Wednesday, February 24, 2010

Migraine

Migraine is recurrent headache associated with visual and GI disturbance. Approximately 12% of the population world-wide suffers from the condition.

Pathology:

Precise mechanisms are still unknown. Although some factors are as follows:

1) Genetic factors play some part;
2) Also, release of neuropeptide, calcitonin-gene-related peptide (CGRP) is implicated as it is a potent dilator of cerebral and dural vessels.
The headache of migraine is usually caused by dilation or edema of cranial vessels and subsequent stimulation of nearby nerve endings. Nitric oxide, a vasoactive substance, also has a role. Magnesium deficiency, nueral excitation by glutamate and asparate as well as alterations in hypothalamic-pituitary axis is also suggested.

Some precipitating factors:
1) Weekend migraine (time of relaxation)
2) Chocolate (phenyl ethylamine)
3) Cheese (high in tyramine)
4) Noise and irritating lights
5) Premenstrual symptoms
6) Also common around puberty and menopause


Clinical Presentation:

1) Migraine with aura - prodromal symptoms are usually visual mostly related to visual cortex depression or retinal problems. Other neurological symptoms like tingling, nausea, numbness and vague weakness of one side may occur. It can last for few minutes to an hour followed by the headache. It is usually hemi cranial but often begins locally. Patient is irritable and prefers dark environment. Diuresis follows resolution after several hours and deep sleep often ensues.

2) Migraine without aura (common migraine) - the usual variety. Prodromal symptoms are vague and headache is recurrent accompanied by nausea and malaise.

3) Basilar migraine - prodrome includes vertigo, diplopia, transient visual disturbance, syncope and dysarthria. They can occur alone or progress to typical migraine

4) Hemi paretic migraine - classical migraine with hemi paretic features, but resolves within 24 hours differentiating from stroke.

5) Ophthalmoplegic migraine - associated with third nerve, or sometimes sixth nerve palsy.

6) Facioplegic migraine - associated with unilateral facial palsy.


Differential Diagnosis:

The sudden headache may resemble meningitis or Sub-Arachnoid Hemorrhage. Prodromal symptoms must be distinguished from Transient Ischemic Attacks - TIAs usually deficit immediate and without headache.
Sensory abnormalities may resemble sensory epilepsy.


MANAGEMENT:

General measures include:
1) Reassurance and relief of anxiety
2) Avoidance of dietary factors - rarely helpful. Also patients taking oral contraceptives may benefit from change of brand or trying without. Severe symptoms are indication for stopping hormonal medications.

During an attack:
After ruling out serious pathology for headache, paracetamol or other simple analgesics should be given, with an antiemetic (e.g. Metaclopromide) if necessary. Repeated use may lead to further headaches.
Also, Triptans (5-HT1 agonists) can be used as well. In 30% cases of severe recurrent migraine, sumatriptan, zolmitriptan and naratriptan are of value by either subcutaneous injection or orally by inhaler. They should be avoided when there is vascular disease. Recently, some CGRP antagonist was effective in treating attacks.

Prophylaxis:
The following are used when attacks are frequent:

1) Pizotifen (antihistamine and 5-HT antagonist) - 0.5mg at night for several days, increasing to 1.5mg (common side-effects: weight gain and drowsiness)
2) Propanolol (beta-blocker) - 10mg three times daily, increasing to 40-80mg thrice daily
3) Amitriptyline - 10mg (or more if required) at night

Sodium valproate, methysergide, SSRIs, verapamil, topiramate and nifedipine are also used.

Hopefully the article would help my fellow medical students understand migraine better for it is a common problem encountered by most GPs and even by us students during daily life.

(Sources: Kumar and Clark, Davidson)

Monday, February 15, 2010

Pulmonary Edema

PULMONARY EDEMA
Fluid accumulation in lungs, causing impaired gaseous exchange leading to respiratory difficulty/ failure.

TYPES:
Cardiogenic
Non-cardiogenic

CLINICAL FEATURES:
Dyspnea
Cough
Pink frothy sputum
Restlessness
Excessive sweating

In chronic cases, there maybe:

Nocturia
Pedal edema
Orthopnea
Paroxysmal nocturnal dyspnea

MANAGEMENT OF ACUTE PULMONARY EDEMA

Diagnosis:

Clinical Signs:
Decreased peripheral perfusion
Pulmonary congestion
Use of accessory respiratory muscles
Wheezing, specially in basal zones
Pink frothy sputum

Radiographic Signs: on CXR:
Cardiomegaly
Vascular engorgement (interstitial and perihilar)
Kerley B lines
Pleural effusion (varies with severity)


Treatment:
Start on clinical judgement only, no time to waste.

Position: Nurse the patient in a propped up position, so the secretions don’t pool in the bases of lungs.
Relieving the dyspnea: Administer oxygen, so arterial pO2 comes up to 60%.
Administer IV furosemide (loop diuretic), which actys as a venodilator before its diuretic action comes into play, thus immediately relieves edema. Nitroglycerin potentiates the effects of loop diuretic, so it is usually also given. Mechanical ventilation is indicated if hypercapnea coexists.
Relieving the pain: Provide analgesia(morphine sulfate) if patient experiences any pain, as pain may exacerbate the dyspneic symptoms.
Supportive: Inotropic agents are indicated if patient is in cardiac block or shock, eg. dobutamine or PDE inhibitors.
Recombinant BNP: Nesiritide, indirectly increases cardiac output. It also produces diuresis and natriuresis, in conjunction with furosemide.
Acute hemodialysis and ultrafiltration: consider in patient with significantly renal dysfunction and diuretic resistance.
Heart catheterization
Correction of precipitating factors:
HTN, MI, ischemia, acute valvular regurgitation, arrhythmias or volume overload should be corrected for.

Sunday, February 7, 2010

Alzheimer's Disease - Dementia

What is Dementia?

An acquired global impairment of personality, intellect and memory without any impairment in consciousness.

Dementia can either be progressive or non progressive depending upon the cause. It is noteworthy that Dementia is NOT a disease, it is simply a collective name given to a a group of disorders that may bring about the changes in memory, intellect and personality.

ALZHEIMER'S DISEASE

A TYPICAL CASE SCENARIO of Alzheimer's Disease:

"A woman in her early 50s was admitted to a hospital because of
increasingly odd behavior. Her family reported that she had been
showing memory problems and strong feelings of jealousy. She also
had become disoriented at home and was hiding objects. During a
doctor's examination, the woman was unable to remember her
husband's name, the year, or how long she had been at the hospital.
She could read but did not seem to understand what she read, and
she stressed the words in an unusual way. She sometimes became
agitated and seemed to have hallucinations and irrational fears."


Alzheimer's Disease is the leading cause of Dementia amongst the older people today.

According to the latest epidemiological survey, this progressively detoriating cause of dementia effects about four million people in the United States of America. 1 in every 10 people will suffer from Alzheimer's disease in the population of people greater than 65 years of age. This figure, however, becomes a staggering 1 in ever 2 persons for people over the age of 85 years. Approximately, fifty thousand deaths in the USA are directly caused by Alzheimer's disease. So yes, you are dealing with a big problem!

What causes Alzheimer's Disease?

Extensive research has been targetted at finding the basic cause of the development of this progressive dementia however, no single factor can yet be labelled as the soitary cause of Alzhiemer's Disease. Many pathology causing theories have been put forward amongst which the most widely accepted conclude the presence of :

*Neurofibrillary tangles in the Cortex of the Brain
*Amyloid or Senile Plaques
*Widespread loss of Acetylcholine in the CNS
*Selective neuron loss in the Hippocampus and Entorhinal areas the brain
*Decrease in the number of synapses in the CNS
*Tau protein abnormalities

Signs and Symptoms

The presence of signs and symptoms, in the early stages of the disease, are very much dependant on the pre-morbid personality of the individual. A shy, reserved and introvert type of a person will show more signs of the disease at an early stage whilst a socially skilled person can go on functioning adequately till much later stages of the disease.

*Memory Impairment --> This is the foremost sign of AD. Initially the short term memory is effected. The patients will have trouble understanding new concepts or new routines. They will forget their new neughbour's name however will not forget how to ride a bicycle, in the initial AD stages. In later stages the long term memory is also hampered.

*Mood Disturbances/Behavioural Changes --> Fluctations in the moods are present varying from depression to anger to aggressive behaviour. Many patients lose their social inhibitions and commit various embarassing actions like undressing in public etc.

*Catastrophic Reactions --> Patients, when moved from routine, can show signs of aggression

*Organic Orderliness --> A patient of Alzheimer's Disease likes to live by a very strict routine.

*Psychotic Symptoms --> Some of the patients may harbour Depression while some have been reported to have haluucinations. The most common Hallucinations known to occur in an Alzheimer's patient are Persecutory Hallucinations (patients complain of theft or robbery when nothing has happened in actuality).

Risk Factors

Genetics and Family History

Advancing Age

Smoking

Alcohol

Atherosclerosis

Increases plasma Homocysteine levels

Diabetes Mellitus

Down's Syndrome

Mild Congnitive Impairment (MCI) ---> One study claims that 40 percent of over 65 years inviduals who had MCI developed Alzheimer's Disease within the next three years!

Diagnosing Criteria

Comprehensive History and Examination to rule out any other problems
Mini Mental State Exam
MRI
EEG

According to DSM IV, the presence of the following features is necessary to label a person suffering from Alzheimer's Disease:
*Memory Impairment

*One or more of --> Aphasia,
Apraxia,
Agnosia,
Disturbance in Executive Functioning

*Exclusion of other organic disorders

Treating Alzheimer's Disease
Though there is no cure for Alzheimer's, the treatment aims to increase the quality of the life of the patients. A BioPsychoSocial standard plan for the treatment of Alzheimer's disease is given below.

Bio or Medical Therapy: Though there are devised medications for the treatment of Alzheimer's disease, it is important to remember that this a disease that runs on a one way road only, there is NO cure for Alzheimer's as yet. Medications will help the symptoms of the disease to get better but it cannot slow down or cure the disease.

*Choline esterase inhibitors (Tacrine, Donezapil, Rivastigmine, Galantimine) are the mainstray therapy. They work to increase the amount of Acetylcholine in the CNS, as these patients have increasingly low levels of AcH in their systems.

The following are given to the patients with specific symptoms:
*Anti Convulsants
*Sedatives
*Anti Depressants

Psychosocial Help
Secure Environment and Understanding:
The patients of Alzheimer's Disease require continous care by the ones looking after them. They need understanding and love. A normal routine life in a loving and caring environment is perhaps the answer to alot of poblems they face. These patients should be kept away from harm's way. All harmful objects in a household should be kept locked away from their way and they should not be allowed to drive themselves or go wandering about by themselves.
Care takers might feel burdened by the round the clock care needed by their loved ones suffering from Alzheimer's so it is necessary to take timely shifts in doing the duty.

Cognitive Therapy, Leisure activities and Exercise should be encouraged amongst these patients.
Support Groups help can seeked as needed.






Saturday, February 6, 2010

Thyroid Examination

Thyroid Examination

  1. Greet the patient -> handshake
    • Handshake
      1. Sweating
      2. Normal temperature
      3. Pulse?
  2. Explain
  3. Seek permission
  4. Right side always
  5. Proper exposure
  6. Ensure privacy


General Inspection:

  • Appropriately dressed for temperature outside?
  • Comment on obesity, weight loss
  • Anxious, agitated, lethargic?
  • Exophthalmos
  • Dry skin (hypothyroidism)
  • Hair – loss?
  • Facial myxedema?


Examination of the hands:

  • Check pulse (bradycardia, tachycardia, atrial fibrillation)
  • Check for presence of sweating, increase in temperature, palmar erythema?
  • Onycholysis (separation of the nail from its bed)
  • Thyroid acropathy (similar to clubbing)
  • Ask the patient to extend arms and hold hands with palms facing downwards. Check for fine tremors.
    • Rest piece of paper over hands
  • Elicit Pemberton's sign
    • It is the development of facial flushing, distended neck and head superficial veins, inspiratory stridor and elevation of the jugular venous pressure (JVP) upon raising of the patient's both arms above his/her head simultaneously, as high as possible.


Examination of the thyroid gland:


Inspection:

  • Comment on symmetry, scars
  • Obvious thyroid enlargement?
  • Midline masses?
  • Ask the patient to swallow (only goiter or thyroglossal cyst rises upon swallowing)
  • Protrude the tongue (thyroglossal cyst moves with protrusion of tongue)
  • Comment on the mass
    • The 7 S's (BOX)
    • Distention
    • Discharge
    • Extension

Inspection 7 S's

  1. Site (anterior triangle)
  2. Size (3x3 cm)
  3. Shape (spherical, uniformly enlarged or nodular)
  4. Surface (smooth, rubbery, hard)
  5. Surrounding skin (normal, ulcers, sinuses)
  6. Scars (none)
  7. Subcutaneous veins (not)


Palpation:

  • Stand behind the patient
  • Thumbs on back of neck, patient's head slightly flexed
  • Palpate neck
  • Ask to swallow and feel the gland move under your fingers (Get below the swelling)
  • Palpate right lobe
    • Turn neck slightly to right
    • Ask to swallow
    • If palpable, describe size, shape, consistency, tenderness, mobility
      • Temperature à surrounding and then on lump
      • Tenderness
      • Texture
      • Trachea
    • Repeat for left lobe!
  • Lymph nodes palpation; also check Virchow's glands


Percussion:

  • From down upwards; check for retrosternal extension
  • Also percuss clavicle


Auscultation:

  • Bruit is a sign of increased blood flow; maybe present in thyrotoxicosis
    • Take breath in and hold while auscultating
    • Auscultate over two major lobes
    • Auscultate with bell
      • Also auscultate mitral area


Examination of the eyes:

  • Lid lag, lid retraction
  • Chemosis, Proptosis
  • Exophthalmos (examine from above & behind, from side. Eyes should not be visible beyond the supraorbital ridge)
  • Check eye movements (ophthalmoplegia); seeing double?


Miscellaneous:

  • Check reflexes
  • Proximal myopathy
  • Pretibial myxedema
  • CVS examination (failure?)
  • Internal carotid