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Fall Pharm > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Natriuretic VS Diuretic

A

Natriuretic = increase Na+ secretion (increase water secretion)
Diuretic = increases urine volume
(all natriuretics are diuretics but not all diuretics are natriuretics)

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2
Q

4 main targets of diuretics:

A

1) Membrane transport proteins
2) water permeable segments of nephron
3) enzyme inhibition
4) interference with hormone receptors

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3
Q

2 main regions of kidney:

A

Cortex (outer section)

Medulla (inner section)

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4
Q

Parts of nephron:

A

Renal corpuscle (bowman’s capsule and glomerulus)–> proximal convoluted tubule (S1 and S2)–> Descending limb of loop of henle–> Ascending limb of loop of henle–> Distal convoluted tubule–> collecting duct

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5
Q

Glomerulus

A

arterial capillary network in the bowman’s capsule

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6
Q

What happens with RBC and WBC at the glomerulus?

A

they do not cross over into the nephron unless there is damage to the glomerulus

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7
Q

Most common reason for diuretic use:

A

Peripheral or pulmonary edema related to CHF, kidney disease, hepatic cirrhosis, or idiopathic edema

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8
Q

Non-edematous uses for diuretics:

A

HTN
Renal Stones
Hypercalcemia
Diabetes Insipidous

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9
Q

5 Classes of diuretics:

A 
Carbonic Anhydrase Inhibitors (CA-I)
Loop diuretics 
Thiazides
Potassium sparing
Agents that alter water excretion
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10
Q

Rate of excretion

A

Rate of exertion= filtration rate + secretion rate - reabsorption rate

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11
Q

Low sodium effect on nephron

A

increases NO and prostaglandin –> dilates afferent arteriole–> increases filtration

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12
Q

Increased sodium effect on nephron

A

signals ATP synthesis–> increased adenosine –> constricts afferent arteriole–> decreases filtration

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13
Q

What is the purpose of two capillary beds in the nephron?

A

The capillary bed at the renal corpuscle exchanges glomerular filtrate.
The other capillary bed is all along the nephron and exchanges O2 and CO2 as well as reabsorption and secretion of things that were not filtered at the renal corpuscle.

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14
Q

How much filtrate is there per day?

A

180grams (80% is reabsorbed at the proximal convoluted tubule

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15
Q

Vasa Recta

A

area of capillary beds around the loop of henle that exchange O2 and CO2.

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16
Q

Juxtaglomerular apparatus (JGA) is made up of..

A

..macula densa cells of the distal tubule and juxtaglomerular cells along the afferent arteriole.

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17
Q

what signals the arterioles in the nephron to constrict or dilate?

A

Na+

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18
Q

Renin response to 2 things:

A

-Stretch receptors in the afferent arteriole.
(decrease stretch in AA–> renin released–> activates angiotensin/aldosterone system–> allows reabsorption of water)
-Beta agonism

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19
Q

Things that regulate GFR:

A
  • Renal auto-regulation
  • Neural regulation (direct nerve input into JGA)
  • Hormonal regulation (sympathetic nervous system: beta receptors increase renin release and alpha receptors on vessels)
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20
Q

The Proximal Convolute Tubule (PCT) absorbs how much filtrate?

A

80%

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21
Q

Things that are reabsorbed in PCT:

A 
NaHCO3
NaCl
Glucose
Amino acids
Organic solutes
K+
H2O
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22
Q

What is secreted in the S2 segment of the PCT?

A

Drugs that are too big to filter through the glomerulus

Uric acid, NSAIDS, Diuretics, antibiotics

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23
Q

Molecular targets in PCT:

A

NHE3 (Na+H+ exchanger type 3)

Carbonic Anhydrase

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24
Q

Drugs that effect PCT:

A
  • Carbonic Anhydrase Inhibitors (CA-I) blocks NaHCO3 reabsorption which decreases H2O reabsorption
  • Caffeine weakly blocks Adenosine receptors causing dilation of AA and increased GFR. Caffeine also blocks NHE3.
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25
Q

Blood osmolality:

A

290-310mOsm/kg

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26
Q

Loop of Henle (L of H): osmotic gradient

A

at deepest part of loop, 1200mOsm/kg

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27
Q

Descending limb of L of H:

A

Water leaves to balance osmolarity.

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28
Q

Ascending limb of L of H:

A
  • Impermeable to water

- Ions leave to balance osmolarity.

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29
Q

Molecular target in L of H:

A

NKCC2

Na+K+2Cl- transporter

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30
Q

Drugs that effect L of H:

A

Thick ascending limb: loop diuretics inhibit NKCC2 transporter

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31
Q

Distal Convoluted Tubule (DCT) absorption:

A
  • very little H2O and Na+ movement

- Active Ca++ reabsorption by parathyroid hormone (PTH)

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32
Q

Molecular target in DCT:

A

NCC

Na+Cl- transporter

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33
Q

Drugs that effect DCT:

A

Thiazides inhibit NCC.

also very limited effect on carbonic anhydrase in PCT

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34
Q

What happens at the collecting tubule in the presence of a diuretics that blocks NaCl upstream?
(ex of this kind of diuretic)

A

There is an increases in NaCl reaching the CT–> more Na+ moves into cell–> creates a more negative gradient–> pushes Cl- out of tubule

(ex: Loop diuretics and thiazides)

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35
Q

What happens at the collecting tubule in the presence of a diuretic that blocks NaHCO3 upstream?
(ex of this kind of diuretic)

A

More NaHCO3 is reaching the CT–> more Na+ moves into cell creating a negative gradient–> HCO3- collects creates a more negative gradient–> K+ leaves the cell and enters the tubule to balance the charge

(ex: Acetazolamide)

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36
Q

Aldosterone

A
  • secreted by adrenal cortex
  • Increases water and Na+ reuptake at ENaC
  • Increase blood volume and pressure
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37
Q

Antidiuretic Hormone (ADH)

A

aka Vasopressin

  • Increases water reabsorption
  • Binds to receptor on CT wall–> stimulates adenylyl cyclase–> produces cAMP–> causes vesicles with aquaporins to fuse to cell wall–> water flows into cell from lumen side
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38
Q

Acetazolaminde: drug class

A

Diuretic: Carbonic Anhydrase Inhibitor

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39
Q

Acetazolaminde: Targets

A

inhibits carbonic anhydrase in the PCT
block 80% of HCO3 reabsorption
Highly K+ wasting

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40
Q

Acetazolaminde: clinical uses

A

Glaucoma
Alkalinization of urine for drug trapping
Metabolic alkalosis
Acute motion sickness

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41
Q

Acetazolaminde: Toxicity

A

Depletion of blood buffering capacity (risk for metabolic acidosis)
Kidney stones

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42
Q

Furosemide: Drug class

A

Loop diuretic

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43
Q

Loop diuretics: targets

A

Inhibit NKCC2 in the TAL of the loop of henle
blocks NaCl reabsorption
increases loss of K+, Mg++, Ca++

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44
Q

Furosemide: precautions

A

Sulfa allergy

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45
Q

Hydrochlorothiazide: Drug class

A

Thiazide diuretic

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46
Q

Thiazides: targets

A

Inhibit NCC in the DCT
blocks NaCl reabsorption
K+ wasting

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47
Q

Thiazides: precautions

A

Sulfa allergy

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48
Q

Spironolactone: Drug class

A

Potassium sparing diuretic

Aldosterone receptor antagonist

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49
Q

Spironolactone: targets

A

Blocks aldosterone receptors in collecting tubule (which decreases reabsorption of Na)

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50
Q

Amiloride: Drug class

A

Potassium sparing diuretic

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51
Q

Amiloride: targets

A

inhibits Na+ flux through ion channels in luminal membrane

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52
Q

Potassium sparing diuretics: clinical uses

A

Primary: Conn’s syndrome and Ectopic ATCH production
Secondary: CHF and Nephrotic syndrome

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53
Q

Mannitol: Drug class

A

Osmotic Diuretic

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54
Q

Mannitol: Clinical uses

A

to decrease ICP

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55
Q

Osmotic diuretics: precautions

A

Hypernatremia in healthy patients
Hyponatremia in renal impaired patients
Hyperkalemia
Use in-line filter, mannitol can crystalize

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56
Q

Conivaptan: Drug class

A

ADH antagonist (diuretic)

57
Q

Vasopressin (desmopressin): Drug class

A

ADH agonist (decreases diuresis)

58
Q

COPD=

A

bronchitis + emphysema

59
Q

Asthma

A

1) Airway hyper reactivity (causes constriction)
2) Inflammation
3) Mucosal thickening

60
Q

Eosinophils vs Neutrophils

A

Eosinophils more associated with Asthma

Neutrophils more associated with COPD

61
Q

Emphysema

A

hyperinflation of alveoli which leads to damage to cell membrane, destruction of alveoli, and/or development of scar tissue along the alveoli

62
Q

FEV1

A

Forced expiratory volume
A way to measure bronchial hyper-reactivity
Fall in FEV for 1 second after administration of histamine or methacholine

63
Q

PEF

A

Peak expiratory flow

Max flow of forced expiration

64
Q

Early vs late response in asthma:

A

Early response is a Type1 hypersensitivity like reaction (Histamine, Leukotriene, PG)

Late response is due to inflammation (eosinophils, cytokine)

65
Q

Histamine

A
  • Released during mast cell degeneration.
  • Induces smooth muscle contraction/bronchospasm.
  • Causes mucosal edema/secretions due to dilation of vasculature
66
Q

4 Histamine receptors

A

H1- lungs
H2- GI system
H3- CNS
H4- CNS

67
Q

H1

A

Bronchoconstriction

vasodilation

68
Q

Diphenhydramine: Drug class

A

(Benadryl)
Antihistamine
H1 inverse agonist

69
Q

Diphenhydramine: Clinical use

A

Type 1 Hypersensitivity reactions

very limited use in asthma

70
Q

Leukotrienes

A

Slow reaction
released during mast cell degeneration.
released from lungs during inflammation.
Causes same things that histamine causes only slower.

71
Q

Prostaglandins

A

Potent bronchoconstriction.
Enhance histamine effect.
Short duration of action.

72
Q

Which prostaglandin contributes the most to bronchoconstriction?

A

PGD2

73
Q

Thromboxane (TXA2)

A

Produced when COX has its effect on arachidonic acid.

Constricts blood vessels.

74
Q

T-Helper cells type 2 (TH2)

A

-Release cytokines that attract additional WBC (eosinophils) to the area, increasing the inflammatory response.
Eosinophils stimulate IgE production

75
Q

Sympathetic activity on bronchiolar smooth muscle:

A

Relaxes
Beta2
no direct nerve innervation

76
Q

Parasympathetic activity on bronchiolar smooth muscle:

A

Constricts
Muscarinic 3
direct nerve innervation

77
Q

Epi for treatment of asthma: drug class

A

Sympathomimetic agent
Beta2 agonist
non-selective alpha and beta

78
Q

Epi for treatment of asthma: precautions

A

B1 activity as well (tachycardia, arrhythmias, worsening angina)

79
Q

Beta2 agonists

A
  • Relax airway SM
  • Inhibit microvascular leakage
  • Increase mucociliary transport.

Short term asthma tx.
can cause tremors

80
Q

Isoproterenol: Drug class and clinical use

A

Sympathomimetic agent
Beta2 agonist
non-selective

Short term asthma tx

81
Q

Isoproterenol: precautions

A

arrhythmias

UK study- increased mortality

82
Q

Terbutaline: Drug class and clinical use

A

Sympathomimetic agent
Selective Beta2 agonist

Short term asthma tx

83
Q

Salmeterol/Formotorol: Drug class and clinical use

A

Sympathomimetic agent
Selective Beta2 agonist

longer term asthma tx (12hr effect)
(Can develop tolerance)

84
Q

Albuterol: Drug class and clinical use

A

Sympathomimetic agent
Selective Beta2 agonist

Short term asthma Tx

85
Q

Theophylline: Drug class and clinical use

A

Methylxanthine

Short term asthma tx

86
Q

Methylxanthine: MOA

A
  • Main: Inhibit PDE
  • Inhibit adenosine receptors
  • anti-inflammatory action
87
Q

Theophylline: precautions

A

Positive chronotrope and inotrope
arrhythmia
N/V

88
Q

Theophylline: dose and toxicity

A

Dose: 5-20mg/L

Toxic: >20mg/L

89
Q

Atropine: Drug class and clinical use

A

M3 antagonist

Short term asthma tx

90
Q

M3 antagonists: MOA

A

Compete with ACh at H3-R

  • Block contraction of airway SM
  • Block mucous secretion
91
Q

Ipratropium Bromide: Drug class and clinical use

A

M3 antagonist (more selective than atropine)

Short term asthma tx and COPD tx

92
Q

Tiotropium: Drug class and clinical use

A

M3 antagonist

Longer term asthma tx and COPD tx

93
Q

Ipratropium Bromide VS Tiotropium

A

both have NO CNS effects and NO B2 activity

Tiotropium last longer (24hr)

94
Q

Black Haw, Evening primrose, and Feverfew

A

contains mild amount of theophylline (asthma tx)

95
Q

Corticosteroids: MOA

A
  • Inhibit production of cytokines

- Inhibit lymphocytic, eosinophilic airway mucosal inflammitory

96
Q

Corticosteroids: precautions

A

Increased risk for osteoporosis
Stunts growth in children
Inhibit immune response (Oropharyngeal candidiasis)

97
Q

Prednisone: Drug class

A

Corticosteroid

98
Q

Fluticasone: Drug class

A

Corticosteroid

99
Q

Mast cell Stabilizers

A

Prevent mast cell degranulation (prophylactic).

No direct effect on airway SM

100
Q

Mast Cell Stabilizers: Drug examples

A

Cromolyn

Nedocromil

101
Q

Anti-IgE monoclonal antibodies

A

Bind to antibody on mast cell and prevent degranulation

102
Q

Omalizumab

A

Anti-IgE monoclonal antibody
1dose/wk injection
prophylactic

103
Q

Leukotriene pathway inhibitor: MOA

A

2 ways:

1) inhibit 5-lipoxygenase
2) inhibit receptor binding

104
Q

Montelukast: Drug class and clinical use

A

Leukotriene pathway inhibitor

Long term asthma tx

105
Q

Montelukast: MOA

A

inhibits leukotriene receptor binding

106
Q

Tx for ASA induced asthma:

A

leukotriene pathway inhibitor

107
Q

Autacoid groups

A

(means they have their effect locally)

Histamine, serotonin, PG, leukotrienes.

108
Q

1st generation H1 antagonists:

A

Bendryl, phenergan, dramamine

109
Q

2nd generation H1 antagonists:

A

Claritin, Allegra, Zyrtec

110
Q

Buspirone

A

5HT1A agonist

GAD, OCD, anti-anxiety

111
Q

Triptans

A 
5HT1B/D agonist
Migraine HA
prevent blood vessel dilation and stretch 
non-prophylactic 
Serotonin syndrome
112
Q

Ondansetron

A

Zofran

5HT3 antagonist

113
Q

SSRIs

A

Prozac
Zoloft

Inhibit SERT

114
Q

SNRIs

A

Cymbalta
Pristique

Inhibit SERT and NET

115
Q

TCAs

A

Elavil

Inhibit SERT, NET, and have anticholinergic effects

116
Q

MAOIs

A

Nardil

refractory depression

117
Q

Pheytoin: clinical use

A

Dilatin

partial, tonic-clonic

118
Q

Pheytoin: MOA

A

Modification of ion conductance
Enhance inhibitory-GABA
Inhibit excitatory-Glutamate

Highly protein bound

119
Q

Pheytoin: AE

A 
Nystagmus
diplopia
sedation
gingival hyplasia
hirsuitism
120
Q

Pheytoin: levels

A

Therapeutic: 10-20mcg/ml
Toxic: 30-50mcg/ml
lethal: >100mcg/ml

121
Q

Carbamazepine: clinical use

A

Tegretol (TCA)

Partial(drug of choice) , TGN, BiPolar

122
Q

Carbamazepine: MOA

A

Modification of ion conductance
Enhance inhibitory-GABA
Inhibit excitatory-Glutamate

Induces hepatic enzymes

123
Q

Carbamazepine: AE

A

Diplopia
ataxia

can develop tolerance (induces hepatic enzymes, decrease in half life over time)
can speed up break down of drugs

124
Q

Phenobarbital: clinical use

A

Barbituate

DOC in infants
partial
GTCS

125
Q

Phenobarbital: MOA

A

sedation
Enhances inhibitory-GABA
Induces hepatic enzymes

126
Q

Phenobarbital: AE

A

Can worse other seizures (absence, drop, or infantile)
can speed up breakdown of drugs (tolerance)
severe resp. depression

127
Q

Lamotrigine: clinical use

A

partial and absence seizures

128
Q

Lamotrigine: MOA

A

Modification of ion conductance

129
Q

GABA analogs: Drugs

A

Vigabatrin

lyrica

130
Q

GABA analogs: clinical use

A

adjunct
partial
neuralgia
Infantile spasms

131
Q

Ethosuxamide: clinical use

A

Absence seizures DOC

132
Q

Ethosuxamide: MOA

A

Modification of ion conductance

133
Q

Ethosuxamide: AE

A

GI

lethargy

134
Q

Valproic Acid: clinical use

A

Depakene

generalized seizures (except TC)
bipolar
migraine

135
Q

Valproic Acid: MOA

A

Modification of ion conductance
Enhance inhibitory-GABA
Inhibit excitatory-Glutamate

136
Q

Valproic Acid: AE

A 
DISPLACES PHENYTOIN
 Inhibits metabolism of some drugs 
GI
sedation
tremor
hepatotoxicity
137
Q

Benzodiazepines: clinical use

A

status epilepticus (Diazepam)

138
Q

Benzodiazepines: MOA

A

Enhance inhibitory-GABA

139
Q

Diazepam: half life/duration

A 
Long half life (20-100H) 
short duration (30min)

Fall Pharm (8 decks)

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