Hey,Hello! awesomites ,this blog is just a small review of some old and new things I learned about Parkinson's disease.
The very first thing I learned is:- parkinson's disease and parkinsonism are two different terms !!!.
-Parkinsonism is a complex term it includes many symptoms while parkinson's disease is a progressive neurodegenerative disorder .
-Parkinosons disease is actually cause of parkinsonism .
Let's start with Parkinson's disease
-Main cause is decrease dopamine secretion in body mainly due to injury to substantia nigra which sends dopamine secreting nerve fibers to caudate nucleus and putamen.
Signs and symptoms:
- Characteristics features is tremors .Tremors occurs during all walking hours and therefore it is a type of involuntary tremor in case of cerebellar disease there is an intension tremor because tremors are seen when patient perform any work.
-Also festinant gait is found
-Akinesia is also seen
-Lead-pipe rigidity is seen earlier in hands and legs followed by neck and trunk.
Causes:
-Any serious injury that affects dopamine secretion !
-Also some medication which decreases dopamine secretion or blocks dopamine receptors.
-Apart from that certain drugs also induces Parkinson's disease like drugs used to treat schizophrenia and other neuroleptic drugs like
Clozapine.
Risperdal.
Quetiapine.
Apart neuroleptic drugs,others drugs like prochlorperazine,metoclopramide.
Also calcuim channel blockers causes Parkinson's
Drug induced Parkinson's remains same ,it doesn't progress
Categories of drugs used for treatment of parkinsonism:-
-Dopamine agonist.
-Anticholinergic.
-COMI inhibitors.
~Ojas
Today I am gonna give some brief review about how to treat constipation .So let's start with basics
Why constipation occurs ?
-Water serves as a transporter of stools ,decrease in concentration of water in intestine can lead to constipation ,it may be either due to increase absorption from the extracellular space or decrease water content in body.
-Decrease bowel moment
How to treat constipation?
-As now we know cause of the constipation ,we can treat constipation either by :-increasing water content or decrease loss of water from intestinal lumen
And also by increasing bowel moments so less water or salts are absorbed (Yet some drugs uses another mechanism.)
Drugs used :-
1)We can use Dietary fibers which will just form a bulk in intestine and will increase water content of faeces ,also due to bacterial degradation some osmotic active substances are produces which further increases water content Hey but there is one drawback ,it may causes gas :D.
2)Stool softeners:
-They permit water and lipid to penetrate stool .
-They are either given orally or rectally!
(Yes a drug acting on intestine can also given rectally)
-Again there is one drawback ,prolong use can cause impair absorption of fat soluble vitamins ( A,D,E,K)
3)Osmotic laxatives (Laxative is term used for drugs for treatment of constipation)
-Colon can neither concentrate /dilute fecal fluid so fecal fluid is isotonic throughout the colon
-Generally we use non-absorable sugars /salts eg:-Magnesium citrate & sodium phosphate.
-Osmotic laxatives are commonly used but should not be used in patient with renal insufficiency.
-But patient using sodium phosphate must take adequate water to compensate fluid loss due to it
,It may causes hyperphosphatemia,hyper natremia , hypocalcemia,hypokalemia.
-So should not be used in cardiac patients
4)Stimulant laxatives
a) Anthraquinones:It after hydrolysis produces bowel moment in 6-12hrs if given orally or within 2 hrs if given rectally.!
-It may causes melanosis coli.
b)Diphenylmethane derivatives : It increases bowel moments in 6-10hrs when given orally and in 30-60mins when given rectally.
-It has minimum systemic absorption
5) Opioid receptor antagonism
-Now this is an interesting type of drug mechanism rather than increasing motility it "decreases" motility .
Confused ?!!
Still it is used in prevention of constipation ?!
Yes ,by decreasing motility it prolonges the transient time required for absorption of water and salts from surrounding
Eg:-Methylnaltrexone & alvimopan.
~Ojas
Hello readers,today I am gonna tell you about some blood indices -there meaning, normal values, and units ! . Hopefully they will be useful . I always use to mess up them during my very first year :(
1)Mean corpuscular volume (MCV):It denotes the volume in a single RBC .It correspond to size of RBCs ,so when MCV is in normal range it denotes normocyte .When MCV increases , RBCs are known as macrocytic eg : megaloblastic anemia and when it decreases ,cell are microcytic eg: iron deficiency anemia.
MCV can be calculated by automated hematology analyzer or by using hematocrit value
MCV:-Hematocrit (%) ×10/RBC count
(million /cubic mm).
Unit of MCV is femtolitre(fL)
Normal value is 80-95 fL
2)Mean corpuscular hemoglobin(MCH):-
It's the quantity or amount of hemoglobin present in one RBC. It's normally expressed in picogram or microgram .
Normal range is 27-31 pg
Formula -
MCH :-Hb (gm per 100mL)/Total RBCs in blood(million per cubic mm) . I think no need to tell MCH decreases in anemia :D
3)Mean corpuscular hemoglobin concentration: It is concentration of hemoglobin in one RBC.It is actually the amount of hemoglobin expressed in relation to volume of RBC.(It's actually
Combination of above two terms )
So we express it in gram /dL
Normal value is 33-36 gm/dL
Formula :
MCHC:
Hb(g/100mL)×100/Hematocrit(%).
When RBC size decrease , RBC is known as hypochromic
In pernicious anemia RBCs are macrocytic and normochromic While in iron deficiency RBCs are microcytic and hypochromic.
We don't have hyperchromic RBC because content of RBC is limited !
~Ojas
Hello awesomites ! Some days back I revised my concepts on regulation of blood pressure so would like to share with you ,so lets start it .This is short -term regulation of blood pressure.
Changes in blood pressure is normally detected by 9th cranial nerve from carotid sinus and by 10th cranial nerve from aortic arch both of them carries signal to NTS (nucleus of tractus solitarius) present in medulla oblongata which in turn co-ordinate 3 centres present in medulla oblongata.
- Cardio inhibitory centre .
- Cardio stimulatory centre.
- Vasomotor centre.
Now suppose there is increase in blood pressure ,let's see microscopically what changes we are gonna seen in nerve endings of 9th and 10th nerve.
An increase in blood pressure will stretch carotid sinus and aortic arch ,which in turn will cause stretching or spreading of nerve endings ,which will increase influx of the sodium ions . Ultimately increase in depolarisation wave will cause stimulation of NTS (Even decrease in depolarisation wave will stimulate NTS ,which happens during decrease in blood pressure).Now as we know there is increase in blood pressure , NTS-our main character in this process will control these 3 centres to control blood pressure. Let's see what it do to these three centres present in medulla oblongata.
1)Cardio-inhibitory centre : This centre will be stimulated which in turn send fibers to SA node and AV node via right and left vagus nerve respectively.Leading to decrease in heart rate ,obviously cardiac output will decrease so will be blood pressure!.
2)Cardio-stimulatory centre: This centre will be inhibited which causes decrease in heart rate and cardiac output via it's fibers (post-ganglionic) which passes to lateral horn of spinal cord and then post-ganglionic fibers goes to sympathetic ganglion from where post-ganglionic sympathetic fibers acts on heart causing decrease in heart rate and cardiac output.
3)Vasomotor centre:This centre do's more work compared to above two mentioned centres .It acts on three areas ,
Arteries
Veins
Adrenal medulla
Let's see how it reacts when there is increase in blood pressure.
a) On arteries :It causes vasodilation leading to decrease in Total peripheral resistance which is directly proportional to diastolic pressure hence causes decrease in diastolic blood pressure.
b )On veins :It causes vasodilation leading to decrease in venous return which is directly proportional to EDV and which in turn causes decrease in Cardiac output and hence decrease in systolic blood pressure.
c )On adrenal medulla: Decreases release of epinephrine and nor-epinephrine which is responsible for decrease in HR,so decrease in blood pressure.
Woahh! Was such a long blog!
I think it's not necessary to mention occlusion of carotid artery causes false phenomenon of decrease in blood pressure so opposite effects will be seen:)
~Ojas.
Hi everyone,
this is notes on community medicine topic. levels of prevention and mode of intervention.
Hope it helps.
That's all
Shubham Patidar jmc 013
Hello awesomites ! Today I am gonna talk about a drug named as "Metoclopramide".
Basically it's a anti-emetic drug.First let us know what is emesis !.In simple words emesis means vomiting.Chemoreceptor trigger zone (CTZ) is located in area postrema and the nucleus tractus solitarius (NTS) of medulla oblongata.They both act as a important relay areas for afferent impulses arising in g.i.t.,throat and other viscera.
Metoclopramide is a Pro kinetic drug
It acts on GIT causing increase in peristaltic movement with relaxation of pylorus .
Mechanism of action includes :
a)D2 antagonism:It Decreases dopamine concentration and obviously acetylcholine concentration increases !.Which causes activation of ACh receptors leading to increase in LES tone and gastric pressure .
b)5-HT4 agonism:Activates 5-HT4 receptors on primary afferent neurons (PAN) of the ENS,via excitatory interneurons.
Gastric hurrying and LES tonic effects are mainly due to this action which is synergised by bethanechol and attenuated by atropine .
c)5-HT3 antagonism: At high concentrations it can block 5-HT3 receptors present on inhibitory myenteric interneurons and in NTS/CTZ .Increase in ACh concentration is also seen in minor condition
Long term use can cause parkinsonism-since decrease in dopamine , galactorrhea and gynecomastia .
It hastens use of many drugs like aspirin and diazepam by its action
~Jaskunwar Singh & Ojas
