Monday, June 15, 2015
Tuesday, January 05, 2010
It is characterized by 5 of the following for 2 weeks, including depressed mood and anhedonia (inability to attain pleasure from normally pleasurable events or things).
1. Sleep disturbances
2. Loss of Interest
4. Loss of Energy
5. Loss of Concentration
5. Change in appetite
6. Psychomotor retardation
8. Suicidal ideations
9. Depressed mood.
Recurrent Depression- Requires two or more episodes with a symptom free interval of 2 months. Lifetime prevalence- 5 to 12% males; females- 10 to 25%.
Friday, May 02, 2008
Buerger's disease is also called Thromboarteritis obliterans. It occurs in young males mostly below 40 years. It is common in Israel, South America and India. It is strongly associated with heavy smoking and caffeine. It mostly involves smalls and medium arteries and veins of the extremities.
- Recurrent neutrophilic vasculitis with micro abscesses.
- Segmental thrombosis- leads to vascular insufficiency.
- Severe pain (claudication) in the affected extremity
- Raynaud phenomenon
- Ulceration and gangrene
View a case: Example
Thursday, May 01, 2008
Arteriosclerosis can be defined as a group of diseases that result in arterial wall thickening.
1. Monckeberg medial calcific sclerosis:
- Medial calcification of medium sized arteries
- Femoral, tibial, radial and ulnar arteries are affected mostly.
- It is mostly asymptomatic and can be detected by X ray
- Occurs in diabetes, hypertension and aging
- Affects small arteries and arterioles
- Microscopic appearance-
- Hyaline arteriosclerosis- pink, glossy arterial wall thickening with luminal narrowing is noted. Hyperplastic arteriosclerosis- Smooth muscle proliferation resulting in concentric (onion skin) wall thickening and luminal narrowing.
- Def: Lipid deposition and intimal thickening of large and medium sized arteries, resulting in fatty streaks and atheromatous plaques.
- Aorta, coronary arteries, carotid, cerebral, iliac and popliteal arteries
- Fatty streak- flat, yellow intimal streak. Microscopically, lipid laden macrophages can be seen (also called foam cells).
- Atheromatous plaque- Raised, yellow-white plaques, Microscopically-Fibrous cap is seen which contains smooth muscles, lymphocytes and foam cells. Necrotic core contains cholesterol clefts, foam cells and necrotic debris.
Major Risk Factors
Minor Risk Factors
Sedentary life style
Stress (Type A personality)
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- Ischemic heart disease
- Cerebrovascular accidents
- Atheroemboli (Transient ischemic attacks and renals infarcts)
- peripheral vascular disease
- Aneurysm formation
- Mesenteric artery occlusion
Wednesday, April 30, 2008
Definition: Congenital or acquired weakness of vessel wall media, resulting in a localized dilation or out pouching.
The bulge in the aneurysm may burst and death may occur any time.
1. Atherosclerotic aneurysms:
- Weakening of media secondary to atheroma formation
- Occur in the abdominal aorta below the real arteries
- Associated with hypertension
- Half of aortic aneurysms > 6cm in diameter will rupture within 10 years
- Its due to cystic medial necrosis of tunica media.
- Blood from the vessel lumen enters the intimal tear and dissects through the layers of media.
- It presents with severe tearing pain.
- It may compress and obstruct the aortic the aortic branches (eg- renal or coronary arteries)
- HTN and Marfan syndrome are predisposing factors.
- Involves ascending aorta
- Syphilitic (leutic) aortitis causes an obliterative endarteritis of the vasa vasoram. Leading to ischemia and smooth muscle atrophy of aortic media.
- May dilate the aortic valve ring causing aortic insufficiency.
- Congenital aneurysm of Circle of Willis.
6. Mycotic aneurysms: aneurysm usually due to bacterial infections.
Tuesday, April 29, 2008
Most common form of vasculitis. Affects females more than males. Primarily affects the elderly population. Temporal arteritis is associated with HLA-DR4
Distribution of the disease:
1. Small and medium sized arteries
2. Cranial arteries (temporal, facial and ophthalmic arteries)
2. Aortic arch-giant cell aortitis (uncommon)
1. Throbbing headache- Mostly unilateral
2. Tender firm temporal arteries
3. Visual disturbances- Blurred vision, double vision, visual loss.
4. Facial pain
5. Fever, Malaise, Weight loss, muscle aches, anemia
6. Polymyalgia rheumatica: systemic flu like symptoms and joint involvement (pain, morning stiffness in neck, shoulders and hips).
Laboratory findings- Elevated ESR
1. Segmental granulomatous vaculitis
2. Fragmentation of internal elastic lamina
3. Intimal fibrosis with luminal narrowing.
Temporal arterial biopsy, classical presentation or rapid onset may be treated empirically
Monday, April 28, 2008
Wagner's granulomatosis is a kind of autoimmune disorder affecting the arteries. Medium sized and small arteries are involved. This is a kind of necrotizing vasculitis with granulomas. Its more common in males than in females. Mostly occurs at the age group of 40-60. Classically involves Nose, Sinuses, Lungs and kidneys.
- Bilateral pneumonitis with nodular and cavity pulmonary infiltrates.
- Chronic sinusitis.
- Nasopharyngeal ulcerations.
- Focal necrotizing glomerulosclerosis and Crescentic glomerulosclerosis are the two important forms of Renal pathology observed.
Fibrinoid necrosis, Neutrophils and granulomas.
Cytoplasmic antineutrophil cytoplasmic auto antibodies(C-ANCA)
Auto antibody against proteinase 3
Diagnosis is confirmed by biopsy
Treatment is by giving immunosuppresive drugs like Cyclophosphamide.
Thursday, April 24, 2008
It is derived from the Mesenchyme and usually arise within the left atrium near the fossa ovalis. It restrict the blood flow to left ventricle. Shows constitutional signs of fever, weight loss and anemia.
Microscopic picture- Stellate shaped cells in the myxoid background.
Complications- Embolism (mostly in the brain), Ball valve obstruction of valves.
Benign tumour arising from myocardium.. Associated with Tuberous sclerosis.
Most commonly from Lungs. This is more common than primary cardiac tumors.
Wednesday, April 23, 2008
Gross sequence of Changes in MI
0 to 18 hours
No gross changes
18 to 24 hours
Vague pallor and softening
1 to 7 days
7 to 28 days
Central scar formation with red border
Thick white Firm scar formation
Microscopic changes in MI
Wavy myocyte fibers, contraction bands
1 to 3 days
3 to 7 days
7 to 28 days
Monday, April 21, 2008
1. Decreased synthesis of ATP by oxidative phosphorylation.
2. Decrease function of Na-K ATPase pump-
- Influx of sodium and efflux of potassium
- Swelling of cell and endoplasmic reticulum.
- Depletion of cytoplasmic glycogen,
- Increased lactic acid production
- Decreased PH of the cell
5. Plasma membrane blebs and myelin figures
1. Severe membrane damage-
- Massive influx of calcium into the cell- Large flocculant densities in the matrix.
- Efflux of intra cellular enzymes into circulation.
- Mitochondrial swelling
- Large densities in mitochondrial matrix
- Irreparable damage of oxidative phosphorylation
- Inability to produce ATP
- Release of lysosomal digestive enzymes into cytosol
- Activation of acid hydrolases followed by autolysis
- Pyknosis- degeneration and condensation of nuclear chromatin
- Karyorrhexis- Nuclear fragmentation
- Karyolysis- dissolution of nucleus.
1. Myocardial injury- CK MB, Troponin, Lactate dehydrogenase.
2. Biliary tract obstruction- Alkaline phosphatase.
3. Pancreatitis- Amylase, lipase.
4. Hepatitis- Transaminases.
Friday, April 18, 2008
- Atenolol is not lipid soluble therefore it has longer half life than Metaprolol which is lipid soluble.
- Carvedilol blocks both alpha and beta receptors and is the most common beta blocker used in chronic congestive heart failure because it has Antioxidant and Antimitogenic properties in addition.
- Esmolol has the shortest and Nadolol has the longest half life among all beta blockers.
- Beta Blockers must not be used in compensated (i.e) acute heart failure.
- Beta blockers that are excreted in kidneys (lipid insoluble): Nadalol, Satolol, Atenolol, Acebutalol, Bisprolol, Betaxolol, Celioprolol- Should be avoided in renal failure.
- Endogenous Norepinephrine is metabolized by COMT and MAO. Exogenous Norepinephrin is metabolized by reuptake.
- Hemicholimium- Blocks the reuptake of Choline
- Vesamicol- prevents entry of choline into storage vesicles.
- Glucagon is DOC in beta blockers overdose. Other drugs that are used- Norepinephrine and Calcium chloride.
- Cardioselective Beta Blocker used in Glaucoma treatment- Betaxolol.
- Beta Blockers having local anaesthetic activity- Propranolol, Metaprolol, Labetolol, Acebutolol, Pindolol- These drugs must not be used for treatment of glaucoma (more risk of corneal ulcer formation)
- Longest acting ocular beta blokcer- Betaxolol.
- Latanoprost- It is a PGF2alpha derivative used in Glaucoma.
- Intramuscular injection of Atropine causes an initial Bradycardia- due to inhibition of M1 receptors (which normally decrease Ach release).
- Hyoscine (scopolamine) is a CNS depressor in low doses. Atropine is a CNS elevator in low dose and depressor in high dose.
- Glycopyrrolate is an anticholinergic drug that is used in pre anaesthetic medications and also during surgeries- to decrease secretions and avoid reflex bronchospasm.
- Tropicamide- fastest mydriatic (antimuscuranic with shortest half lie).
- Rate limiting enzyme in the synthesis of Catecholamines- Tyrosine hydroxylase.
- Vasomotor reversal of Dale is seen in case of Epinephrine because it has both alpha and beta2 agonist activity.
- Vasoconstrictors must not be used in secondary shock
- Adrenergic neuron blocking drugs have no action on exogenous (injected) adrenaline. They only block the release of adrenaline from nerve endings.
- Ergot alkaloids are the alpha blockers that can cause vasoconstriction.
- Aplha1 inhibitors cause faster and greater symptomatic relief but do not affect the disease progression. 5 alpha reductase inhibitors (Finasteride) slows disease progression.
- Most dangerous effect of belladona in very young children- Hyperthermia (not dehydration)
- Cocaine inhibits the re-uptake of Dopamine and Noradrenaline in CNS.
- The effect of parasympathetic system (and atropine) is of longest duration in Eye.
- Adrenaline in anaphylaxis- If used IM, dose is 1:1000; If used IV, dose is 1:10,000
Thursday, April 17, 2008
Alpha 1 receptors are located in-
Eye radial (i.e dilator) muscle
Arterioles and viens,
Male sex oegans, Urinary bladder,
Kidney and Liver.
Alpha 1 receptors use Gq Coupled secondary mediators and cause increase in phospholipase C, IP3, DAG and calcium levels in the cell.
Selective Blockers- Prazosin, Doxazocin, Terazocin
Non selective Alpha blockers (both alpha 1 and alpha 2 receptor blockers)-
Phentolamine(competitive inhibitor), Phenoxybenzamine (non competitive inhibitor)
Effects of Alpha1 receptor blockage:
Arterioles and veins- Reduced sympathetic tone in blood vessels- This results in vasodilation, Decrease in preload and after load on heart, lowering of peripheral vascular resistance and thus a fall in blood pressure is noted. The drop in blood pressure causes a reflex tachycardia.
Prazosin: Prazosin can lower BP rapidly so patients are recommended to relax for 1 hour after taking the first dose and for any increase in dose.
Ohter side effects: Orthostatic hypotension, First dose syncope, Urinary incontinence
Prazosin is used in case of lowering blood pressure in hypertensive emergencies (though I.V Sodium nitroprusside is the drug of choice in hypertensive emergencies). It decreases the tone of Urinary sphincters so it is used effectively for the treatment of BPH(Benign prostatic hypertrophy).
Tuesday, April 15, 2008
Excitation (Muscle, CNS)- Nicotinic effects
TEPP- 50mg- IM or 100mg- Orally
OMPA 80mg IM or 175mg Orally
Parathion 80mg IM or 175mg Orally
HETP 60mg IM or 350mg Orally
Malathion and Diazinon 1gm Orally
Cause of Death:
Paralysis of respiratory muscles, respiratory failure and intense bronchoconstriction.
For Muscaranic effects- Atropine is drug of choice (Tachycardia is not a contraindication for atropine administration)
For Regeneration of AchE- Pralidoxime (2-PAM)
Time dependent aging requires administration of PAM as soon as possible.
Monday, April 14, 2008
Diagnosis of sperm DNA integrity of semen sample is important for consistently high reproductive
efficiency. The conventional parameters of semen analysis take into account morphology, motility,
and concentration of spermatozoa in the sample, which are insufficient for evaluation of reproductive
potential. Current studies have implicated abnormal organization of genomic material in sperms as
a probable cause in 20 per cent cases of male infertility. This is especially important in the era of
assisted reproduction technique (ART) when a majority of infertile couples opt for assisted
reproduction and in where cases DNA integrity is a better diagnostic and prognostic marker as
compared to routine semen analysis.
This article reviews and discusses some of the current techniques employed for evaluating chromatin
structure or DNA damage in spermatozoa. These different techniques include single cell gel
electrophoresis (COMET assay), Terminal tranferase dUTP Nick End Labelling (TUNEL), sperm
chromatin structure assay (SCSA), In situ nick translation (ISNT) and acridine orange test. These
techniques are independent measure of sperm quality and assist in semen quality assessment by
detecting defects in DNA integrity or chromatin structure. The discussed techniques vary in their
level of accuracy, cost input, sophistication of analysis and their application depends upon the
sensitivity required for analysis.
The article also briefly outlines the DNA packaging and the causes of DNA damage in spermatozoa.
During chromatin packing 85 per cent of the histones are replaced by protamine while the residual
histones act as marker of genes which are expressed in early embryonic development. Among the
different aetiological factors observed to be responsible for DNA damage in human spermatozoa
increased reactive oxygen species (ROS), oxidative stress is highly correlated with greater DNA
fragmentation index (DFI). Oxidative stress leads to single and double strand breaks in sperm DNA.
Apoptosis and abnormal chromatin packing also contribute to DNA damage.
The significance of chromatin structure studies is more stressed owing to the greater awareness to
transmission of genetic diseases because of higher incidence of gene imprinting defects, increased
cancer frequency and other congenital and non-congenital defects in children conceived through
assisted reproduction techniques.
Source: Indian Journal of Medical Reasearch
Contact : Sri Sathya Sai Institute Higher Medical Sciences,
WhiteField, Bangalore. India.
Email us, General Queries: adminblr@sssihms. org.in
Write to us: Sri Sathya Sai Institute of Higher Medical Sciences
EPIP Area, Whitefield, Bangalore 560 066,
Karnataka , INDIA .
Call us: Telephone: +91- 080- 28411500
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Employment related +91- 080- 28411500 Ext. 415
Wednesday, April 02, 2008
Mechanism of Action
Inhibition of bacterial cell wall
Penicillins, Cephalosporins, Imipenem, Aztreonam, Vancomycin
Inhibition of protein synthesis
Macrolides, Aminoglycosides, Choramphenicol, Tetracyclines, Streptogramins, Linezolid
Inhibition of Nucleic synthesis
Disruption of cell membrane function
Anti fungal agents
Inhibition of Folic acid synthesis
Sulphonamides, pyrimethamine, Trimethoprim
Sunday, March 30, 2008
Events in the Heart
0.18 0.12 to 0.2
Atrial depolarization and conduction through AV node
0.08 to 0.10
Ventricular depolarization and Atrial repolarization
0.40 to 0.43
Ventricular depolarization and repolarization
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Saturday, March 29, 2008
- Blood volume in lungs= 450ml, 9% of total blood volume.
- Blood flowing through Bronchial arteries- 1-2% of total Cardiac Output
- Pulmonary Vascular resistance= 1/7 of systemic vascular resistance
- Mean pressure= 15mmHg
- Pulmonary arteries constrict in response to hypoxia.
- Perfusion and Ventilation both are more in lower lobes
- Ventilation/resistance is maximum at the apex.
- Pulmonary veins are collapsed in upper and middle lobes, distended in lower lobes. This is because pressure in pulmonary veins of upper and middle lobes is less than atmospheric pressure. This causes the veins to collapse.
Tuesday, March 25, 2008
Sino-Atrial node is located at the junction of superior vena cava with right atrium, Just deep to the epicardium, near the sulcus terminalis. The SA node is made of modified cardiac muscle that has fewer strations and indistinct boundaries. These cells are small round with few organelles which are connected by gap junctions. These cells are called P cells (pacemaker cells). SA node is the fastest discharging part of the myocardium (70 to 80/min)
Blood supply of SA node- Right coronary artery supplies the SA node in 65% of the cases.
Nerve supply- SA node develops from the structures on the right side of the embryo, therefore SA node is supplied by Right vagus nerve and Right sympathetics. Noradrenergic nerve fibers are epicardial while vagal fibers are endocardial.
Atrio-ventricular node is located in the right postero-infero region of the interatrial septum near the opening of coronary sinus. There are 3 bundles of fibers that connect the SA node with the AV node. Namely Anterior internodal tract of Bachman, Middle internodal tract of Winckebach and Posterior internodal tract of Thorel.
Blood supply- Right coronary artery.
Nerver supply- AV node develops from structures in the left side of the enbryo. Therefore it is supplied by Left vagus and left sympathetics.
The depolarization of SA and AV nodes depends on calcium channels rather than on Sodium channels. Rate of impulse generation in decreasing order- SA node> AV node (40 tp 60/min)> Bundle of His (40/min)> Purkinjee fibers (24/min).
Wednesday, October 10, 2007
A serious note about heart attacks - You should know that not every heart attack symptom is going to be the left arm hurting. Be aware of intense pain in the jaw line.
You may never have the first chest pain during the course of a heart attack. Nausea and intense sweating are also common symptoms. 60% of people who have a heart attack while they are asleep do not wake up. Pain in the jaw can wake you from a sound sleep. Let's be careful and be aware. The more we know the better chance we could survive.
A cardiologist says if everyone who reads this message sends it to 10 people, you can be sure that we'll save at least one life. Read this & Send the link to a friend. It could save a life. So, please be a true friend and send this article to all your friends you care about.
Thursday, March 01, 2007
Acne vulgaris is a self limiting disorder of teenagers and young adults.But 10-20% of adults may continue to experience this disorder. In adolescence, there is increased secretion of sebum from sebaceous glands. The glands get blocked with the retained sebum and kerotinous debris. Small cysts called Comedons are formed due to blockage of hair follicles. Proprionobacterium acnes is the cyst and caused production of fatty acids within the cysts. Thus causing infection of the cyst and bursting of the cyst wall. The extrusion of oily, keratinous debris triggers a foreign body reaction develops.
These are of two types-
- Closed comedones = White heads.
- Opened comedones = Black heads.
The closed comedones are mostly associated with inflammatory lesions like papules, cysts and nodules. These are seen as small white heads with the naked eye or sometimes are not visible to the naked eye.
The Open comedones are seen as Black heads. These are more stable and have a dilated orifice (opening) at their peak. Material in these comedones can be easily expressed out. These rarely cause inflammatory cysts and nodules.
The earliest lesion seen is mildly inflammed comedone at the forehead. Later cheeks, chin and nose are involved. Chest and back are also not uncommon.
Usually Scarring is not seen in case of acne lesions but in case of large inflammatory cysts and nodules, they may leave significant scarring. Helmets, chin straps may produce friction on the comedone scausing their burst and subsequent inflammation. Cosmetics containing comedogenic substances (glucocorticoids, lithium etc) or drugs that may cause acne (phenytoin, phenobarbital, glucocorticoids) may produce acneiform lesions.
Washing face with a mild soap to avoid accumulation of oil and debris, avoiding over cleaning and rubbing of the skin, maintaining good hygiene and trimming of nails etc prevent and reduce the incidence of Acne.
Topical agents (agents applied locally, on the site) - Retinoic acid, Benzoyl peroxide, salicylic acid are useful in altering the epidermal desquamation and comedome formation. They aid in resolution of previous cysts.
Topical antibacterial agents - Benzoul peroxide, azelaic acid, topical erythromycin, clindamycin.
It is an inflammatory disorder predominantly affecting the central face. Mostly seen in women but males are the severe sufferers. It is rarely seen below the age of 30. Initially flushing is seen over the face as a reaction to hot drinks, emotional stimuli, spicy foods, heat etc, but later the flushing becomes permanent. Papules , pustules and telangiectases become superimposed on the flush. Rosacea of long standing duration may cause connective tissue over growth (particularly of nose - rhinophyma). Rosacea is complicated by various eye disorders like blepharitis, iritis, keratitis which are sight-threatening and require an ophthalmic evaluation.
Topical metronidazole, sulfacetamide are useful. More severe diseases require oral tetracycline. Laser therapy is useful for residual telangiectasia. Glucocorticoids are best avoided.
Monday, February 26, 2007
Pemphigus vulgaris is a blistering autoimmune skin lesion mostly seen in elderly patients.The disorder is characterised by a process called Acanthoysis (loss of cohesion between epidermal cells).Lesions are mostly flaccid blisters over the skin.These blisters burst out and the surounding skin gets denuded.In severe cases, substantial portions of the body get denuded.Manual pressue over these blisters can cause separation of epidermis.This is known as Nikolsky's sign.This finding is a characteristic feature of Pemphigus vulgaris but not the specific feature. Nikolsky's sign is also seen in Stevens Johnson Syndrome, Toxic epidermal necrolysis and few other skin conditions.
Sometimes the disorder starts with pruritis(itching).Lesions in Pemphigus vulgaris are usually seen over the oral mucosa, scalp, axilla, trunk, face, neck.Blisters are usually seen in the mouth first and then on other mucosa (pharyngeal, laryngeal, oesophageal, conjunctival, vulval or rectal) in severe cases.Severe pain may be seen associated with extensive denudation of body surface area. Lesions usually heal without scarring except at sites complicated by secondary infections or with mechanical dermal wounds.Post inflammatory hyper pigmentation is usaually seen at sites of healed lesions for some time.
On biopsy, the lesions show acantholytic epidermal cells and intra epithelial vesicles.Basal keratocytes are attached to the basement membrane, hence blister formation takes place in suprabasal portion of epidermis.Eosinophil predominant leukocytosis is seen in these regions.
Direct immuofluoresence microscopy shows - IgG antibodies both in the lesional and normal skin.But in the lesional skin, there are compliment components which are absent in the normal skin.These IgGs are derived from autoantibodies directed against cell surface antigens on the epidermal cells.These autoantibodies are targeted against desmogleins (Dsgs, these are transmembrane desmosomal glycoprotiens that belong to cadherin supergene family of calcium dependent adhesion molecules).These autoantibodies can be demonstrated by indirect imunofluoresence microscopy or by ELISA.Anti Dsgs titers relate with the activity of the disease.Mostly anti Dsgs3 is seen in these patients but in severe cases, antiDsgs3 and anti Dsgs1 autoantibodies are seen.Anti Dsg antibodies are pathogenic for blister formation and their titers correspond with the disease activity.
Prior to availability of Glucocorticoids, the mortality rate was 60 to 90%. Now it has been reduced to 5%.Prednisolone 60 to 80 mg/day is given. If new blister appear after 1 or 2 weeks of treatment, the dose must be increased. Immunosuppressants are given along with glucocorticoids if needed. Azathioprine (1 to 2 mg/day), Cycliphosphamine (1 to 2 mg/day), Mycophenolate mofetil (20 to 35 mg/day).
Sunday, February 25, 2007
Iron deficiency anemia is a condition where there is anemia and a clear evidence of iron deficiency. It is categorized under ‘Hypoproliferative Anemias’.
Stage of negative iron balance – The demand (or loss) for Iron exceeds that of the body’s capacity to absorb from the diet. Most common causes of the above condition are pregnancy, blood loss from bleeding, growth spurts in adolescence. Blood loss of 25-30 micrograms/dL can exceed the total body’s capacity to absorb iron from diet. The iron from reticulo-endothelial system and other iron stores is utilized.
In this condition, iron in stores like ferritin or stainable iron in bone marrow decrease. As long as iron stores are present and mobilized, serum iron, total iron binding capacity (TIBC) red cell protoporphyrin levels remain normal. At this stage, RBC morphology and indices are normal.
Stage of Iron deficient erythopoiesis – When the iron stores are depleted, TIBC and red cell protoporphyrin levels increase. Marrow iron stores are absent when serum ferritin levels fall to 15 micrograms/dL. Once the transferrin saturation falls to 15 – 20%, hemoglobin synthesis is impaired.
Stage of Iron deficiency anemia – In this stage, microcytic, hypochromic RBC are visible in the peripheral smear. Hemoglobin and hematocrit begin to fall. Transferrin saturation at this point is 10-15%.
At moderate anemia (Hb -10 to 13 g/dL), the bone marrow is hypoproliferative. At severe anemia (Hb – 7 to 8 g/dL), misshapen red cells called poikilocytes, cigar shaped cells, target cells, are seen. Marrow becomes ineffective. Microcytes and hypochromatic cells become more prominent. With severe prolonged anemia, the erythroid hyperplasia is seen in the marrow rather than hypoproliferation.
Pallor, decreased exercise capacity, fatigue, Cheilosis (fissures at the corners of mouth), Koilonychia (spooning of fingernails) are the few signs and symptoms of iron deficiency anemia.
As a cardinal rule, Iron deficiency anemia in an adult male is due to gastrointestinal bleeding, until proved otherwise.
Serum Iron and Total Iron binding capacity (TIBC)-
Normal serum iron range = 50-150 migs/dL
Normal serum Total iron binding capacity = 300-350 migs/dL
Normal transferrin saturation = 25-50 %
Transferrin saturation = Total serum iron x 100 ÷ TIBC
Iron deficiency states are associated with transferrin saturation <> 50% indicates that disproportionate transferrin bound iron is being delivered to non erythroid tissues. If this condition persists for a long time, tissue iron overload may occur.
There is diurnal variation in serum iron level.
Serum ferritin indicates the total iron stores of the body. Thus serum ferritin estimation is the most appropriate laboratory test for estimating iron stores.Normal serum transferrin levels in adult male – 100 migs/L, levels in female – 30 migs/L.Serum ferritin levels of
Evaluation of Bone Marrow Iron Stores-
Reticulo endothelial stores of iron can be estimated by
1. Iron staining of bone marrow aspirate
2. Serum ferritin levels.
Measurement of Serum ferritin levels has largely replaced iron staining of bone marrow and is a better indicator of iron overload. But iron staining of bone marrow provides information about iron delivery to developing erythroblasts. 20-40% of sideroblasts (developing erythroblasts) have visible iron granules in them.
In myelodysplastic syndrome, mitochondrial dysfunction occurs and accumulation of iron in the mitochondria around the nucleus in a necklace fashion. Such cells are termed as ringed sideroblasts.
Red cell Protoporphyrin levels:
Protoporphyrin is a metabolite used in the production of heme molecule. Heme production is impaired in iron deficiency states causing in increase in protoporphyrin levels in RBC. Most common causes are Iron deficiency and Lead poisoning. Normal value (of red cell protoporphyrin) – 30 migs. In iron deficiency, its value may go up to 100 migs.
Serum levels of Transferrin Receptor Protein:
Erythroblasts have the highest number of transferrin receptors on their surface. Erythroblast receptor protein is released by cells into circulation. Therefore estimation of Transferrin receptor proteins gives an indication about erythroid marrow mass. Normal value = 4-9 migs/L.
Conditions which show microcytic, hypochromic anemia which need to be distinguished from Iron Deficiency Anemia –
1. Thalassemias – Inherited defects in globin chain synthesis. Serum iron levels are normal in this case, which help in differentiating it from iron deficiency anemia.
2. Chronic inflammatory diseases – Here the serum iron levels are normal but iron is not efficiently supplied to erythroid cells.
3. Myelodysplastic syndromes – Most rare condition of the three. Here hemoglobin synthesis is impaired due to defective mitochondria resulting in defective mitochondrial incorporation into the heme molecule. Serum iron levels are normal here and more than adequate iron is delivered to the marrow.
Diets rich in Iron:
Red meat is the easiest source of Iron that is easily absorbed by the body.
Few Foods rich in heme Iron –
• Chicken Liver
• Beef Liver
Foods rich in non heme Iron –
• Enriched breakfast cereals
• Cooked beans and lentils
• Pumpkin seeds
• Blackstrap Molasses
Phytates (found in legumes) and tannins (found in tea) decrease Iron absorption. Iron absorption is increase when the serum iron level is less and decreased when the serum iron is normal to increased.
Parenteral Iron Therapy :
Intravenous Iron is given to patients who can not tolerate oral iron, or who need Iron on an ongoing basis and who have persistent gastrointestinal blood loss. Serious adverse reaction rate to intravenous Iron dextran is 0.7%.Other Iron complexes available are Sodium ferric gluconate (ferrlecit) and iron sucrose (venofer).
Parenteral iron is used for
1. To correct the Hemoglobin deficiency
2. Provide the patient with at least 500 mg of iron stores.
3. To give small doses of parenteral iron over a protracted period – This is usually done in dialysis centers to augment the response to recombinant erythropoietin therapy.100 mg of elemental iron is given weekly for 10 weeks.
Oral Iron Therapy:
It is treatment of choice in patients with established, asymptomatic iron deficiency anemia. Daily dose of 300 mg of elemental iron is given in 3 or 4 divided doses. It causes absorption of 50 mg of elemental iron per day. This supports a erythrocyte production of two to three times that of normal. Oral iron tablets should be taken empty stomach because some foods interfere with the obsorption of iron in the intestines (phytates and phosphates reduce its absorption by 50%). Iron stores of 500 to 1000 mg should be achieved along with correction of the deficiency. To achieve this, sustained treatment for 6 to 12 months is needed. Ascorbic acid helps in the absorption of iron.
Tablet (iron content) in mg
Response – Typically reticulocyte count should begin to increase within 4 to 7 days and peaks at 1.5 weeks. In absence of good response due to incompliance or poor absorption, parenteral therapy should be considered.
This is considered in patients with symptoms of anemia, cardiovascular instability and excessive bleeding. Transfusion not only corrects anemia, but also the transfused RBC provide with iron for reutilization.
Saturday, February 24, 2007
Panic disorder is a type of anxiety disorder.
Anxiety - Is defined as "Subjective sense of unease, dread or foreboding, can indicate a primary psychiatric disorder or can be a component of, or a reaction to a primary medical disease.
Panic disorder - Defined as recurrent and unpredictable panic attacks which are distinct episodes of intense fear and discomfort associated with a variety of physical symptoms including palpitations, sweating, trembling shortness of breath, chest pain, dizziness and a fear of impeding doom or death,Paresthesias, gastrointestinal distress, air hunger and feelings of unreality are common.
First attack is usually outside the home.Onset is usually in late adolescence to early adulthood.Anticipatory anxiety occurs in some people leading to generalized fear and avoidance of places or situations where panic attack may recur.
Panic attack occurs suddenly over a period of 10 mins and resolving over a period of one hour.The attacks usually occur in an unexpected fashion.
Agoraphobia is commonly seen in panic disorder patients.It is an 'acquired irrational' fear of being in places where one might feel trapped or unable to escape.It leads to progressive restriction in lifestyle or in a geography.Frequently patients are embarrassed that they are housebound and dependent on others to go out into the world and do not volunteer this information.
Differential diagnosis :
A variety of cardiovascular, pulmonary, endocrine and neurological conditions can present with anxiety as chief complaint.So the diagnosis of panic attack is made after a medical etiology of panic attack is ruled out.Patients with true panic attack often focus on one specific feature and tend to exclude others.
When the history is nonspecific, physical examination and thorough laboratory testing must be done to rule our anxiety states resulting from medical disorders like Pheochromocytoma, thyrotoxicosis, Hypoglycemia.
ECG may show paroxysmal atrial tachycardia, mitral valve prolapse (these are the cardiovascular disorders usually associated with panic).
Panic disorder is also diagnosed in patients referred for pulmonary function testing or with irritable bowel syndrome.
Diagnostic criteria also requires at least one month of concern or worry about the attacks or the change of behavior related to the attack.
The cause is unknown but genetic predisposition, altered autonomic responsivity and social learning are usually associated with these attacks.
Genome wide screens have identified suggestive risk loculi over 1q, 10q, 13q, 7p15, 11p.Acute panic disorders are associated with increased noradrenergic discharges in locus coeruleus.
Few Precipitating factors observed in some patients - Intravenous infusion of sodium lactate, Alpha2 adrenergic antagonist-Yohimbine, Cholecystokinin tetrapeptide (CCK 4), Carbon dioxide inhalation.
Each of these stimulants activates a pathway involving noradrenergic neurons in coeruleus and serotonergic neurons in dorsal raphe.
1. Tricyclic Antidepressants (TCAs) - imipramine and clomipramine (10-25 mg/day).Low doses are given initially to avoid increase in monoamine levels associated with these drugs.
2. Selective Serotonin Reuptake Inhibitors (SSRIs) - Are equally effective but do not have the adverse effects of TCAs.Usually started at 1/3 to 1/2 of their usual antidepressant dosage.
3. Monoamine Oxidase Inhibitors (MAOIs) - Specifically beneficial in patients with atypical depression with symptoms like hyperosmia, weight gain.They have adverse effects like Orthostatic hypertension, Insomnia and the need to maintain a low tyramine diet (avoidance of cheese and wine)
4. To avoid anticipatory anxiety and for immediate relieving of symptoms - Benzodiazepines (Alprazolam - 0.5 mg to 4 mg/day; Clonazepam - 2 mg to 4 mg/day) are used.But patients should be monitored closely as they may cause dependence.
5. Education of symptoms and their control, assurance, encouraging patients to voluntarily expose themselves to precipitating factors, breathing techniques are very important part of the treatment.
Once satisfactory response if obtained, the treatment is continued for 1 to 2 years.The efficiency of the treatment is 75-80%.
Monday, February 12, 2007
Most common form of Facial paralysis.
Clinical features :
- Pain behind the ear may preced the palsy for one or two days.
- Onset is abrupt and maximal weakness is attained by 48 hours.
- Loss of taste sensation unilaterally (on one side).
- Hyperacusis may be present.
- Mild cerebrospinal fluid Lymphocytosis may be present.
- Presence of incomplete paralysis in first week is most favorable sign.
- 80% patients recover in few weeks to months.
Bell's palsy is associated with presence of Herpes Simplex type I DNA in endonueral fluid and posterior auricular muscle.This indicates that reactivation of this virus may have some role.However this is not proven yet.
Differenctial Diagnosis :
Other causes of Facial Palsy -
1. Tumours of temporal bone - Carotid body tumor, Cholesteotoma, Dermoid cysts.The course is insidious and progressive.
2. Ramsay Hunt Syndrome -
Due to Herpis zoster of geniculate ganglion.Consists of : Severe facial palsy; eruptions in pharynx, external auditory canal and other parts of cranial integument; Eighth nerve is commonly involved.
3. Acoustic Neuromas -
These cause facial paralysis by compresion of facial nerve.
4.Bilateral Facial Paralysis -
This is seen in Guillain Bare syndrome and Uveoparotid fever (Heerfordt syndrome), a form of Sarcoidosis.
5.Pontine lesions -
Infarcts; Demyelinating lesions of Multiple sclerosis and tumours.
6.Milkersson Rosenthal syndrome -
This consists of the triad Facial paralysis; Recurrent (and later permanent) facial edema (particularly of lips); Plication of tongue.
All the above lesions are Nuclear or Peripheral forms of Facial palsy.In Supranuclear facial palsy, Frantalis and orbicularis occuli muslces are less involved.This is because, muscles in upper part of the face are innervated by nerves from Motor cortices of both sides (So if one nerve is paralysed, the muscle gets nervous supply from the other nerve).The muscles of lower face are supplied by nerves of the opposite hemisphere.
In Supranuclear lesions, there is dissociation of emotional and voluntary facial movements.There is some degree of arm and leg and an aphasia may also noted.
All other diseases (mentioned above) are ruled out first.
MRI reveals swelling and uniform enhancement of Geniculate ganglion or facial nerve can me noticed.Sometimes, entrapment of swollen nerve in temporal bone can be observed.
Glucocorticoids (Prednisolone) is given in the dose of 60 - 80 mg/day for first 5 days then the dose is slowly decreased.
Acyclovir (400 mg five times a day for 10 days) given along with Prednisolone has shown to give better results than prednisolone alone.
More reading on Bell's Palsy :
Saturday, February 10, 2007
SA (Sinoatrial) node is the pacemaker of human heart.AV (Atrio-ventricular) node is the conduction junction between Atria and ventricles.It transmits the impulses originating in the SA node (present on right atrium) to the ventricles.Any conductional defects in the AV node may cause ventricular tachyarrhythmias and ventricular failure.
In any suspected case of conduction disturbances, the physician must assess
- The site of block
- The risk of turning into a complete block
- The probability that a subsidiary escape rhythm develops distal to the block.
If the escape rhythm pace maker is in the HIS bundle, the ectopic impulse is stable and the rate is usually 40 - 60 beats/min.QRS complex is normal in duration.If ectopic rhythm is present in HIS-Purkenjee system, ectopic rhythm is unstable and rate is usually 25 - 45 beats/mins.QRS complex id prolonged.
Seen in following conditions-
Chronic athlets have hypervagal stimulation.Mobitz type two AV conduction block is mostly seen in them.
Drugs-Digitalis toxicity,Over dosage of Calcium channel blockers, Beta blockers.
Infections-Viral myocarditits, Infectious mononucleosis, Sarcaidosis, Rheumatic heart disease.
Amyloidosis, SLE,Kyme disease.
Myocardial infarction, Coronary spasms.
Levis Disease - Calcification of myocardial skeleton.Usually involve aortic and mitral valves.
Lenegre's Disease - Primary sclerodegenerative disease of conducting tissue.No involvement of myocardium.
Hypertension and Aortic.mitral valve stenosis accelerate the sclerodegenerative process of conducting system and even have a direct sclerosis and fibrosis of conducting system.
First degree Block : (Prolonged PR Interval > 0.2 sec)
PR interval depends on Atrial, AV nodal, HIS purkinjee system activation.
Normal QRS duration with prolonged PR interval - Seen in AV Nodal block
Normal PR interval with prolonged QRS interval - seen in His-purkinjee block
If both QRS and PR intervals are prolonged - Block can be present anywhere in the three sites.
Second degree Block :
Some impulses fail to reach ventricles.
It is of two types - Mobitz type 1 (Winkebach phenomenon) and Mobitz type 2
- Mobitz type 1 - Progressive Prolongation of PR interval followed by a missed P wave.The pause is less than two normal sinus intervals.The block is always localised to AV node with normal QRS interval.It is seen in inferior wall infarction or drug intoxication with digitalis, Beta blockers and calcium channel blockers.Also seen in normal people with high vagal tones ( athletes).It never progresses to complete block.Even if it progresses, it is stable and pacemaker implantation or aggressive therapy is rarely indicated.
- Mobitz type 2 - Sudden loss of P wave with no prior changes in PR interval.It is a HIS-Purkinje system.If QRS interval is normal, the block is intra HIS block.It is seen in atrio-septal infarction, sclerodegenerative disorders of fibrous skeleton of heart.It progresses to complete heart block with unstable ectopic pacemakers.Therefore, pacemaker implantation becomes mandatory.
In high degree AV blocks, there are two or more consecutively blocked P waves.But intermittent conduction is present.Third degree Block :
In this case, there is no conduction from atria to the ventricles.The rate is usually 40 to 55 beats/min.In case of Congenital AV block, the block is limited to AV node.The rate increases with Atropine or exercise.But if the escape pacemaker is in the HIS bundle, the escape pacemaker is less responsive to these perturbations.
Some people with Infra HIS bundle block are capable of 'retrograde conduction'(reverse conduction).In these people, a dual chamber pacemaker is needed because a normal pacemaker may cause 'Pacemaker syndrome' in these patients.
AV Block Summary -
- QRS normal, PR interval prolonged - AV nodal Block (PR > 0.3 secs)
- QRS prolonged, PR interal normal - HIS bundle block or HIS-Purkinje system block.
- Atropine and exercise - Improves conduction - AV Block
- Atropine and exercise - worsens conduction - HIS or HIS purkinje block.
- Carotid sinus pressure - worsens conduction - AV block
- Carotid Sinus pressure - Improves conduction - HIS and HIS purkinjee block.
- Retrograde conduction is present in HIS and HIS Purkinje system blocks.