Case Presentation

1. CASE PRESENTATION ON
By
BASIL WILSON
13Q0408
PHARM D IVth yr
ACCUTE IDIOPATHIC
PARKINSONISM &
TYPE 2 DIABETES MELITUS

2. Definition
Parkinsonism is a general term that refers to a group
of neurological disorders that cause movement
problems similar to those seen in Parkinson’s
disease, such as tremors, slow movement and
stiffness.
The defining feature of parkinsonism is
bradykinesia, or slowness with decrement and
degradation of repetitive movements (“fatigue”).
Parkinsonism is a symptom complex, and differs
from Parkinson's disease which is a progressive
neurodegenerative illness.

3. Parkinsonism is an umbrella term, which
means that the person has symptoms similar
to Parkinson’s disease (like tremor, rigidity,
slowness of movements and balance
problems), although a doctor is not sure
whether those symptoms are due to the loss
of dopamine. A number of patients with
Parkinsonism do not have PD. Only 85% of
all Parkinsonism are due to idiopathic
Parkinson’s disease.

4. Atypical Parkinsonism should be
considered particularly in patients with:
•Poor response to dopamine
•Early loss of balance
•Prominent intellectual changes (dementia)
•Rapid onset or progression
•Conspicuous postural hypotension, urinary
and bowel incontinence
•Little or no tremor.

5. Etiology
Parkinson’s disease is the most common
neurodegenerative cause of
parkinsonism. Other causes include multiple
system atrophy, progressive supranuclear
palsy and corticobasal degeneration.
These other neurodegenerative conditions are
sometimes grouped together under term of
“atypical parkinsonism” or “parkinson-plus
syndromes”.

6. Parkinsonism can also be symptomatic,
as a result of various vascular, drug-
related, infectious, toxic, structural and
other known secondary causes. Of
these, drug-induced parkinsonism is
probably the most common and
includes agents that block post-synaptic
dopamine D2 receptors with high
affinity (such as antipsychotic and anti-
emetic medications) and sodium
valproate.

9. Pathophysiology
Parkinson’s disease is primarily associated with the
gradual loss of cells in the substantia nigra of the brain.
This area is responsible for the production of dopamine.
Dopamine is a chemical messenger that transmits signals
between two regions of the brain to coordinate activity.
For example, it connects the substantia nigra and the
corpus striatum to regulate muscle activity.
If there is deficiency of dopamine in the striatum the nerve
cells in this region “fire” out of control. This leaves the
individual unable to direct or control movements..

10. This leads to the initial symptoms of Parkinson’s disease.
As the disease progresses, other areas of the brain and
nervous system degenerate as well causing a more
profound movement disorder.
The exact cause for the loss of cells is unknown. Possible
causes include both genetic and environmental factors

11. Diagnosis
There is no definitive test to detect Parkinson’s disease
or Parkinsonism. For diagnosis, doctors take a
thorough medical history and may request a number of
movement tests. Because of the observational nature of
the diagnosis, Parkinson’s can sometimes be confused
with Parkinsonism, and the diagnosis may need to be
revised over time based on speed of disease
progression, response to medications and other factors.
All the Parkinsonisms have a loss of dopamine, so a
DatScan cannot be used to differentiate between them
and idiopathic Parkinson’s disease.

12. Treatment
There is overlap in treatment for Parkinson’s
and Parkinsonisms. Dopaminergic therapy (the
first line treatment for Parkinson’s) can be
effective in some Parkinsonisms. Other
common treatments for both Parkinson’s and
Parkinsonisms include physical, occupational
and speech therapy; antidepressants and
botulinum toxin (Botox) for dystonia. For all
the conditions, health care providers aim to
treat the symptoms that most affect a person’s
quality of life.

13. Demographic Details
Name : ABC Age : 70 Sex : M
I.P No : 3393 Dept. : Medicine Unit : A
D.O.A : 30/01/2017 D.O.D : 03/02/2017

14. Reason For Admission
C/O Giddiness since 15 days
C/O Generalised weakness since 15 days
Past Medical History
K/C/O Type 2 Diabetes Mellitus
since 20 years
Not a K/C/O HTN/TB/Asthma

15. Patient was apparently alright 15
days back, then developed sudden
giddiness, which is progressive in
nature, aggregate on working,
relieved on rest. C/O generalized
weakness since 15 days.
History Of Present Illness

16. Family History
 Diet : Veg
 Sleep : Decreased
 Appetite : Normal
 Habits : Nil
 B/B : N & R
No Known Allergies

17. General Physical Examination
Patient is moderately built and nourished
Well oriented to TPP
Conscious & Cooperative
PR : 80 bpm
BP : 120/80 mmHg
PALLOR +ve

18. Systemic Examination
CVS : S1S2 +
No Murmur
RS : B/L Air Entry Equal
CNS : Intact
P/A : Soft, Non tender

19. Investigations
MRI – Brain & whole spine
CBC
Urine R
RBC
Sr. Electrolytes
ECG
CXR
RVD
HBA1C
FBS

20. Provisional Diagnosis :
PARKINSONISM ? WITH
TYPE 2 DIABETIS MELLITUS

21. INVESTIGATIONS RESULTS REFERENCE
Hb (g/dl) 14.8 13.5-17.5
WBC 6700 4500-10500
Lymphocytes 25 20-40 %
Monocytes 00 0-7 %
Basophils 01 0-1 %
Eosinophils 0.5 0-5 %
Polymorphs 60 45-75 %
RBC (millions/uL) 4.82 4.7-6.1
Platelet (cells/mm3) 187000 150000-450000
R B S (mg/dl) 425 ↑ 60-140
Laboratory Data

22. INVESTIGATIONS RESULTS REFERENCE
ELECTROLYTES
Sodium (mEq/L) 137 135-147
Potassium (mEq/L) 4.7 3.5-5.2
Calcium (mEq/L) 8.2↓ 8.8-10.2
Magnesium (mEq/L) 1.7 1.8-2.9
RFT
Sr. Urea (mg%) 22 10-50
Sr. Creatinine (mg/dl) 0.7 0.6-1.2

23. Urine Routine
PUS cells : 2-3 / hpf
EPITHELIAL cells : 1-2 / hpf
SUGAR : 0.5 %
Echocardiography
Mild Concentric Left Ventricular Hypertrophy
Grade I Diastolic Dysfunction
Good LV systolic Function
Normal Pulmonary Artery pressure

24. TREATMENT CHART
BRAND NAME GENERIC NAME DOSE ROUTE FREQUENCY DAY
1
DAY
2
DAY
3
DAY
4
IVF 1 pint 40ml/hr IV √ √ √ √
Inj. PANTOP PANTOPRAZO
LE
40 MG IV 1-0-0 √ √
Inj. ACTRAPID HUMAN
INSULIN
SC 1-0-1 √ √ √ √
Tab. RAMIPRIL RAMIPRIL 2.5 MG P/O 0-0-1 √ √ √ √
Tab. SYNDOPA LEVODOPA
CARBIDOPA
110 MG P/O ½-0- ½ √ √ √ √
Tab. PRAMIPEX PRAMIPEXOL
E
0.125MG P/O 1-0-1 √ √ √ √

25. Daily Assessment
Day 2
No Fresh Complaints
PR : 90 bpm
B.P : 110/70 mmHg
S/E
RS : B/L AEE
NVBS +
CVS : S1S2 +
No Murmur
CNS : Intact
P/A : Soft non tender
Treatment Advice
As Per Chart
Patient not willing for MRI Brain & further investigations

26. Day 3
No Fresh Complaints
PR : 80 bpm
B.P : 110/70 mmHg
S/E
RS : B/L AEE
NVBS +
CVS : S1S2 +
No Murmur
CNS : Intact
P/A : Soft, Non tender
Treatment Advice
As Per Chart

27. Day 4
No Fresh complaints
PR : 76 bpm
B.P : 112/80 mmHg
S/E
RS : B/L AEE
NVBS +
CVS : S1S2 +
No Murmur
CNS : Intact
P/A : Soft, Non tender
Treatment Advice
As Per Chart

28. DAYS TIM
E
GRBS(mg/dL) Insulin dose given
DAY 1 2 PM 360
8 PM 245 10 UNITS
DAY 2 7.30
AM
269 14 UNITS
2 PM 132 2 UNITS
8 PM 343 14 UNITS
DAY 3 8 AM 207 10 UNITS
8 PM 379 18 UNITS
DAY 4 8 AM 188 6 UNITS
INSUIN DOSAGE CHART
SLIDING SCALE
<100 Stop
100-150 2 Units
150-200 6 Units
200-250 10 Units
250-300 14 Units

29. FINAL DIAGNOSIS
ACUTE IDIOPATHIC
PARKINSONISM with
TYPE2 DIABETES MELLITUS

30. Discharge Medication
BRAND NAME GENERIC NAME DOSE ROUT
E
FREQUENCY DURATIO
N
Tab. RAMIPRIL RAMIPRIL 2.5 MG P/O 0-0-1 14 Days
Tab. SYNDOPA LEVODOPA
CARBIDOPA
110 MG P/O ½-0- ½(7 days)
½-½- ½ (7 days)
14 Days
Tab.
PRAMIPEX
PRAMIPEXOLE 0.125
MG
P/O 1-0-1(7 days)
2-0-2(cont.)
14 Days
Review after 14 days in Neuro OPD

31. PHARMACEUTICAL CARE PLAN
Subjective Evidence
Objective Evidence
C/O Giddiness since 15 days
C/O Generalised Weakness since 15 days
RBC : 425 mg/dl (60-140)

32. Assessment
Based on the Subjective and Objective evidences ,
it is assessed that the patient is suffering from
ACUTE IDIOPATHIC PARKINSONISM
With
TYPE 2 DIABETES MELLITUS

33. Plan
Treatment Goals
To reduce giddiness
To reduce weakness
To improve the standard of life

34. Standard Recommendations
Dopaminergic therapy (the first line
treatment for Parkinson’s) can be effective in
some Parkinsonism's. Other common
treatments for both Parkinson’s and
Parkinsonism include physical, occupational
and speech therapy; antidepressants and
botulinum toxin (Botox) for dystonia. For all
the conditions, health care providers aim to
treat the symptoms that most affect a
person’s quality of life.

35. Patient Counselling
About disease
Diabetes mellitus type 2 (also known as type 2
diabetes) is a long term metabolic disorder that
is characterized by high blood sugar, insulin
resistance, and relative lack of insulin.
Parkinsonism is a clinical syndrome
characterized by tremor, bradykinesia, rigidity,
and postural instability.

36. About Drugs
LEVODOPA & CARBIDOPA is given in
combination
LEVODOPA is an anti parkinsonism agent which is a
dopamine receptor antagonist
CARBIDOPA is given to increase the amount of
levodopa in brain
ACTRAPID is a fast acting insulin which is produced
by Recombinant Technology

37. Life Style Modification
Healthy eating
Try not to move too quickly.
Aim for your heel to strike the floor first when
you're walking.
If you notice yourself shuffling, stop and check
your posture. It's best to stand up straight.
Look in front of you, not directly down, while
walking.
Distribute your weight evenly between both feet,
and don't lean.
Avoid carrying things while you walk.
Avoid walking backward.