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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
Blood osmolality:
290-310mOsm/kg
26
Loop of Henle (L of H): osmotic gradient
at deepest part of loop, 1200mOsm/kg
27
Descending limb of L of H:
Water leaves to balance osmolarity.
28
Ascending limb of L of H:
- Impermeable to water | - Ions leave to balance osmolarity.
29
Molecular target in L of H:
NKCC2 | Na+K+2Cl- transporter
30
Drugs that effect L of H:
Thick ascending limb: loop diuretics inhibit NKCC2 transporter
31
Distal Convoluted Tubule (DCT) absorption:
- very little H2O and Na+ movement | - Active Ca++ reabsorption by parathyroid hormone (PTH)
32
Molecular target in DCT:
NCC | Na+Cl- transporter
33
Drugs that effect DCT:
Thiazides inhibit NCC. | also very limited effect on carbonic anhydrase in PCT
34
What happens at the collecting tubule in the presence of a diuretics that blocks NaCl upstream? (ex of this kind of diuretic)
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)
35
What happens at the collecting tubule in the presence of a diuretic that blocks NaHCO3 upstream? (ex of this kind of diuretic)
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)
36
Aldosterone
- secreted by adrenal cortex - Increases water and Na+ reuptake at ENaC - Increase blood volume and pressure
37
Antidiuretic Hormone (ADH)
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
38
Acetazolaminde: drug class
Diuretic: Carbonic Anhydrase Inhibitor
39
Acetazolaminde: Targets
inhibits carbonic anhydrase in the PCT block 80% of HCO3 reabsorption Highly K+ wasting
40
Acetazolaminde: clinical uses
Glaucoma Alkalinization of urine for drug trapping Metabolic alkalosis Acute motion sickness
41
Acetazolaminde: Toxicity
Depletion of blood buffering capacity (risk for metabolic acidosis) Kidney stones
42
Furosemide: Drug class
Loop diuretic
43
Loop diuretics: targets
Inhibit NKCC2 in the TAL of the loop of henle blocks NaCl reabsorption increases loss of K+, Mg++, Ca++
44
Furosemide: precautions
Sulfa allergy
45
Hydrochlorothiazide: Drug class
Thiazide diuretic
46
Thiazides: targets
Inhibit NCC in the DCT blocks NaCl reabsorption K+ wasting
47
Thiazides: precautions
Sulfa allergy
48
Spironolactone: Drug class
Potassium sparing diuretic | Aldosterone receptor antagonist
49
Spironolactone: targets
Blocks aldosterone receptors in collecting tubule (which decreases reabsorption of Na)
50
Amiloride: Drug class
Potassium sparing diuretic
51
Amiloride: targets
inhibits Na+ flux through ion channels in luminal membrane
52
Potassium sparing diuretics: clinical uses
Primary: Conn's syndrome and Ectopic ATCH production Secondary: CHF and Nephrotic syndrome
53
Mannitol: Drug class
Osmotic Diuretic
54
Mannitol: Clinical uses
to decrease ICP
55
Osmotic diuretics: precautions
Hypernatremia in healthy patients Hyponatremia in renal impaired patients Hyperkalemia Use in-line filter, mannitol can crystalize
56
Conivaptan: Drug class
ADH antagonist (diuretic)
57
Vasopressin (desmopressin): Drug class
ADH agonist (decreases diuresis)
58
COPD=
bronchitis + emphysema
59
Asthma
1) Airway hyper reactivity (causes constriction) 2) Inflammation 3) Mucosal thickening
60
Eosinophils vs Neutrophils
Eosinophils more associated with Asthma | Neutrophils more associated with COPD
61
Emphysema
hyperinflation of alveoli which leads to damage to cell membrane, destruction of alveoli, and/or development of scar tissue along the alveoli
62
FEV1
Forced expiratory volume A way to measure bronchial hyper-reactivity Fall in FEV for 1 second after administration of histamine or methacholine
63
PEF
Peak expiratory flow | Max flow of forced expiration
64
Early vs late response in asthma:
Early response is a Type1 hypersensitivity like reaction (Histamine, Leukotriene, PG) Late response is due to inflammation (eosinophils, cytokine)
65
Histamine
- Released during mast cell degeneration. - Induces smooth muscle contraction/bronchospasm. - Causes mucosal edema/secretions due to dilation of vasculature
66
4 Histamine receptors
H1- lungs H2- GI system H3- CNS H4- CNS
67
H1
Bronchoconstriction | vasodilation
68
Diphenhydramine: Drug class
(Benadryl) Antihistamine H1 inverse agonist
69
Diphenhydramine: Clinical use
Type 1 Hypersensitivity reactions | very limited use in asthma
70
Leukotrienes
Slow reaction released during mast cell degeneration. released from lungs during inflammation. Causes same things that histamine causes only slower.
71
Prostaglandins
Potent bronchoconstriction. Enhance histamine effect. Short duration of action.
72
Which prostaglandin contributes the most to bronchoconstriction?
PGD2
73
Thromboxane (TXA2)
Produced when COX has its effect on arachidonic acid. | Constricts blood vessels.
74
T-Helper cells type 2 (TH2)
-Release cytokines that attract additional WBC (eosinophils) to the area, increasing the inflammatory response. Eosinophils stimulate IgE production
75
Sympathetic activity on bronchiolar smooth muscle:
Relaxes Beta2 no direct nerve innervation
76
Parasympathetic activity on bronchiolar smooth muscle:
Constricts Muscarinic 3 direct nerve innervation
77
Epi for treatment of asthma: drug class
Sympathomimetic agent Beta2 agonist non-selective alpha and beta
78
Epi for treatment of asthma: precautions
B1 activity as well (tachycardia, arrhythmias, worsening angina)
79
Beta2 agonists
- Relax airway SM - Inhibit microvascular leakage - Increase mucociliary transport. Short term asthma tx. can cause tremors
80
Isoproterenol: Drug class and clinical use
Sympathomimetic agent Beta2 agonist non-selective Short term asthma tx
81
Isoproterenol: precautions
arrhythmias | UK study- increased mortality
82
Terbutaline: Drug class and clinical use
Sympathomimetic agent Selective Beta2 agonist Short term asthma tx
83
Salmeterol/Formotorol: Drug class and clinical use
Sympathomimetic agent Selective Beta2 agonist longer term asthma tx (12hr effect) (Can develop tolerance)
84
Albuterol: Drug class and clinical use
Sympathomimetic agent Selective Beta2 agonist Short term asthma Tx
85
Theophylline: Drug class and clinical use
Methylxanthine Short term asthma tx
86
Methylxanthine: MOA
- Main: Inhibit PDE - Inhibit adenosine receptors - anti-inflammatory action
87
Theophylline: precautions
Positive chronotrope and inotrope arrhythmia N/V
88
Theophylline: dose and toxicity
Dose: 5-20mg/L Toxic: >20mg/L
89
Atropine: Drug class and clinical use
M3 antagonist Short term asthma tx
90
M3 antagonists: MOA
Compete with ACh at H3-R - Block contraction of airway SM - Block mucous secretion
91
Ipratropium Bromide: Drug class and clinical use
M3 antagonist (more selective than atropine) Short term asthma tx and COPD tx
92
Tiotropium: Drug class and clinical use
M3 antagonist Longer term asthma tx and COPD tx
93
Ipratropium Bromide VS Tiotropium
both have NO CNS effects and NO B2 activity Tiotropium last longer (24hr)
94
Black Haw, Evening primrose, and Feverfew
contains mild amount of theophylline (asthma tx)
95
Corticosteroids: MOA
- Inhibit production of cytokines | - Inhibit lymphocytic, eosinophilic airway mucosal inflammitory
96
Corticosteroids: precautions
Increased risk for osteoporosis Stunts growth in children Inhibit immune response (Oropharyngeal candidiasis)
97
Prednisone: Drug class
Corticosteroid
98
Fluticasone: Drug class
Corticosteroid
99
Mast cell Stabilizers
Prevent mast cell degranulation (prophylactic). | No direct effect on airway SM
100
Mast Cell Stabilizers: Drug examples
Cromolyn | Nedocromil
101
Anti-IgE monoclonal antibodies
Bind to antibody on mast cell and prevent degranulation
102
Omalizumab
Anti-IgE monoclonal antibody 1dose/wk injection prophylactic
103
Leukotriene pathway inhibitor: MOA
2 ways: 1) inhibit 5-lipoxygenase 2) inhibit receptor binding
104
Montelukast: Drug class and clinical use
Leukotriene pathway inhibitor Long term asthma tx
105
Montelukast: MOA
inhibits leukotriene receptor binding
106
Tx for ASA induced asthma:
leukotriene pathway inhibitor
107
Autacoid groups
(means they have their effect locally) | Histamine, serotonin, PG, leukotrienes.
108
1st generation H1 antagonists:
Bendryl, phenergan, dramamine
109
2nd generation H1 antagonists:
Claritin, Allegra, Zyrtec
110
Buspirone
5HT1A agonist | GAD, OCD, anti-anxiety
111
Triptans
``` 5HT1B/D agonist Migraine HA prevent blood vessel dilation and stretch non-prophylactic Serotonin syndrome ```
112
Ondansetron
Zofran | 5HT3 antagonist
113
SSRIs
Prozac Zoloft Inhibit SERT
114
SNRIs
Cymbalta Pristique Inhibit SERT and NET
115
TCAs
Elavil Inhibit SERT, NET, and have anticholinergic effects
116
MAOIs
Nardil refractory depression
117
Pheytoin: clinical use
Dilatin partial, tonic-clonic
118
Pheytoin: MOA
Modification of ion conductance Enhance inhibitory-GABA Inhibit excitatory-Glutamate Highly protein bound
119
Pheytoin: AE
``` Nystagmus diplopia sedation gingival hyplasia hirsuitism ```
120
Pheytoin: levels
Therapeutic: 10-20mcg/ml Toxic: 30-50mcg/ml lethal: >100mcg/ml
121
Carbamazepine: clinical use
Tegretol (TCA) Partial(drug of choice) , TGN, BiPolar
122
Carbamazepine: MOA
Modification of ion conductance Enhance inhibitory-GABA Inhibit excitatory-Glutamate Induces hepatic enzymes
123
Carbamazepine: AE
Diplopia ataxia can develop tolerance (induces hepatic enzymes, decrease in half life over time) can speed up break down of drugs
124
Phenobarbital: clinical use
Barbituate DOC in infants partial GTCS
125
Phenobarbital: MOA
sedation Enhances inhibitory-GABA Induces hepatic enzymes
126
Phenobarbital: AE
Can worse other seizures (absence, drop, or infantile) can speed up breakdown of drugs (tolerance) severe resp. depression
127
Lamotrigine: clinical use
partial and absence seizures
128
Lamotrigine: MOA
Modification of ion conductance
129
GABA analogs: Drugs
Vigabatrin | lyrica
130
GABA analogs: clinical use
adjunct partial neuralgia Infantile spasms
131
Ethosuxamide: clinical use
Absence seizures DOC
132
Ethosuxamide: MOA
Modification of ion conductance
133
Ethosuxamide: AE
GI | lethargy
134
Valproic Acid: clinical use
Depakene generalized seizures (except TC) bipolar migraine
135
Valproic Acid: MOA
Modification of ion conductance Enhance inhibitory-GABA Inhibit excitatory-Glutamate
136
Valproic Acid: AE
``` DISPLACES PHENYTOIN Inhibits metabolism of some drugs GI sedation tremor hepatotoxicity ```
137
Benzodiazepines: clinical use
status epilepticus (Diazepam)
138
Benzodiazepines: MOA
Enhance inhibitory-GABA
139
Diazepam: half life/duration
``` Long half life (20-100H) short duration (30min) ```

Fall Pharm (8 decks)

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