Friday, April 30, 2010

Tetanus

Etiology:


Pathogenesis:

C. Tetani is an aerobic bacteria that can always be found in soils, feces of some animals such as cats, sheeps, cattles, horses, chickens and etc. This bacteria produce exotoxin that can be transported through axon by retrograde intraneural system. Basically, this toxin, known as tetanoplasmin, cleave synaptobrevin, protein important for the synaptic release. As a result, glycine or GABA is not released into synaptic cleft. The condition increases the resting firing rate of alpha motor neuron. This causes the contraction of both agonist as well as antagonist muscle even by light stimulation.

Causes:
i) Mother is not immunized
ii) Delivery at home
iii) unsterilized treatment of umbilical cord stump

Sign and Symptoms:

i) Neck stiffness
ii) Facial rigidity
iii) Abnormal rigidity
iv) Generalized rigidity
v) Trismus
vi) Abnormal crying
vii) Diminish sucking
viii) Impaired feeding
ix) Fever
x) Cyanosis

Diagnosis:
i) The birth setting at home
ii) Improper management of umbilical cord stump
iii) Nonimmunized mother
iv) Neurological signs and symptoms should raise suspision of tetanus.


Treatment:
i) Enteral feeding
ii) IV infusion for electrolytes
iii) Penicillin G 10 000 unit/kg for 10 days
iv) Immunoglobulin 500 unit, i.m. , in divided dose.
v) Fever management
vi) Mechanical ventilation and endotracheal intubation.
vii) Sedatives - high dose of diazepam 20 - 40 mg/kg/day.

Thursday, April 29, 2010

Chocolate

This session focus on the effect of chocolate on stress...

Basically, chocolate is thought to cause the release of endorphins in our brain which is important as pain killer.

According to medicinenet.com, eating dark chocolate ( 1.4 ounches) everyday for 2 weeks seemed to reduce the level of stress hormones (cortisol). Moreover, dark chocolate can also reduce the level of fight-and-flight hormones - cathecolamines. Cocoa foun in dark chocolate serve as antioxidant (flavonoids). As a result, there is an improvement of insulin sensitivity, reduction of blood pressure and elavation of mood. Other disorders that can be reduced are anxiety.







By the way, Thanks a lot to my friend, Abg Ahmad for giving these chocolates :)

References:
1. CNN food
2. Medianet.com

Optic Nerve Atrophy

There are two types of optic nerve atrophy:
a) Acquired
b) Heredodegenerative

A. Acquired

Pathogenesis:

The axon of optic degenerate due to certain causes that will be replaced by glial cells.

Causes:

i) vascular occlusion
ii) trauma
iii) metabolic disease such as Diabetes mellitus
iv) degenerative disease
v) toxic
vi) post neuritis
vii) post papilledema
viii) congenital abnormality
ix) glaucoma

Types of atrophy:

i) Primary atrophy - pale and clear border
ii) Secondary atrophy - pale and the border is not clear
iii) consekutive atrophy - occur due to abnormality of retina.

Sign and symptoms:

i) Decrease in visual acuity
ii) Decrease in color perception
iii) Disturbance in visual eye field
iv) Abnormality in papil examination:
- diffuse vs localized
- light or severe
- total or partial

Sectoral atrophy:
i) bowtie shape atrophy in both eyes due to chiasma opticum lesion
ii) right disc bowtie shape atrophy due to the lesion on left optic tract or left corpus geniculatum

Leber Disease

Pathogenesis:

Follow maternal inheritance, this disease is transferred through maternal mitochondria. Paternal mitochondrial DNA is not transferred because of the ovum mechanism that destruct paternal mitochondria during fertilization.

Onset:

Second to third decades in young man adult.

Characteristics:

1.Sudden central visual disturbance with 20/200 or hand counting visual acuity.
2.Central scotoma that is large and deep.
3. Elavation and hyperemia of papil (in acute phase).
4. Headache and meningeal sign due to inflammation of arachnoids.
5. Atrophi of papil, with flat and pallor region.
6. Atrophi of the optic nerve.

Monday, April 26, 2010

Ischemic stroke

Pathophysiology

Pathophysiology
Basically, if the blood supply is < 16 -18 mL/ 100 g tissue per min, the tissue will be dead (infarction) within an hour. But if the blood supply is < 20 mL/100 g tissue per min, there is only ischemia without infarction unless the condition is prolonged from hours to days.
Focal cerebral infarction occurs through two pathways: (1) Apoptosis and (2) necrosis due to the rapid cytoskeleton breakdown due to the failure of energy of cells.
The occlusion of the vessels can lead to the deprivation of the oxygen and nutrients to the affected area. Basically, the lack of glucose can lead to many devastating conditions. Glucose is an important energy source that can only be used by the brain. ATP production is impaired in this condition. So, this can lead to the failure of ion channels to transport ions out of the cells. As a result, cells become depolarized. The depolarization can lead to the release of glutamate due to the influx of calcium ions. Glutamate acts on post-synaptic membrane receptor, leading to the influx of calcium ions in these neurons. Free radicals are also generated due to lipid peroxidation and mitochondrial dysfunction. Many conditions can worsen the condition of the stroke such as fever and hyperglycemia ( > 200 mg/dl).


Management:

A. Medical support:


1. Airway, Breathing and Circulation.
2. Prevent bedridden complication:
i. infections: pneumonia, skin and UTI.
ii. Deep venous thrombosis – pneumatic compression stockings and subcutaneous heparin.
3. Fever- antipyretics and surface cooling
4. Glucose level must be less than 110mg/dL – insulin administration
5. Blood pressure – The blood pressure must be lowered in the case of malignant hypertention, concomitant myocardial ischemia or if the blood pressure is >185/110 and antithrombotic therapy is anticipated. We can use beta adrenergic blocker (esmolol).
6.Cerebral Edema – Basically this condition is dangerous because of the risk of brain herniation or obtundation. This may peak at day 2 or 3 but the mass effect can be seen in approximately at day 10. Use of mannitol and fluid restriction but not to cause hypovolemia condition as it can cause hypotension and worsen the conditions. Moreover, hemicraniectomy can also be performed.
7. Cerebellar herniation – Lead to several conditions such as coma and respiratory arrest due to the compression of brainstem. Other symptoms mimic labyrinthitis such as vomiting and vertigo.

B. Intravenous Trombolysis (recombinant tissue plasminogen activator)
Indication:
i. Less than 3 hours after the onset
ii. Age must be 18 years old and above
iii. Clinical diagnosis of stroke
iv. CT scan show no evident of hemorrhage or edema of 1/5 of medial cerebral territory.
v. Informed consent from the patient.
Contraindication:
i. Gastric bleeding in preceding 21 days.
ii. Major surgery in preceding 14 days.
iii. History of head trauma or previous stroke within 3 months.
iv. Coma or stupor
v. Minor stroke symptoms.
v. Recent myocardial infarction.
vi. Hypertension 185/110 mm hg
Etc ...... Refer to Harrison’s Principle of Internal Medicine.

C. Endovascular techniques.
Use of intraarterial thrombolytics pro- urokinase for acute medial cerebral occlusion for up to six hours following the onset of stroke.
Endovascular mechanical thrombectomy – in the condition for which the thrombolytics is contraindicated of the vascular recanalization of IV is not possible.

D. Antithrombotic agents

i. Aspirin – safe and produce small net effect. Produce small reduction in early mortality, recurrent ischemic stroke and dependency at discharge or death. Used for acute ischemic stroke.

E. Neuroprotection:
Hypothermia – the condition that prolong the brains tolerance towards ischemia.

F.Stroke centre and Rehabilitation
Proper rehabilitation – physical, occupational and speech therapy.
Education of patient and family
The goal of rehabilitation is to return the patient to home and maximize the recovery.

Sunday, April 25, 2010

Gadjah Wong

This is my first review for the restoran. The review focus on Gadjah Wong Restoran. There are many types of food served in this restoran; Indonesian, Indian, Italian, Sea Food, Charcoal and Roast.

These are the range of the price:

i. Indonesian food: Rp 46 000 - 52 000
ii. Indian Food: Rp 57 000 - 64 000
iii. Italian Food: Rp 62 000 - 68 000
iv. Sea Food: Rp 82 000 - 98 000
v. Charcoal and Roast: Rp 56 000 - 105 000
vi. Desert: Rp 18 000 - 34 000
v. Drinks: Rp 16 000 - 29 000

By the way, thanks a million to my sweet Sister, Kak Nadiah Kamarudzman for accompanying me.

Here are some pictures:

Happy Belated Birthday , kak Nadia... :)






At the entrance... With lovely flower. In this compartment, you can read magazines such as Da Man (fashion Magazines).


Australian Tenderloin: Juicy beef medallions served with mushrooms sauce and French fries.

Ranapakel: Indian dish of grilled lamb shoulder, lime rice, home-made pineapple chutney, Chapati bread, lemon grass and mint leaves.


Yogurt Lassy: Strawberry and Pineapple.

Saturday, April 24, 2010

Parkinson Disease

Introduction:
Parkinson Disease is progressive neurodegenerative disease.

Characteristics:
Motor Feature

(a) Resting tremor – The frequency of the tremor is around 4 – 6 Hz. This form of tremor usually appears during rest. One of the known terms for this characteristic is pill-rolling.

(b) Rigidity – Increase in muscle tone in antagonist muscle during movement or increase in resistance during passive movement about the joint. Regular interruptions during passive movement due to subclinical tremor give rise to the cog-wheeling sensation.

(c) Bradykinesia (slow movement)

(d) Decreased in fine motor movement – eg: micrographia.

(e) Gait disturbance – shuffling short step, festinating (involuntary tendency to take short accelerating steps in walking) gait and freezing gait.

(f) Abnormal posture – flexed head, stooping or tilting of the upper back, flexed hands during walking.

Non-motor Feature

(a) Sleep disturbance –
Due to the emergence of rigidity and bradykinesia during an effort to turn direction and tremor and involuntary movements (leg restless syndrome or myoclonic jerks).

Sleep apnea

Vivid dream and hallucination that is due to the effect of dopamimometics drugs.

(b) Pain – That is due to the prominent symptoms or due to the effect of antiparkison drugs that are wearing off.

(c) Loss of smell (anosmia)

(d) Cognitive impairment

(e) Anxiety and Depression

(f) Autonomic symptoms – constipation, orthostatic hypotension, seboorhea, urinary urgency or frequency, and excessive sweating.

Orthostatic hypotension occurs due to the sympathetic denervation to the heart, impaired vasomotor reflex or as a side effect of dopamimomemitic therapy.

Pathology:

Macroscopically, there is a mild atrophy of frontal lobe with loss of melanin pigment normally found in midbrain. Microscopically, there is a loss of dopaminergics cells with Lewy body in the remaining cells and processes of substansia nigra pars compacta; other brainstem nuclei; and other region such as medial temporal, limbic and frontal cortices.

Pathogenesis:

Basically, although most of the cases are thought to be sporadic, there are some evidences stated that genetic factors may play some roles.

(a) PARK 1, PARK 4 and PARK 5 are related to autosomal dominant pattern of inheritance and are early onset and rapidly progressed. Basically, PARK 1 gene mutation is associated with the aggregation of alpha – synuclein. PARK 5 gene encodes for Ubiquitin Carboxy-terminal hydroxylase L1 (UCH-L1). Because of ubiquitination is an important step before degradation process in proteosome system can proceed, this mutation can lead to the aggregation of proteins.

(b) PARK 2 and PARK genes are related to autosomal recessive pattern of inheritance. PARK 2 gene encodes the E3 Ubiquitin protein ligase.

(c) PARK 6 and LRRK 2 gene mutation are related to the abnormal kinase activity.


Management:


Pharmacology:

(1) Levodopa –
Description:
It is dopamine precursor that is able to cross blood brain barrier. It is converted into dopamine in neurons. Basically, this medication is very useful to treat tremor, rigidity and bradykinesia symptoms. The dose given must be adequate or combined with other drug (such as carbidopa) in order to increase bioavailability of the drug in CNS. This is because, levodopa undergo first pass effect in the liver and peripheral tissue. Levodopa is converted into dopamine by dopa decarboxylase. This reaction can be reduced by using peripheral decarboxylase antagonist which is carbidopa.

Side effect –

GIT symptoms – Nausea, vomiting and anorexia that is due to the stimulation of chemoreceptor trigger zone in medulla.

Cardiovascular symptoms – Have beta adrenergic effect on heart. Can be reduced by using propranolol.

Endocrinology – Decrease prolactin secretion due to the stimulation of tubulainfundibular system.

Behaviour – elevate the mood of patient.

On/Off effect – Due to the composite of amino acids uses the same transporter across the gastric mucosa.

(2) Dopamine agonist

i. Apomorphine
Be used in certain conditions such as in acute, intermittent treatment of hypomobility, off effect associated with advanced PD as well as adjunct to other medication.

ii. Amantadine

This is used to treat rigidity, tremor and bradykinesia symptoms. The mechanism is uncertain but probably it is associated with the increase in dopamine release, prevent presynaptic reuptake of catecholamines as well as blocking NMDA receptor.

Side effect – sedation, hallucination, dry mouth, hypotension and livido reticularis (patchy discolorization)

(3) MAO Inhibitors

This acts by inhibiting MAO, so dopamine degradation is decreased. There is
possibility for increased side effect due to the increased level of dopamine.
i. Selegiline

(4) COMT inhibitors (carbidopa)
Prevent peripheral decarboxylase from metabolizing levodopa.

References:

1. Harrison's Principles of Internal Medicine, 17th Edition.
2. Dorland's Pocket Medical Dictionary, 27th Edition.

Friday, April 23, 2010

Learn Spanish I

Hola Hello (O-la)
Adiós Goodbye
Buonos Días Good morning
Buenas Tardes Good afternoon
Buenas Noches Good evening
Sí Yes
No No
Gracias Thank you
No entiendo I do not understand
Con permiso Excuse me
¿Cómo está usted? How are you?
Bien Good
Mal Bad
¿Como se llama? What's your name? (formal) (yah-mah)
¿Como te llamas? What's your name? (inf)
Me llamo Fareez My name is Fareez
Mucho gusto Nice to meet you
¿Cuál es su dirección? What is your address?
Hasta leugo See you later (as-tah)
Un momento Just a moment
Por favor Please (fah-bor)
Por supuesto Of course
Por supuesto que no Of course not
¿Me ayuda? Can you help me?

Ticks Paralysis


Pathogenesis


Some ticks have neurotoxin secreted into their saliva and are injected into human during feeding. The injection of neurotoxin causes reduction of nerve conduction, leading to the weakness.

Clinical manifestation
1. Local
i. Soft ticks – attach for less than hour and may produce erythematous macular lesion equal or less tah 3 cm.
ii. Hard ticks – attach for several days and may attach for more than a week. These ticks may produce induration with surrounding erythema and occasionally necrotic ulcer develops.
Chronic nodules – reach several centimetres

2. Fever with malaise, nausea and headache. Usually resolve within or more than 36 hours after tick removal.

3. Limb weakness and paralysis (ascending) started within 6 days after ticks attachment. It is associated with paralysis of cranial nerves as well as diminishes deep tendon reflex but normal sensory examination and normal lumbar puncture exam. (Rare complication)

4. Dysarthria (difficulty in speech), dysphagia (difficulty in eating) and death from respiratory muscle paralysis or aspiration. (Rare complication)

Diagnosis:
Depend on the ticks finding.

Managements:
1. Removal of ticks by firm traction with a forceps placed near the point of attachment. Gloves are recommended to be worn to avoid ticks’ fluid containing pathogen transfer during removal. The area must be disinfected.
2. While awaiting the result of seroconversion to Lyme disease, patient that is associated with deer ticks bites, can be treated with short term oral doxycycline.

References:
1. Harrison’s Principle of Internal Medicine, 17th edition.

Vitiligo

Definition:

Vetiligo is a common skin disease that affect about 1 % of population. It is related to the hypopigmentation disorder.

Etiology:

There are three theories proposed the development og vitiligo;

(a) Autoimmune disorder - Some of autoimmune conditions are associated with vililigo. Lab study of autoantibody present in the blood showed that there is an increase of autoantibody towards melanocytes.

(b) Neural theory - according to this theory, there is an elaboration of specific neural mediator released by nerve endings that can lead to the dustrucion of melanocytes.

(c)Self-destructive process - This process is related to the condition in which melanocytes itself lost it protective mechanism against cytotoxic melanin percursors.


Clinical manifestation:

(a) Characteristics:

Hypopigmentation or depigmentation of skin.

In hypopigmented area, the hair present is white in colour. The border is well-circurmscribe with hyperpigmentation around the border. This condition is known as trichrome vitiligo.

i. Inflammatory vitiligo - the border maybe raised and the hypopigmented area is itchy.

ii. Generalized - depigmenation of all cutaneous region except pigment of eyes.

Ocular involvement - occur in 40% of patient but do not really affect visual aciuty because the area affected is distal to fovea. This manifestation occur due to the destruction of melanin in epithelial or choroid of retina.

(b) Onset:

i. Age - 50% of patirent develop vitiligo prior to age 20.


(c)Common sites - bony prominents, area of the skin exposed to the sun, and intertriginous area as well as nose and mouth part.


(d) Progression:

Often begin about pigmented nervi in halo fashion. This condition is always preceded by strong physical or emotional stress. Repigmentation always take place. The rate of repigmentation depends on the availibility of melanocytes. Basically, melanocytes can migrate from hair follicle the skin area. So, in the case in which the hypopigmented skin area is lack of hair follicles or the hais is white in color, the rate become slower. Moreover, the repigmentation is always spotty and parafollicular. The tendency of hypopigmented area to be recovered is almost absent when there is well-established depigmented area for several years.

Treatment:

The treatment of vitiligo must be individualized because the efficacy of most agents are not satisfactory and require prolonged patient participation and comitment.

(a) Staining - This method can be done by using the freshly cut surface of green-black walnut husk can give temporary relief. If this procedure is overdone, the irritation is the resul.

(b) PUVA therapy - this therapy uses some of the drugs such as trimethoxypsoralen, 8-methoxypsoralen and 5-methoxypsoralen.Patient taking oral psoralen followed in by 1 - 2 hours of exposure of either natural sunlight or UVA omitting bulb can lead to the recovery in 50 -70% patient. In this treatment, patient must be told that this treatment usually takes 20-25 times before any response achieved. It is time-consuming and expensive as well as have some phototoxic effect(topical).

(c) Surgery -

(i) Transplantation of normal skin into diseased skin.

(ii) Total depigmentation of skin by using 20% monobenzyl ether of hydroquinone. Psychological therapy must be considered in darkly complexioned individual.

(d) Topical corticosteroid in small and few lesions of recent onset.

References:

1. Dermatology, third edition, Samuel L abd Harry J.

Learn Japanese II

1. Dōmo Thank you or Hi!
2. Īe No or Don’t mention it.
3. Sō, Sō You’re right, you’reright
4. Dame Prohibited or that’s bad
5. Zenzen Not at all or It was nothing.
6. Ii desu ne That’s a great idea.
7. Yatta Yahoo! I did it.
8. Omedetō Congratulations
9. Yōkoso Welcome!
10. Shinpai shinaide Don’t worry
11. Makasete Count on me!
12. Sono tōri You’re absolutely right.
13. Hontō Really?
14. Mochiron Of course!
15. Dōshiyō What shall I do?

Wanna sound like Japanese?

You just need to memorize all these terms below and apply that!

Enryo shinaide – Don’t be shy.
Mottainai - What a waste.
Osakini – Pardon me, but I’m leaving now.
Sasuga- I’m impressed by you, as usual.
Gambatte- Try your best.
Shōganai- There’s no choice.
Okage-sama de- Luckily.
Gokurō-sama- Thank you for your trouble.
Yoroshiku- I’m pleased to meet you./I appreciate your helping me.
Taihen desu ne – That’s tough.

Learn Japanese I

1. Hajimemashita. How do you do?
2. Onamae wa. What’s your name?
3. Watashi no namae wa Fareez. My name is Fareez.
4. Dōzo yoroshiku. I’m pleased to meet you.
5. Ohayō gozaimasu. God morning.
6. Konnichiwa. Good afternoon.
7. Konbanwa. Good evening.
8. Oyasuminasai. Good night.
9. Jā, mata. See you again.
10. Chotto sumimasen. Excuse me.
11. Dare desu ka. Who?
12. Dō desu ka. How?
13. Doko desu ka. Where?
14. Dore desu ka. Which one?
15. Dō Shimashita ka. What happened?
16. Dōshite desu ka. Why?
17. Nanji desu ka. What time?
18. Nan desu ka. What?
19. Benkyō shinasai. Study!
20. Kikinasai Listen!
21. Yasui. Cheap.
22. Takai. Expensive.
23. Ikura desu ka. How much?
24. Irasshaimase. Welcome.
25. Gomen nasai. Sorry.

Thursday, April 22, 2010

Toxoplasmosis

The Pathogenesis

This microorganism needs cat in order to form oocytes containing sporozoites. This process need cat’s gut as a medium. Basically, the oral transmission occur when a person eat food contaminated by infected soil. Ingestion of beef or pork containing cyst (bradyzoites) can also lead to the infection of toxoplasmosis. The ingestion of sporozoites or cysts causes the release of bradyzoites and sporozoites by digestion process. Basically, bradyzoites cannot be digested by pepsin. Bradyzoites are then invaded enterocytes and undergo transformation process. This process provokes the secreation of sIgA. Moreover, tachyzoites are formed in the process. Tachyzoites can be spread by blood and lymphatics system and prone to infect some tissues such as placenta, retina, CNS, skeletal muscle and heart. Toxoplasmosis gondii invade, multiply and cause the rupture of the cells, creating focal necrosis that is surrounded by acute inflammatory reaction. In immunocompetent people, the infected cells and tachyzoites are killed by the action of immune system; antibody, interferon gamma, CD8 T cells and macrophage activation via radical immediate release. Some of tachyzoites corvert themselves into bradyzoites that has slow metabolic rate. Although bradyzoites are metabolically slow, the ruptures of the cells containing cysts do occur. This condition leads to persistant infection of individual infected by this microorganism.

Acute Bacterial Meningitis (ABF)


Definition:

Acute purulent bacterial infection in the subarachnoid space that is associated with the decrease in consciousness level, seizure, increase in ICP as well as stroke.
If the brain’s parenchyma, subarachnoid space and meninges are involved, the term used is meningoencephalitis.

The pathogenesis
The bacteria such as N.meningitidis and S. Pneumonia get assess into the blood through the nasopharynx. These bacteria attach to the epithelial cells of nasopharynx, migrating into blood through the tight junction between cells or transported across the cells through vacuole. Once in the blood, these bacteria have the ability to avoid immune mechanism due to its cell wall. The cell wall present protects the exposure if LPS or peptidoglycans and techoic acid present in S. Pneumonia.So, complement component and neutrophils are failed to destroy them. S. Pneumonia get assess into CSF through direct attachment to the cerebral capillary. Some bacteria provoke inflammatory reaction that can lead to the damage of choroid plexus. Once in the CSF, bacteria start to multiply due to the present of conducive environment in CSF; low level of complement proteins, immunoglobulins and immune cells. The multiplication of bacteria can cause the release of peptidoglycans and techoic acid from s. Pneumonia and LPS from N.meningitis. These antigens cause the release of IL-1 and TNF from microglial, astrocyte, endothelial cells and monocytes. The increased in these cytokines cause the increase in blood-brain barrier permeability. This leads to the recruitment of leucocytes as well as proteins into CSF. The accumulation of proteinaceous matrix and leucocytes can cause obstruction of ventricular system, leading to the non-communicating hydrocephalus. Moreover, communicating hydrocephalus can also occur. The recruitment of leucocytes causes the release of oxygen reactive molecules and NO. These substances can cause brain damage( cell death).
The epidemiology;
1. Hib – was the most common cause of acute bacterial meningitis. Due to the increase in the availability of vaccination toward this bacteria, the incidence of ABF decreases.
2. Pneumococcal pneumonia (50%) – due to the increase in bacterial resistance towards penicillin and ampicillin.
3. N. Meningitidis (25%) – due to the emergence of new strain (serogroup c serotype 2a), increase in penicillin resistance.
4. L.monocytogens – Increase in incidence in elderly and people who are immune compromised, malignancy, pregnancy, receiving organ transplantation and Etc. Basically, this infection occur due to the low level of cell mediated immunity.
5. streptococci B – increase in USA and Europe