

what do SNRIs inhibit>

A

SERT and NET

327
Q

TCAs drugs

A

amitriptyline

328
Q

MAOIs drugs

A

nardil and selegiline

329
Q

are MAOIs frequently used?

A

no

330
Q

Is buprprion an NDRI?

A

yes

331
Q

What do NDRIs inhibt?

A

NE and DA reuptake

332
Q

Do benzo treat anxiety?

A

yes

333
Q

biggest side effect of antidepressants?

A

suicidal tendencies

Pharm (11 decks)

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