Pharm (Fall 2025) > Test 3 > Flashcards

Test 3 Flashcards

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1
Q

What are the three principal activities of nephrons in producing urine?

A

Filtration at the glomerulus, reabsorption of water and solutes back to blood, and secretion of wastes or drugs from blood into the tubular fluid.

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2
Q

Where does 100% of blood plasma filtration occur in the nephron?

A

Bowman’s (glomerular) capsule.

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3
Q

Where does most selective reabsorption of essential solutes and water happen?

A

Proximal tubule via active and passive transport.

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4
Q

What is the site of action for carbonic anhydrase inhibitors like acetazolamide?

A

Proximal convoluted tubule where they block NaHCO3 reabsorption.

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5
Q

What major imbalance do carbonic anhydrase inhibitors cause and what are they used to treat?

A

They cause metabolic acidosis and potassium depletion; used for metabolic alkalosis and altitude sickness.

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6
Q

What is the mechanism of action for loop diuretics such as furosemide?

A

They inhibit NaCl reabsorption by blocking the NKCC2 cotransporter in the thick ascending limb.

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7
Q

How do loop diuretics affect magnesium and calcium?

A

They increase urinary excretion of magnesium and calcium, lowering serum levels.

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8
Q

Loop diuretics are contraindicated in patients with what allergy?

A

Sulfonamide (sulfa) allergy.

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9
Q

Where is the primary site of action for thiazide diuretics?

A

Distal convoluted tubule, blocking the NCC cotransporter.

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10
Q

How do thiazides affect calcium handling in the distal convoluted tubule?

A

They increase calcium reabsorption into blood by enhancing the basolateral Na+-Ca2+ exchanger (NCX1).

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11
Q

What is the mechanism of potassium wasting caused by upstream sodium reabsorption blockade?

A

More sodium reaches the collecting tubule, enters principal cells via ENaC, and drives potassium secretion into the lumen.

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12
Q

Which diuretics tend to cause hyperkalemia?

A

Potassium-sparing diuretics.

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13
Q

What is the specific mechanism of action for spironolactone?

A

It antagonizes aldosterone receptors (mineralocorticoid receptor blocker).

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14
Q

What is the specific mechanism of action for amiloride?

A

It directly blocks the ENaC channel in principal cells.

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15
Q

What are potassium-sparing diuretics primarily used for?

A

Mineralocorticoid excess (e.g., primary hyperaldosteronism); secondarily for heart failure and nephrotic syndrome.

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16
Q

What is the mechanism of action for osmotic diuretics like mannitol?

A

They increase tubular fluid osmolality, retaining water in the lumen and reducing sodium and water reabsorption.

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17
Q

What is a primary therapeutic use for mannitol?

A

Reducing intracranial pressure and promoting removal of renal toxins.

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18
Q

How can mannitol affect serum sodium and potassium after diuresis?

A

It can cause hypernatremia and hyperkalemia due to free water loss (renal failure patients may become hyponatremic).

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19
Q

How is airway obstruction defined in asthma?

A

Reversible obstruction due to inflammation, bronchial smooth muscle constriction, and increased mucus.

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20
Q

What is the primary airflow limitation difference between asthma and COPD?

A

Asthma is reversible; COPD is chronic and largely irreversible.

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21
Q

What is the pathology of emphysema?

A

Destruction of alveolar walls with enlarged airspaces, elastic recoil loss, and air trapping.

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22
Q

In an allergic response, which cell presents allergen to Th2 cells?

A

Dendritic cells.

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23
Q

Which cytokine stimulates B cells to become plasma cells producing IgE?

A

Interleukin-4 (IL-4).

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24
Q

What event occurs when an allergen cross-links IgE on mast cells?

A

Mast cell degranulation with rapid release of histamine and leukotrienes.

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25
List two key mediators in the early stage of asthma.
Histamine & platelet-activating factor; Prostaglandin D2
26
Which mediators characterize the late stage of asthma?
Proteases, Leukotrienes (LTC4, LTD4, LTE4) from eosinophils, macrophages, and T cells.
27
What are the two main arachidonic acid pathways and one product of each?
Cyclooxygenase makes prostaglandins and thromboxane; 5-lipoxygenase makes leukotrienes.
28
Which autonomic division provides resting bronchomotor tone?
Parasympathetic (vagus nerve).
29
What are the two broad drug strategies for asthma and COPD?
Bronchodilation & inflammation control
30
Which class is first-line for rescue inhalers in asthma?
Short-acting beta agonists (SABA), e.g., albuterol.
31
What is the molecular MOA of beta-2 agonists like albuterol?
They increase cAMP in airway smooth muscle, causing relaxation.
32
What is the MOA for methylxanthines such as theophylline?
Phosphodiesterase inhibition increases cAMP, and they also antagonize adenosine receptors.
33
How do inhaled corticosteroids reduce airway inflammation?
They suppress transcription of inflammatory cytokine genes.
34
Which muscarinic antagonist is commonly used in COPD?
Ipratropium bromide.
35
What is recommended long-term controller therapy for moderate asthma?
Low to medium dose inhaled corticosteroid plus a long-acting beta agonist.
36
Which histamine receptor mediates vasodilation, increased permeability, and bronchoconstriction?
H1 receptors.
37
Which histamine receptor stimulates gastric acid secretion?
H2 receptors.
38
What differentiates first-generation from second-generation H1 antihistamines?
First-generation (e.g., diphenhydramine) are sedating and cross the blood-brain barrier; second-generation (e.g., fexofenadine, loratadine) are minimally sedating.
39
Name two H2 blockers used for heartburn.
Ranitidine (historical) and famotidine; currently famotidine is commonly used.
40
List two common side effects of first-generation antihistamines.
Sedation and antimuscarinic effects such as urinary retention or blurred vision.
41
Where is most serotonin located and what is its function there?
About 90% is in the gut enterochromaffin cells, stimulating peristalsis.
42
What is the precursor for serotonin?
Tryptophan.
43
Which serotonin agonist targets 5-HT1A for anxiety?
Buspirone.
44
Which serotonin agonist is used acutely for migraines?
Sumatriptan (a 5-HT1B/1D agonist).
45
What is sumatriptan’s molecular target in migraine therapy?
5-HT1B/1D receptors on cranial vessels and nerves to prevent pathologic dilation and neuropeptide release.
46
What causes serotonin syndrome?
Any drug or combination that raises CNS serotonin excessively.
47
What is the immediate management for serotonin syndrome?
Airway, breathing, and circulation with sedation and intubation as needed; supportive care.
48
What causes malignant hyperthermia and how is it treated?
Triggered by volatile anesthetics or succinylcholine in susceptible patients; treat with dantrolene and supportive care.
49
List the four antidepressant classes from first-line to last resort.
SSRIs, SNRIs, TCAs, MAOIs.
50
What is the MOA of SSRIs?
They block the serotonin transporter (SERT) to increase synaptic serotonin.
51
Which antidepressant class is rarely used due to dangerous interactions?
MAO inhibitors, reserved for refractory depression.
52
What is a seizure that starts focally then generalizes called?
Focal to bilateral tonic-clonic (secondarily generalized).
53
What are automatisms and where do they often arise? What seizure type do they appear in?
Repetitive involuntary movements like lip smacking or fumbling; Originate commonly at temporal lobe Focal Imparied Awareness
54
Which seizure type is sudden brief jerks of a muscle group?
Myoclonic seizure.
55
What is the drug of choice for absence seizures?
Ethosuximide.
56
What are the three primary MOAs for antiseizure drugs?
Modulate Na+, K+, and Ca2+ channels; enhance GABAergic inhibition; inhibit glutamatergic excitation.
57
How do GABA-enhancing AEDs reduce seizures?
They increase inhibitory chloride current through GABA-A receptors, hyperpolarizing neurons.
58
What is first-line for focal seizures?
Carbamazepine (Tegretol).
59
Which AED is broad spectrum for many seizure types?
Valproic acid.
60
What class and drug are first-line for status epilepticus?
Benzodiazepines; lorazepam IV.
61
What is the primary MOA for carbamazepine and phenytoin?
Block voltage-gated Na+ channels to reduce high-frequency firing.
62
What kinetic property of phenytoin causes toxicity at high levels?
Zero-order (capacity-limited) elimination leading to disproportionate increases in concentration.
63
Name two signs of chronic phenytoin toxicity.
Gingival hyperplasia and hirsutism; coarse facial features may occur.
64
How does valproic acid increase phenytoin toxicity risk?
It displaces phenytoin from albumin, increasing free (active) phenytoin.
65
Why are benzodiazepines rarely used chronically for seizures?
Tolerance, dependence, sedation, and respiratory depression risks.
66
What is the MOA of ethosuximide?
Blocks T-type calcium channels in thalamic neurons
67
What is fosphenytoin?
A water-soluble prodrug of phenytoin that can be given IM or IV.
68
What diet therapy can help pediatric epilepsy?
Ketogenic diet (high fat, adequate protein, very low carbohydrate).
69
Which opioid should be avoided in seizure-prone patients?
Meperidine (due to normeperidine metabolite).
70
Define sedative versus hypnotic effects.
Sedatives reduce anxiety; hypnotics induce sleep and maintain sleep.
71
What is the MOA of benzodiazepines such as midazolam?
They positively modulate GABA-A receptors to increase chloride channel opening frequency.
72
What drug reverses benzodiazepine effects?
Flumazenil (a benzodiazepine receptor antagonist).
73
Why has barbiturate use declined?
Lethal overdose risk, narrow therapeutic index, and high abuse potential.
74
Which barbiturate is ultra-short-acting for induction?
Thiopental.
75
How does GABA-A receptor activation change neuronal excitability?
It opens chloride channels, hyperpolarizing the neuron and preventing excitatory postsynaptic potentials.
76
How is propofol formulated?
As an oil-in-water emulsion containing soybean oil and often egg lecithin.
77
What is the MOA of propofol?
Potentiates GABA-A receptor activity; also has some glycine receptor effects.
78
Name a non-anesthetic use of propofol.
Antiemetic, antipruritic for opioid-induced itching, or anticonvulsant.
79
What is propofol infusion syndrome?
A rare, potentially fatal syndrome with high-dose infusion causing metabolic acidosis, rhabdomyolysis, acute kidney injury, and cardiovascular collapse.
80
How do high doses of sedative-hypnotics affect sleep architecture?
They decrease REM sleep and reduce deep NREM stage 3/4 slow-wave sleep.
81
How does acute alcohol use affect sleep onset to deep stages?
It can cause rapid onset of deep slow-wave sleep initially, followed by disrupted sleep later.
82
Which enzyme converts ethanol to acetaldehyde in the main pathway?
Alcohol dehydrogenase.
83
What drug inhibits alcohol dehydrogenase for toxic alcohol ingestion?
Fomepizole.
84
What is the molecular action of disulfiram?
It inhibits aldehyde dehydrogenase, causing acetaldehyde accumulation with alcohol intake.
85
Differentiate tolerance, dependence, and addiction.
Tolerance: reduced effect requiring higher dose; dependence: physiologic adaptation causing withdrawal; addiction: compulsive drug seeking despite harm.
86
What are the three elements of Virchow’s triad for thrombosis?
Stasis, endothelial injury, and hypercoagulability.
87
Where do red thrombi form and what is a key consequence?
In low-pressure venous systems such as deep veins; risk of pulmonary embolism.
88
Where do white thrombi form and what is a key consequence?
In high-pressure arteries; risk of downstream ischemia or infarction.
89
List two acquired risk factors for deep vein thrombosis.
Prolonged immobilization or bedrest, recent surgery or trauma, obesity, estrogen therapy, active cancer, chronic venous disease, or long flights.
90
What is the pathophysiology of disseminated intravascular coagulation?
Widespread clotting activation consumes platelets and factors, leading to bleeding tendency and organ ischemia.
91
What causes heparin-induced thrombocytopenia?
Antibodies against the heparin–platelet factor 4 complex that activate platelets and promote thrombosis.
92
What is the treatment for confirmed HIT?
Stop all heparin and start a non-heparin anticoagulant such as argatroban or fondaparinux.
93
What is the general MOA of indirect thrombin inhibitors like heparin?
They accelerate antithrombin activity to inhibit thrombin and factor Xa.
94
How do UFH versus LMWH or fondaparinux differ in activity?
Unfractionated heparin inhibits both thrombin and factor Xa; LMWH and fondaparinux primarily inhibit factor Xa.
95
What reverses unfractionated heparin?
Protamine sulfate.
96
Which lab test monitors the intrinsic pathway for heparin therapy?
Activated partial thromboplastin time (aPTT).
97
What is the target INR range for most patients on warfarin?
2.0 to 3.0 (normal is about 0.8 to 1.2).
98
How does aspirin act as an antiplatelet agent?
It irreversibly inhibits COX-1 in platelets, blocking thromboxane A2 synthesis.
99
What is the MOA of clopidogrel and ticlopidine?
They irreversibly block P2Y12 ADP receptors on platelets.
100
How does desmopressin help in bleeding disorders?
It increases factor VIII activity & releases vWF, Helpful in hemophilia A & von Willebrand disease.
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