1 Flashcards
(124 cards)
1
Q
Studies how drugs affect the body and how drug concentrations influence their effects.
A
pharmacodynamics
2
Q
A substance that changes biological functions by binding to receptors.
A
drug
3
Q
A protein where drugs bind to produce effects.
A
receptor
4
Q
Drug (Key) fits into Receptor (Lock). Must match in size, shape, and chemical properties.
A
Lock & Key Model
5
Q
Drugs binding to receptors.
A
ligands
6
Q
Activates the receptor.
A
agonist
7
Q
Blocks the receptor.
A
antagonist
8
Q
Weakly activates the receptor.
A
partial agonist
9
Q
Reverses receptor activity.
A
inverse agonist
10
Q
Fast action receptors (e.g., nicotine receptors).
A
ligand-gated ion channels
11
Q
Slow but powerful receptors (e.g., adrenaline receptors).
A
G Protein-Coupled Receptors (GPCRs)
12
Q
Control growth (e.g., insulin receptors).
A
enzyme-linked receptors
13
Q
Work inside cells (e.g., steroid hormones).
A
intracellular receptors
14
Q
They are the most common drug targets.
A
GPCRs
15
Q
Increases heart rate and relaxes muscles.
A
cAMP
16
Q
Releases calcium for muscle contraction.
A
IP3
17
Q
Activates enzymes for cell growth.
A
DAG
18
Q
How much drug is needed for effect (lower EC50 = more potent).
A
potency
19
Q
Maximum effect a drug can produce.
A
efficacy
20
Q
Dose that works in 50% of people.
A
ED50
21
Q
Dose that is toxic in 50% of people.
A
TD50
22
Q
therapeutic index (TI)
A
TI = TD50 / ED50.
23
Q
What does a high TI indicate?
A
Safer drug (e.g., penicillin).
24
Q
What does a low TI indicate?
A
Dangerous drug (e.g., warfarin).
25
It needs close monitoring.
Warfarin
26
Sympathomimetics
Adrenergic Agonists
27
Mimic the sympathetic nervous system
fight-or-flight response
28
Bind directly to receptors (e.g., epinephrine).
Direct-Acting
29
Increase norepinephrine release (e.g., amphetamines).
Indirect-Acting
30
Both direct + indirect (e.g., ephedrine).
Mixed-Action
31
Blood vessels, bladder, eye
Vasoconstriction, urinary retention, pupil dilation
Alpha-1
32
Brain, blood vessels
__________: ↓ Norepinephrine → Sedation
Alpha-2;
Presynaptic
33
Vasoconstriction
Postsynaptic
34
Heart, kidney
↑ Heart rate, ↑ renin release
Beta-1
35
Lungs, uterus, liver
Bronchodilation, uterine relaxation, glycogenolysis
Beta-2
36
Fat cells, bladder
Lipolysis, bladder relaxation
Beta-3
37
Kidney, brain
Renal vasodilation (D1), antiemetic/psychosis (D2)
Dopamine (D1/D2)
38
Renal vasodilation
D1
39
antiemetic/psychosis
D2
40
Non-Selective Agonists
Alpha + Beta
41
Non-Selective Agonists (Alpha + Beta):
o Anaphylaxis, cardiac arrest, asthma.
o Side effects: ↑HR, tremors, anxiety.
Epinephrine
42
Beta-Selective Agonists:
Heart failure, stress tests
Dobutamine (Beta-1)
43
Beta-Selective Agonists:
Asthma (bronchodilator).
Albuterol (Beta-2)
44
Beta-Selective Agonists:
Stops preterm labor.
Beta-Selective Agonists
Ritodrine (Beta-2)
45
Alpha-Selective Agonists:
Nasal decongestant, hypotension.
Phenylephrine (Alpha-1)
46
Alpha-Selective Agonists:
Hypertension (CNS sedation).
Clonidine (Alpha-2)
47
Dopamine Agonists:
Hypertensive crisis
Fenoldopam (D1)
48
Adrenergic Antagonists
Sympatholytics
49
rest-and-digest response
Block sympathetic effects
50
Alpha Blockers:
Hypertension, BPH.
Prazosin (Alpha-1)
51
Alpha Blockers:
Rarely used (erectile dysfunction)
Yohimbine (Alpha-2)
52
Beta Blockers:
Hypertension, anxiety.
Propranolol (Non-selective)
53
Beta Blockers:
Heart disease, migraines.
Metoprolol (Beta-1)
54
Dopamine Antagonists:
Nausea, gastroparesis.
Metoclopramide (D2)
55
Dopamine Antagonists:
Psychosis (blocks dopamine).
Haloperidol (D2)
56
Side Effects:
Bradycardia, fatigue, ED, asthma worsening
Beta Blockers
57
Side Effects:
Dizziness, low BP (1st-dose effect)
Alpha Blockers
58
Non-Selective Agonists (Alpha + Beta):
Shock (septic/neurogenic) → Strong vasoconstriction.
Norepinephrine (Levophed)
59
Dopamine Agonists:
Parkinson’s, hyperprolactinemia
Bromocriptine (D2)
60
Side Effects:
↑HR, tremors, hypertension, anxiety
Sympathomimetics
61
rest-and-digest response
Block sympathetic nervous system effects
62
Mechanism: Block α1 (vasodilation) or α2 (CNS effects).
Alpha Blockers
63
Non-Selective (α1 + α2):
Reversible, used for hypertensive crises (e.g., pheochromocytoma).
Phentolamine
64
Non-Selective (α1 + α2):
Irreversible, long-lasting.
Phenoxybenzamine:m
65
α1-Selective ("-zosin"):
Treat BPH + hypertension.
Prazosin, Doxazosin, Terazosin
66
α1-Selective ("-zosin"):
BPH-only (uroselective).
Tamsulosin
67
Side Effects:
▪ Orthostatic hypotension (1st-dose effect).
▪ Reflex tachycardia.
α1-Selective ("-zosin")
68
α2-Selective:
CNS stimulant (rarely used).
Yohimbine
69
Mechanism: Block β-receptors → ↓ heart rate, BP, and cardiac output.
Beta Blockers
70
Non-Selective (β1 + β2):
Prototype; also for migraines, anxiety.
Propranolol
71
Side Effects: Bronchospasm (avoid in asthma), fatigue
Non-Selective (β1 + β2)
72
β1-Selective ("Cardioselective"):
Safer for COPD/asthma.
Metoprolol, Atenolol, Bisoprolol
73
Uses: HTN, HF, arrhythmias.
β1-Selective ("Cardioselective")
74
With Intrinsic Sympathomimetic Activity (ISA):
Partial agonists; less bradycardia.
Pindolol, Acebutolol
75
α + β Blockers:
For HF, severe HTN.
Carvedilol, Labetalol
76
Side Effects:
• Bradycardia, erectile dysfunction, masking hypoglycemia (caution in DM).
Beta Blockers
77
Antihypertensives First-Line Agents:
ACE Inhibitors ("-pril")
ARBs ("-sartan")
Calcium Channel Blockers (CCBs)
Thiazide Diuretics
78
ACE Inhibitors ("-pril"):
↓ Angiotensin II → vasodilation.
Lisinopril, Enalapril
79
o Uses: HTN, HF, diabetic nephropathy.
o Side Effects: Dry cough (switch to ARB), hyperkalemia
ACE Inhibitors ("-pril")
80
o Uses: HTN, HF, diabetic nephropathy.
o Side Effects: Dry cough (switch to ARB), hyperkalemia.
ACE Inhibitors ("-pril")
81
ARBs ("-sartan"):
Block AT1 receptors (no cough).
Losartan, Valsartan
82
o Uses: Similar to ACEi (alternative if cough).
ARBs ("-sartan")
83
Calcium Channel Blockers (CCBs):
o Dihydropyridines ("-dipine")
Vasodilation → ↓ BP
Amlodipine
84
▪ Side Effects: Peripheral edema, reflex tachycardia.
Calcium Channel Blockers (CCBs):
o Dihydropyridines ("-dipine")
85
Calcium Channel Blockers (CCBs):
o Non-Dihydropyridines
Also for arrhythmias (avoid in HF).
Verapamil, Diltiazem
86
Thiazide Diuretics:
- ↓ Blood volume
o Side Effects: Hypokalemia, hyperuricemia.
Hydrochlorothiazide
87
Pros: Renal protection (DM)
Cons: Cough (ACEi), teratogenic
ACEi/ARBs
88
Pros: No electrolyte issues
Cons: Edema (DHP), avoid in HF (non-DHP)
Calcium Channel Blockers (CCBs)
89
Pros:↓ MI risk, arrhythmias
Cons: Fatigue, bronchospasm
Beta Blockers
90
Pros: BPH relief
Cons: 1st-dose hypotension
Alpha Blockers
91
Drugs:
• Furosemide, Bumetanide, Torsemide
Uses:
• Heart failure (↓fluid overload)
• Pulmonary edema
• Hypercalcemia/Hyperkalemia
Loop Diuretics
91
Mechanism:
• Inhibits ____________ → reduces bicarbonate reabsorption (PCT)
Uses:
• Glaucoma (↓aqueous humor)
• Metabolic alkalosis
Side Effects:
• Metabolic acidosis
• Low potassium (Hypokalemia)
Avoid in: COPD, Liver disease
Carbonic Anhydrase Inhibitors
91
Strongest Diuretics – "High Ceiling"
Loop Diuretics
91
Function: Increase urine output
Main Uses: Edema, Hypertension (HTN)
DIURETICS
92
Mechanism:
• Blocks Na+/K+/2Cl− pump in Loop of Henle
Loop Diuretics
93
Side Effects:
• Ototoxicity (ear damage)
• Electrolyte loss (Na+, K+, Mg²⁺, Ca²⁺)
• HYPERuricemia, HYPERglycemia
Loop Diuretics
94
Mild Diuretics – "Low Ceiling"
Thiazide Diuretics
95
Mechanism:
• Blocks Na+/Cl− pump (DCT)
Thiazide Diuretics
96
Drugs:
• Hydrochlorothiazide, Chlorthalidone
Uses:
• 1st-line for HTN
• Heart failure
• Hypercalciuria (↓kidney stones)
Thiazide Diuretics
97
Side Effects:
• HYPOnatremia, HYPOkalemia
• HYPERcalcemia
• HYPERglycemia, HYPERuricemia
Thiazide Diuretics
98
Weakest Diuretics
Potassium-Sparing Diuretics
99
Mechanism:
• Blocks Na+ reabsorption (Collecting Duct) → saves K+
Potassium-Sparing Diuretics
100
Potassium-Sparing Diuretics:
o Blocks aldosterone → ↓Na+ retention, ↑K+
o Side Effects: Hyperkalemia, Gynecomastia (men), Menstrual issues (women)
Aldosterone Antagonists (Spironolactone)
101
Potassium-Sparing Diuretics:
o Directly block Na+ channels
o Side Effects: Kidney stones (________), Hyperkalemia
Sodium Channel Blockers (Amiloride, Triamterene);
Kidney stones (Triamterene)
102
Uses:
• Prevent hypokalemia (when combined with other diuretics)
• Heart failure
Potassium-Sparing Diuretics
103
Mechanism:
• Pulls water into urine (no effect on Na+)
Drug: Mannitol
Osmotic Diuretics
104
Uses:
• ↓Intracranial pressure (brain swelling)
• Kidney issues
Side Effects:
• Dehydration (___________)
• High sodium (___________)
Osmotic Diuretics;
Side Effects:
• Dehydration (Hypovolemia)
• High sodium (Hypernatremia)
105
Mechanism: ↓Bicarbonate (PCT)
Key Drugs: Acetazolamide
Main Uses: Glaucoma
Side Effects: Metabolic acidosis, Low K+
Carbonic Anhydrase
106
Mechanism: Blocks Na+/K+/2Cl− (Loop
of Henle)
Key Drugs: Furosemide
Main Uses: Heart failure, Edema
Side Effects: Ototoxicity, Low electrolytes
Loop
107
Mechanism: Blocks Na+/Cl− (DCT)
Key Drugs: Hydrochlorothiazide
Main Uses: HTN
Side Effects: Low Na⁺/K⁺, High Ca²⁺/sugar
Thiazide
108
Mechanism: Saves K⁺ (Collecting Duct)
Key Drugs: Spironolactone
Main Uses: Prevents low K⁺
Side Effects: High K⁺, Gynecomastia
K⁺-Sparing
109
Mechanism: Pulls water (no Na⁺ effect)
Key Drugs: Mannitol
Main Uses: Brain swelling
Side Effects: Dehydration, High Na⁺
Osmotic
110
Definition: Elevated lipids (cholesterol, triglycerides) in blood → ↑risk of heart disease, stroke.
DYSLIPIDEMIA (High Cholesterol)
111
o Sources: Liver (70%) + diet (30%).
o Functions: Cell membranes, hormones (testosterone/estrogen), vitamin D, bile acids.
Cholesterol
112
Deposits in arteries → plaque.
LDL ("Bad")
113
Removes cholesterol → liver.
HDL ("Good")
114
o Stored fat from excess calories (carbs/fats).
o High levels → ↑heart disease risk.
Triglycerides
115
TREATMENT GOALS
1. Lower LDL (main target).
2. Lower Triglycerides.
3. Raise HDL.
116
1st-line for high LDL
Mechanism: Block cholesterol production in liver → ↑LDL uptake from blood.
STATINS (HMG-CoA Reductase Inhibitors)
117
STATINS (HMG-CoA Reductase Inhibitors):
Atorvastatin, Rosuvastatin
High potency
118
STATINS (HMG-CoA Reductase Inhibitors):
Simvastatin, Pravastatin.
Moderate
119
STATINS (HMG-CoA Reductase Inhibitors):
(except long-acting: Atorvastatin/Rosuvastatin).
Take at night
120
Uses:
• Hypercholesterolemia.
• Prevents heart attacks/strokes (stabilizes plaques).
STATINS (HMG-CoA Reductase Inhibitors)
121
Side Effects:
• Muscle pain (______) → Check CK levels if severe (rhabdomyolysis).
• Liver damage (rare) → Monitor LFTs.
STATINS (HMG-CoA Reductase Inhibitors);
• Muscle pain (myalgia)
