Exam 2 Flashcards
(177 cards)
1
Q
Somatic nervous system controls what?
A
Voluntary muscle movements
2
Q
Autonomic nervous system controls what?
A
Involuntary functions
3
Q
What is included in the autonomic nervous system?
A
Sympathetic, parasympathetic and enteris
4
Q
Sympathetic nervous system mediates what response?
A
Fight or flight
5
Q
what does the fight or flight response do?
A
Increase HR, BP and Breathing
6
Q
What does the parasympathetic nervous system mediate?
A
Rest and digest
7
Q
what does rest and digest do?
A
conserve energy. slow HR and promote digestion
8
Q
Parasympathetic nervous system involves primarily cranial nerve _____
A
- Vagus nerve
9
Q
what is the enteric nervous system?
A
complex network of neurons controlling gastrointestinal functions
10
Q
Parasympathetic nervous system has ____(longer/shorter) preganglionic and _____(longer/shorter) postganglionic fibers
A
longer
shorter
11
Q
Sympathetic has ____(longer/shorter) preganglionic and _____(longer/shorter) postganglionic fibers
A
shorter
longer
12
Q
Parasympathetic nervous system primarily uses ____ as a neurotransmitter, while sympathetic nervous system primarily uses _____
A
Acetylcholine
Norepi
13
Q
____ receptors are mainly muscarinic and nicotinic, while ____ receptors are mainly alpha and beta adrenergic.
A
Parasympathetic
Sympathetic
14
Q
_____ are clusters of neuron cell bodies in the sympathetic nervous system, located close to the spinal cord.
A
Chain ganglia
15
Q
_____ are networks of neurons in the enteric nervous system, similar in function to the chain ganglia.
A
PNS plexi
16
Q
What are sympathomimetics?
A
Drugs that mimic the effects of the sympathetic nervous system
17
Q
What are parasympathomimetic (cholinomimetic)
A
Drugs that mimic the effects of the parasympathetic nervous system.
18
Q
What are sympathoplegic (α and β blockers)?
A
Drugs that block the sympathetic nervous system.
19
Q
What are parasympathoplegics (anticholinergics)
A
Drugs that block the parasympathetic nervous system.
20
Q
List the sympathetic receptors, subtypes, and second messengers
A
Receptor: Adrenergic receptors
Subtype: Alpha and Beta
Second messengers: cAMP, IP3, DAG
21
Q
List the parasympathetic receptors, subtypes and second messengers
A
Receptor: Cholinergic receptors
Subtype: Muscarinic and Nicotinic
Second messengers: cAMP, IP3, DAG
22
Q
What are the adrenergic alpha receptor subtypes?
A
Alpha 1 and 2
23
Q
What are the adrenergic Beta receptor subtypes?
A
Beta 1 and 2
24
Q
What G protein is coupled with Alpha 1, Alpha 2, Beta 1 and Beta 2?
A
QISS
A1: Gq (activates phospholipase C)
A2: Gi (inhibitory..inhibit adenylate cyclase)
B1/B2: Gs (stimulates..increase cAMP)
25
Where are alpha 1 receptors found and what do they cause?
Vascular smooth muscle, causing vasoconstriction.
26
Where are the Alpha-2 adrenergic receptors found and what does this cause?
Presynaptic, inhibiting neurotransmitter release.
27
Where are the Beta-1 adrenergic receptors found and what does this cause?
Cardiac muscle, increasing heart rate and contractility.
28
Where are the Beta-2 adrenergic receptors found and what does this cause?
Vascular smooth muscle, causing vasodilation. Bronchi causing bronchodilation
29
Where are the Muscarinic cholinergic receptors found and what does this cause?
Smooth muscle (relax)
Heart (decrease HR and contractility)
30
Where are the Nicotinic cholinergic receptors found and what does this cause?
Skeletal muscle (muscle contraction.)
31
How does the autonomic (sympathetic and parasympathetic) feedback loop work in terms of MAP
Sympathetic: vasoconstriction, increase HR, increase contractile force, increase venous tone = increased BP
Parasympathetic: vasodilation, decrease HR = decrease BP
32
How does the hormonal feedback loop work in terms of MAP
Decreased blood pressure is sensed by the kidneys, leading to renin release, angiotensin II production, and aldosterone secretion to increase blood volume and pressure.
33
What are the organ system effects of stimulation of the parasympathetic system?
Slowed heart rate, bronchoconstriction, increased digestive activity.
34
What are the organ system effects of stimulation of the sympathetic system?
Increased heart rate, bronchodilation, decreased digestive activity.
35
describe how vasodilation occurs in skeletal muscle blood vessels.
vasodilation of skeletal muscle blood vessles via acetylcholine released from postganglionic parasympathetic fibers.
36
List the six main classes of neurotransmitters
1.esters of choline
2.monoamines
3.amino acids
4. purines
5. peptides
6. inorganic acids
37
Example of esters of choline neurotransmitter (1)
Acetylcholine
38
Example of monoamines neurotransmitter (3)
norepi
dopa
serotonin
39
example of amino acids neurotransmitter (2)
glutamate
gaba
40
example of purines neurotransmitter (2)
adenosine and ATP
41
example of peptides neurotransmitter (2)
substance P
endorphins
42
example of inorganic acids neurotransmitter (1)
nitric oxide
43
Recall the function of three CNS neurotransmitters in emotion.
Dopamine
Serotonin
Norepo
44
List three types of synapses described in lecture.
chemical synapses
electrical synapses
on-pause synapses.
45
Describe the possible fate of neurotransmitters in the synapse. (4)
1. diffusion away from synapse
2. degraded by enzymes
3. uptake into pre-synaptic cell
4. uptake into surrounding cells
46
What is the difference between excitatory and inhibitory neurotransmitters
Excitatory: Cause depolarization (e.g., glutamate).
Inhibitory: Cause hyperpolarization (e.g., GABA).
47
What role does CHT play in the presynaptic neuron?
Choline transporter into neuron
48
Describe the formation of acetylcholine
acetyl-CoA + choline via ChAT
49
Describe the transport of acetylcholine (specifically VAT)
VAT transports ACh into vesicle
50
Describe the enzymatic cleavage of acetylcholine
enzymatic cleavage occurs by acetylcholinesterase (AChE)
51
What is the SNARE complex?
Anchoring (docking). includes SNAP-25 and VAMP
52
List targets for drug action in the synapse. (5)
Synthesis
Storage
Release
Receptors
Degradation/Reuptake
53
What is an example of drug action for the synthesis synapse
Inhibition of tyrosine hydroxylase to block norepinephrine synthesis
54
What is an example of drug action for the storage synapse
Reserpine to inhibit vesicular storage of neurotransmitters
55
What is an example of drug action for the release synapse
Botulinum toxin to block neurotransmitter release
56
What is an example of drug action for the receptors synapse
Agonists and antagonists acting on muscarinic, nicotinic, alpha, beta, dopamine, and serotonin receptors
57
What is an example of drug action for the reuptake synapse
SSRI - reuptake inhibitor
58
List the major clinical uses of cholinomimetic agonists (cholinergic agonists). (4)
Acetylcholine - pupillary constriction
Methacholine - astha (Dx)
Carbachol - Decrease IOP
Bethanechol – Bladder dysfunction, GERD
59
Describe direct-acting cholinomimetic agent
Mimic activity of acetylcholine. (bind to and activate M or N receptors)
60
Describe indirect-acting cholinomimetic agent
Block acetylcholinesterase
61
The indirect cholinomimetic ______ is useful in the diagnosis of Myasthenia gravis
Edrophonium
62
Describe the differences between a nicotinic and muscarinic receptor.
Nicotinic receptors are ion channels
muscarinic receptors are G-protein coupled receptors.
63
List the effects of cholinomimetics in the major organ systems (eye, CV system, respiratory system and GI)
eye (pupillary constriction)
cardiovascular system (decreased peripheral resistance, increased heart rate)
respiratory system (bronchoconstriction)
gastrointestinal tract (increased secretions and motility).
64
What are the two different types of glaucoma?
Open-angle and closed-angle
65
Cholinomimetics are used for which type of glaucoma and contraindicated in what other type of glaucoma?
used for - open-angle
contraindicated for: closed-angle
66
List the major signs and symptoms of organophosphate insecticide poisoning
"SLUDGE-M"
salivation
lacrimation
urination
defecation
gastrointestinal motility
emesis
miosis
67
List the major signs and symptoms of acute nicotine toxicity.
tremors
vomiting
respiratory stimulation
convulsions
coma
68
What is the function of acetylcholinesterase?
Breaks down acetylcholine
69
what is the function of organophosphate aging?
organophosphates can irreversibly inhibit this enzyme through covalent binding and "aging".
70
Antimuscarinics: main uses for the following according to lecture:
Atropine is for _____
Scopolamine is for ____
Tropicamide is for _____
Ipratopium is for _____
1. bradycardia
2. motion sickness
3. eye
4. COPD
71
Describe the effects of atropine on the major organ systems. (Eyes, CV system, Respiratory system, GI)
atropine can reverse the effects of cholinomimetics
eye (pupillary dilation)
cardiovascular system (increased heart rate)
respiratory system (bronchodilation)
gastrointestinal tract (decreased secretions and motility).
72
Symptoms of atropine overdose
BRAND
Blind
Red
Absent bowel sounds
Nuts (cray cray)
Dry
73
Treatment of atropine overdose
neostigmine or pyridostigmine
74
the use of cholinomimetics myasthenia gravis
Neostigmine:
treat the muscle weakness by increasing acetylcholine levels at the neuromuscular junction.
75
the use of cholinomimetics glaucoma
pilocarpine:
open-angle glaucoma
increasing drainage of aqueous humor.
Atropine can be used in open angle with caution
76
the use of cholinomimetics in post-operative ileus.
neostigmine:
used to treat the paralysis of the gastrointestinal tract that can occur after surgery.
77
List the major clinical indications for the use of muscarinic antagonists such as atropine.
poisonous mushrooms (muscarinic excess)
Organophosphare exposure
Premedication before anesthesia to reduce secretions
78
List the major clinical contraindications for the use of muscarinic antagonists such as atropine.
Closed-angle glaucoma - Atropine can worsen the condition by further constricting the angle and impeding drainage
79
Name the two categories of muscle relaxants.
Depolarizing muscle relaxants
Non-depolarizing muscle relaxants
80
Differentiate depolarizing muscle relaxants and give examples
(e.g., succinylcholine) cause initial depolarization of the muscle followed by paralysis.
81
Describe non-depolarizing muscle relaxants and give examples
(e.g., rocuronium, vecuronium) competitively block acetylcholine at the NMJ without causing depolarization.
derivatives of curare
82
Recall the basic structure of catecholamines.
catechol group (a benzene ring with two hydroxyl groups) and an amine group.
83
Mechanism of Action (MOA) of Direct Acting Catecholamines
These directly bind to and activate adrenergic receptors
84
Mechanism of Action (MOA) of Indirect Acting Catecholamines
Release catecholamines from presynaptic terminal
85
Why cant catecholamines be taken orally?
because it is broken down in the gut by COMT
86
Describe what happens in the cardiovascular system after the administration of an alpha-agonist
vasoconstriction
87
Describe what happens in the cardiovascular system after the administration of an a beta-agonist
Beta 1- increase HR, increase contractility
Beta 2- bronchodilation, vasodilation = decrease BP
88
Describe what happens in the cardiovascular system after the administration of a mixed agonist.
mixed agonists like epinephrine (increase both blood pressure and cardiac output).
89
Norepi has effects on ____ and ____receptors and has little effect on _____ receptors.
Alpha
Beta 1
Beta 2 (little effect)
90
Name a typical nonselective α agonist
Phenylephrine
91
Name a typical selective α2 agonist (2)
Dexmedatomidine and Clonidine
92
Name a typical nonselective β agonist
Isoproterenol
93
Dobutamine is a _____ selective agonists and is used for treating ______ and ______
beta 1
cardiac shock
acute heart failure
94
Name a typical selective β2 agonists.
Albuterol
95
List tissues that contain significant numbers of α1 receptors.
peripheral vasculature
96
List tissues that contain significant numbers of α2 receptors.
central nervous system.
97
Tissues Containing Significant β1 Receptors
Heart (increases heart rate and contractility).
Kidney (renin release).
98
Tissues Containing Significant β2 Receptors
Bronchial smooth muscle (bronchodilation).
Vascular smooth muscle in skeletal muscle (vasodilation).
99
Define the triphasic effects of dopamine.
low doses cause vasodilation
medium doses increase cardiac effects
high doses increase blood pressure.
100
List the most common toxicities associated with sympathomimetics.
Cardiac arrhythmias
Addiction
CNS effects
101
Effects of an α Blocker on blood pressure
Vasodilation, lower BP
102
phentolamine, prazosin, terazosin, and doxazosin are examples of what?
alpha blockers
103
Phentolamine and phenoxybenzamine can be used in the treatment of _____ linked to pheochromocytoma (tumor of the adrenal glands that secrete epi and norepi)
Hypertension
104
propranolol, metoprolol, atenolol, lebetalol and esmolol are examples of what?
beta blockers
105
What are the clinical uses for alpha and beta blockers?
hypertension, angina, certain arrhythmias, and pheochromocytoma (for alpha blockers)
106
Explain the following sentence: Phentolamine converts a pressor (epinephrine) into a depressor.
phentolamine, an alpha blocker, can block the pressor effects of the alpha agonist epinephrine, leading to a decrease in blood pressure.
107
Selective beta-blockers metoprolol and atenolol are typically safer for treating ____ and _____ and are mainly beta _____ selective.
COPD and diabetics
beta 1
108
non-selective beta-blocker propranolol works on which beta receptor
beta 1 and 2
109
Describe the clinical indications of typical α and β blockers.
hypertension, angina, certain arrhythmias, and pheochromocytoma (for alpha blockers).
110
Describe the toxicities of typical α and β blockers.
bradycardia, bronchospasm, hypoglycemia, and weight gain (for long-term use of beta blockers).
111
How do you calculate MAP
diastolic pressure plus 1/3 of the difference between systolic and diastolic pressures.
112
Cardiac output as a regulator of BP
Increased CO raises BP
113
PVR as a regulator of BP
Resistance in the arteries; increased PVR leads to higher BP
114
Four main anatomic control sites for blood pressure.
the resistance arterioles
the capacitance venules
the pump output of the heart
the renin-angiotensin-aldosterone system.
115
non-pharmacologic intervention for elevated blood pressure.
Controlling salt intake, weight and stress
116
List 4 major groups of antihypertensive drugs
1. Diuretics
2. Sympathoplegics
3. direct vasodilators
4. anti-angiotensins
117
Hydralazine, minoxidil, nitroprusside and fenoldopam are examples of what class of antihypertensives?
Vasodilators
118
______ and _____ are centrally acting sympathoplegic drugs that primarily act on _____ receptors
Methyldopa
Clonidine
Alpha 2
119
Methyldopa is typically used to treat ______.
pregnancy induced hypertension
120
Clonidine is (1)_____ soluble. It is used as a backup (2)_____. More commonly it is used for (3)_____, (4)_____, and (5)_____
1. lipid
2. antihypertensive
3. ADHD
4. tourettes
5. Withdrawl symptoms
121
A major side effect of both clonidine and methyldopa is _____
sedation
122
List the major sites of action of peripheral sympathoplegic drugs in clinical use and give examples of drugs that act at each site.
sympathetic ganglia, the adrenergic nerve terminals, the alpha receptors, and the beta receptors.
Examples of drugs acting at these sites include phenoxybenzamine (alpha blocker), propranolol (beta blocker), and labetalol (alpha and beta blocker).
123
MOA of vasodilators
Relax smooth muscle in blood vessels
124
4 classifications of vasodilators
Calcium channel blockers
NO donors
K channel openers
Alpha blockers
125
Describe the compensatory responses to vasodilators.
increased sympathetic outflow, increased renin release, and sodium and water retention.
126
List the major antihypertensive vasodilator drugs and describe their effects. (2)
Hydralazine and Minoxidil
K channel activation, hyperpolarization of smooth muscle
127
What is sodium nitroprusside typically used for and what are concerns for using this drug?
HTN emergencies. However, it has high toxicity due to the cyanide molecules in its structure.
128
List the three classes of CCBs and major target of each.
Verapamil- More targeted towards the heart
Dihydropyridines (e.g., nifedipine, amlodipine) - More targeted towards the peripheral vasculature
Diltiazem - Somewhere in between the other two classes in terms of its effects on the heart and peripheral vasculature.
129
Describe the differences between ACE inhibitors and Angiotensis receptor blockers
ACE inhibitors (e.g., captopril) - Block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin.
Angiotensin receptor blockers (ARBs) - Directly block the binding of angiotensin II to its receptors, without affecting the production of angiotensin II.
130
What is the side effect of ACE inhibitors that everyone hates and what causes this?
Dry cough. ACE inhibitors lead to an increase in bradykinin levels
131
List and describe mechanisms of action for pulmonary hypertension therapeutics. (2)
Prostaglandins (e.g., prostacyclin) - Cause vasodilation in the pulmonary vasculature.
Endothelin receptor antagonists - Block the endothelin receptors, which are involved in vasoconstriction and smooth muscle proliferation in the lungs. (Bosentan)
132
Define hypertensive urgency
hypertensive urgency is defined as blood pressure greater than 180/110 mmHg without end-organ damage
133
Define hypertensive crisis.
hypertensive emergency is the same high blood pressure with acute end-organ damage.
134
TX for mild/mod HTN
diet, exercise
single-drug therapy (diuretic, Beta-blocker, Ca channel blocker)
135
Treatment for severe/emergent HTN
Continuous IV infusion of parenteral antihypertensives like sodium nitroprusside or fenoldopam.
136
What is arterial tone responsible for?
regulating vascular resistance and blood pressure.
137
What is capillary tone used for?
important for distributing blood flow to different tissues based on their metabolic needs
138
What is venous tone responsible for?
The primary function is to conduct blood back to the heart, rather than regulate pressure.
139
Describe the pathophysiology of effort angina
Effort angina is caused by decreased blood flow to the heart due to coronary artery disease, leading to an imbalance between oxygen demand and supply.
140
Describe the pathophysiology of vasospastic angina
caused by temporary spasm of the coronary arteries, rather than fixed blockages.
141
Describe the major determinants of cardiac oxygen consumption.
heart rate, contractility, and wall tension.
142
Explain the following: coronary blood flow is directly related to duration of diastole.
Coronary blood flow occurs mainly during diastole when the heart muscle relaxes and perfusion to the coronary arteries increases.
143
Strategies and Drug Targets for Anginal Pain Relief
Reduce Oxygen Demand: Use beta blockers or calcium channel blockers.
Increase Oxygen Supply: Use nitrates to dilate coronary vessels.
144
Molecular Pathways of Vascular Tone and Drug Targets
Nitric Oxide Pathway: NO activates guanylyl cyclase, increasing cGMP and leading to vasodilation. Drugs like nitroglycerin target this pathway.
145
name the Primary Nitrates and Nitrites. What do they treat
Nitroglycerin and isosorbide dinitrate.
Angina and heart failure
146
MOA of Primary Nitrates and Nitrites
Donate NO, increasing cGMP for vasodilation.
147
Concerns with Overexposure to Nitrates/Nitrites
Tolerance: Continuous use can lead to decreased efficacy.
Methemoglobinemia: Overexposure can cause abnormal hemoglobin formation.
148
Receptor Differences in Epicardial Arteries
Alpha and Beta Receptors: Epicardial arteries contain both alpha (vasoconstrictive) and beta (vasodilatory) receptors.
149
Is Ranolazine a pFOX inhibitor?
yes
150
Describe MOA of pFOX inhibitors
Inhibit fatty acid oxidation, shifting metabolism to glucose, reducing oxygen consumption.
151
Therapeutic and Adverse Effects of Nitrates for Angina
Vasodilation, but can cause headaches and hypotension.
152
Therapeutic and Adverse Effects of Beta Blockers for Angina
Reduce heart rate, but can cause fatigue and bradycardia.
153
Therapeutic and Adverse Effects of CCBs for Angina
Vasodilation, but may cause edema and reflex tachycardia.
154
Why would we combine Nitrate with Beta Blocker or CCB
Combining nitrates with beta blockers or CCBs can reduce compensatory mechanisms like reflex tachycardia, providing better angina control.
155
Medical Therapy for Angina
Focuses on reducing oxygen demand and increasing supply (e.g., drugs like nitrates, beta blockers).
156
Surgical therapy for angina
Coronary interventions like angioplasty or bypass surgery improve coronary blood flow mechanically
157
Define heart failure
Heart cant pump enough blood to meet body's needs
158
The four factors of cardiac performance
Preload
Afterload
Contractility
Heart rate
159
Define the Starling law.
force of cardiac muscle contraction is directly proportional to the initial length of the muscle fiber (preload).
This means that increased ventricular filling (preload) leads to a more forceful contraction, up to an optimal point.
160
How does ESV contribute to EDV
End-systolic volume (ESV) - Higher ESV leads to higher end-diastolic volume (EDV) through the Frank-Starling mechanism.
161
How does passive filling contribute to EDV
Increased venous return and ventricular compliance during diastole contribute to higher EDV.
162
How does atrial contraction contribute to EDV
The "atrial kick" at the end of diastole further increases EDV by actively filling the ventricles
163
treatment for acute heart failure
Diuretics: Furosemide.
Vasodilators: Nitroglycerin, sodium nitroprusside.
Positive Inotropes: Dobutamine, milrinone.
164
Treatment for chronic HF
ACE inhibitors: Lisinopril.
Beta blockers: Carvedilol, metoprolol.
Aldosterone antagonists: Spironolactone.
ARNI (angiotensin receptor-neprilysin inhibitor): Sacubitril/valsartan.
165
Molecular Mechanisms Controlling Normal Cardiac Contractility
Calcium influx during the plateau phase of the action potential triggers calcium release from the sarcoplasmic reticulum, which binds to troponin C, leading to actin-myosin interaction and muscle contraction.
166
Describe the mechanism of action of digitalis and its major effects.
Digitalis (e.g., digoxin) inhibits the Na+/K+ ATPase pump in cardiac myocytes, leading to increased intracellular sodium.
This, in turn, increases intracellular calcium through the Na+/Ca2+ exchanger, enhancing calcium-mediated contraction of the myofibrils.
The major effects of digitalis include increased contractility, decreased heart rate, and increased cardiac output.
167
Describe the nature and mechanism of digitalis’s toxic effects on the heart.
Digitalis toxicity can lead to cardiac arrhythmias, such as atrial and ventricular tachyarrhythmias.
This is due to the drug's effects on the Na+/K+ ATPase pump, which can disrupt the normal electrical activity of the heart when present in excess.
168
Positive Inotropic Drugs for Heart Failure (Other than Digitalis)
Dobutamine: Beta-1 agonist, increases contractility.
Milrinone: Phosphodiesterase-3 inhibitor, increases cAMP, enhancing contractility and vasodilation.
169
Reasoning for Beta Blockers in Heart Failure
Chronic sympathetic stimulation is harmful in HF. Beta blockers reduce heart rate, improve ejection fraction over time, and prevent adverse remodeling.
170
Effects of Non-Inotropic Drugs in Heart Failure
Diuretics: Reduce preload and alleviate fluid overload.
Vasodilators: Decrease afterload (e.g., ACE inhibitors, hydralazine).
ACE Inhibitors: Reduce RAAS activity, decreasing afterload and preload, and preventing remodeling.
Beta Blockers: Reduce sympathetic overactivity, slow heart rate, and prevent remodeling.
171
Non-Pharmaceutical Interventions for Heart Failure
Lifestyle modifications: Low-sodium diet, fluid restriction.
Exercise: Cardiac rehabilitation.
Surgery: Bypass, VAD
172
List the different types of arrhythmias.
Bradycardia
Tachycardia
Heart block
Bundle branch block
Atrial fibrillation
Ventricular fibrillation
173
Intrinsic Conduction System and EKG Reading
Conduction System: SA node → AV node → Bundle of His → Right and left bundle branches → Purkinje fibers.
174
EKG interpretation
P wave (atrial depolarization), QRS complex (ventricular depolarization), and T wave (ventricular repolarization).
175
Compare the different types of ion channels, their operation, and contribution to the cardiac action potential.
Sodium Channels: Rapid depolarization (Phase 0).
Calcium Channels: Plateau phase (Phase 2).
Potassium Channels: Repolarization (Phase 3).
176
Describe the process of sodium channel recycling and the positions of the m and h gates.
m gate: Activation gate, opens during depolarization.
h gate: Inactivation gate, closes during depolarization, reopens during repolarization.
177
Cardiac Action Potential Phases
Phase 0: Rapid depolarization (Na+ influx).
Phase 1: Initial repolarization (K+ efflux).
Phase 2: Plateau (Ca2+ influx).
Phase 3: Repolarization (K+ efflux).
Phase 4: Resting potential.
