Parkinson's disease is one condition under the branch of 'Parkinsonism' - way to confuse you, I know. Basically, parkinsonism describes the symptoms typical of the disease (tremor, walking difficulties, cognitive decline, etc.). Parkinsonism can develop due to other causes, which we discuss later on. 
- Whereas, Parkinson's disease describes the specific condition involving degeneration of the dopaminergic neurons, primarily in the substantia nigra of the basal ganglia (a part of the brain involved in movement, among other things). 

The substantia nigra ("black substance") appears darker than its surrounds, due to the high density of neuromelanin - a by-product of dopamine-transmitting neurons. This area of the brain degenerates in Parkinson's disease. It plays a role in motor control and rewarding certain behaviour (hence the term, 'dopamine rush' - when you do something fun).
The treatment of Parkinson's disease aims to increase the amount of dopamine in this region of the brain, to counter the decreasing dopamine activity. 

Diagnosing 'PD' is a clinical decision, chiefly made be a neurologist. Their decision can be aided by imaging of the brain, known as a 'DaTscan' - looking for evidence of a reduction in dopaminergic neurons. The scan can help to differentiate between PD and other causes of a tremor - such as a benign essential tremor. 

PD tends to affect one limb more than the other, whereas BET typically affects both limbs equally. BET will also typically get worse with intended movement, whereas PD tremor often disappears when the hand is not at rest. PD tends to present with a classic form of tremor titled 'pill-rolling', it appears as if the patient is trying to change the frequency on a radio (obviously, 'radio-frequency tremor' didn't have the same ring to it).
A suspicion of PD may be raised even earlier than the tremor phase by a GP with a keen eye. In early PD, patients often lose the natural arm swing on one side as they walk. 

There are many possible symptoms of PD as it progresses, so I may list them here... pill-rolling tremor seen at rest, shuffling gait, problems with initiating movement, freezing during a movement, slow movements (bradykinesia), small handwriting, stooped posture and a risk of falls, rigidity (often described as 'lead-pipe'),  cognitive decline/dementia, mood changes, poor sleep, postural hypotension (changes in blood pressure upon standing causing light-headedness and in some cases, a brief loss of consciousness).
- Like we said, there are a lot, and there are even more!

Once diagnosed, the mainstay of treatment is dopamine replacement - in the form of L-dopa (commonly known as the medication, Levodopa). L-dopa is a precursor of dopamine that is able to cross a special bridge known as the blood-brain barrier. Within the brain, it is processed to form dopamine. Dopamine itself cannot cross this barrier and reach the brain, making it fairly useless as a Parkinson's medication! The dosage and timing of L-dopa is a process of trial and error from patient to patient - based on the clinical results. 

There are other medications that support L-dopa is its dopamine-boosting quest.
For instance, dopamine receptor agonists (activators) such as Ropinerole or Pramipexole. 
COMT inhibitors (such as Entacapone) stop an enzyme from breaking down L-dopa before it reaches the brain. 
MAO-B inhibitors (such as Selegiline) stop an enzyme from breaking down dopamine in the brain. 

Deep Brain Stimulation (DBS) involves surgically implanting small wires into the degenerating region of brain, and delivering electrical stimulation - akin to a pacemaker for the heart. This treatment isn't too common but can be very helpful for some. 

The aforementioned Parkinsonism is an umbrella term for the array of symptoms listed earlier. These symptoms can result from other forms of neurological illness or indeed certain medications (such as anti-psychotics which act on the dopamine-neuron pathways).
Other neurological illnesses causing parkinsonism include progressive supranuclear palsy (PSP), Lewy body dementia, Cortico-basal degeneration, multiple system atrophy (MSA), etc. 
- They are differentiated from Parkinson's disease by a neurologist by certain variances in their symptoms or supporting tests/imaging.

The last thing I'll mention is the increased risk of addiction in patients on Parkinson's disease treatment - because it's interesting! Dopamine plays an important role in rewarding us a with a "good feeling" after something fun. The more we chase that dopamine rush, the more likely we are to crave it. This is why we are all addicted to our phones, with their countless, mindless dopamine kicks they provide. By increasing dopamine levels via medication, especially with the additional issue of cognitive decline - Parkinson patients are at an increased risk of showing addictive behaviour. The classic example is elderly people playing the slot machines!