Showing posts with label Medicine. Show all posts
Showing posts with label Medicine. Show all posts

Thursday, November 12, 2015

STUDY GUIDE FOR HEAD AND NECK ANATOMY - MEDICAL MNEMONICS -MUSCLES OF THE HEAD AND NECK REGION ( FREE DOWNLOAD ANATOMY STUDY GUIDES AND MEDICAL MNEMONICS)

MEDICAL MNEMONICS -MUSCLES OF THE HEAD AND NECK REGION

MEDICAL MNEMONICS -MUSCLES OF THE HEAD AND NECK REGION

MEDICAL MNEMONICS -MUSCLES OF THE HEAD AND NECK REGION

MEDICAL MNEMONICS -MUSCLES OF THE HEAD AND NECK REGION

MEDICAL MNEMONICS -MUSCLES OF THE HEAD AND NECK REGION

MEDICAL MNEMONICS -MUSCLES OF THE HEAD AND NECK REGION

Tuesday, December 30, 2014

Vitamin D-What, Where, When, How, Why?


Vitamins are not generally considered to be endocrine substance, but it is a organic dietary factors essential for healthy life. The term ‘ vitamin D ’ refers to two steroid like chemicals, namely ergocalciferol and cholecalciferol . Vitamin D is important for good health, growth and strong bones and may also help to prevent other diseases such as cancer, diabetes and heart disease. A lack of vitamin D is very common. Vitamin D is mostly made in the skin by exposure to sunlight.  A mild lack of vitamin D may not cause symptoms but can cause generalised aches and pains and tiredness. A more severe lack can cause serious problems such as rickets (in children) and osteomalacia (in adults), described below. Treatment is with vitamin D supplements. Some people are more at risk of vitamin D deficiency, and so are recommended to take vitamin D supplements routinely. These include all pregnant women, breast-fed babies, children under 5, and people aged 65 and over. Also, people who do not get much exposure to the sun, people with black or Asian skin types, people who do not go out in the sun and people with certain gut, liver or kidney diseases.  We have checked our own patients and found that 9/10 adults of South Asian origin are vitamin D deficient and something like 60% of our white patients are vitamin D deficient.  Most people present with aches and pains and tiredness.

What is vitamin D?
Vitamins are a group of chemicals that are needed by the body for good health. Foods that contain vitamin D include the following though many foods do not contain much vitamin D and exposure to the sun is a better source of vitamin D than foods. Vitamin D is a fat-soluble vitamin. Most foods contain very little vitamin D naturally , though some are fortified (enriched) with added vitamin D.  Foods that contain vitamin D include:
                -Oily fish (such as sardines, pilchards, herring, trout, tuna, salmon and mackerel).
                -Egg yolk.
                -Fortified foods (this means they have vitamin D added to them) such as margarine, some cereals, infant formula milk.

Action of Vitamin D
The 1,25 - (OH)2 -D 3 receptor belongs to a superfamily of nuclear hormone receptors, which bind to their ligand and alter transcription. The hormone travels in the bloodstream in equilibrium between bound and free forms. The latter form is freely able to enter cells, due to its lipophilic nature. The plasma 1,25 - (OH) 2 - D 3 - binding protein (DBP) recognizes the hormone specifi cally. 1,25 - (OH) 2 - D 3 binds to the nuclear receptor; the complex binds to specifi c hormone response elements on the target gene upstream of transcriptional activation sites, and new mRNA and protein synthesis result.
New proteins synthesized include osteocalcin, an important bone protein whose synthesis is suppressed by glucocorticoids. In the GIT, a calcium - binding transport protein (CaBP) is synthesized in response to the hormone – receptor activation of the genome.


Physiological actions of vitamin D

Bone-Vitamin D stimulates resorption of calcium from bone as part of its function to maintain adequate circulating concentrations of the ion. It also stimulates osteocalcin synthesis.
Gastrointestinal tract-1,25 - (OH) 2 - D 3 stimulates calcium and phosphate absorption from the gut through an active transport process. The hormone promotes the synthesis of calcium transport by enhancing synthesis of the cytosolic calcium – binding protein CaBP, which transports calcium from the mucosal to the serosal cells of the gut.
Kidney- 1,25 - (OH) 2 - D 3 may stimulate reabsorption of calcium into the tubule cells while promoting the excretion of phosphate. The tubule cells do possess receptors for vitamin D and CaBP.
Muscle-Muscle cells have vitamin D receptors, and the hormone may mediate muscle contraction through effects on the calcium fl uxes, and on consequent adenosine triphosphate (ATP) synthesis.
Pregnancy-During pregnancy, there is increased calcium absorption from the GIT, and elevated circulating concentrations of 1,25 - (OH) 2 - D 3 , DBP, calcitonin and PTH. During the last 6 months prior to birth, calcium and phosphorus accumulate in the fetus. The placenta synthesizes 1,25 - (OH) 2 - D 3 , as does the fetal kidney and bone. Nevertheless, the fetus still requires maternal vitamin D.
Other roles- Vitamin D may be involved in the maturation and proliferation of cells of the immune system, for example of the haematopoietic stem cells, and in the function of mature B and T cells.


Our main source of vitamin D is that made by our own bodies. 90% of our vitamin D is made in the skin with the help of sunlight.
Ultraviolet B (UVB) sunlight rays convert cholesterol in the skin into vitamin D. Darker skins need more sun to get the same amount of vitamin D as a fair-skinned person. The sunlight needed has to fall directly on to bare skin (through a window is not enough). 2-3 exposures of sunlight per week in the summer months (April to September) are enough to achieve healthy vitamin D levels that last through the year. Each episode should be 20-30 minutes to bare arms and face. This is not the same as suntanning; the skin simply needs to be exposed to sunlight.
So, vitamin D is really important for strong bones. In addition, vitamin D seems to be important for muscles and general health. Scientists have also found that vitamin D may also help to prevent other diseases such as cancer, diabetes and heart disease.

Who gets vitamin D deficiency?
Vitamin D deficiency means that there is not enough vitamin D in the body. Broadly speaking, this can occur in three situations:

1. Increased need for vitamin D
Growing children, pregnant women, and breast-feeding women.

2. Situations where the body is unable to make enough vitamin D
People who get very little sunlight on their skin are also at risk of vitamin D deficiency. This is more of a problem in the most northern parts of the world where there is less sun. In particular:
                 People who stay inside a lot or cover up when outside or use strict sunscreen
                 People with pigmented (dark coloured) skins and elderly people  
                 Some medical conditions can affect the way the body handles vitamin D.
                     People with Crohn's disease, coeliac disease, and some types of liver                                                     and kidney disease, are all at risk of vitamin D deficiency.
                 Vitamin D deficiency can also occur in people taking certain medicines -                                                  examples include: Carbamazepine, Phenytoin, prim done, barbiturates and some anti-HIV                    medicines
3. Not enough dietary vitamin D
Vitamin D deficiency is more likely to occur in people who follow a strict vegetarian or vegan diet, or a non-fish-eating diet.

How common is vitamin D deficiency?
It is very common. This is why we recommend a regular supplement to our patients.  A recent survey in the UK showed that more than half of the adult population in the UK had low vitamin D. This level is found to be greater in people who have dark skin.  In the winter and spring about 1 in 6 people has a severe deficiency. It is estimated that about 9 in 10 adults of South Asian origin may be vitamin D-deficient. Most affected people either don't have any symptoms, or have vague aches and pains, and are unaware of the problem.  80% of our Asian patients have been found to be deficient and 60% of our white patients have found to be deficient.

What are the symptoms of vitamin D deficiency?
Symptoms of vitamin D deficiency are tiredness or general aches.  Because symptoms of vitamin D deficiency are often very vague, the problem is often missed.

How is vitamin D deficiency diagnosed?
Vitamin D deficiency can be diagnosed by a blood test.  However, on balance if you have dark skin and live in the UK you should take supplements. It may be suspected from your medical history, symptoms, or lifestyle. A simple blood test for vitamin D level can make the diagnosis.

RECOMMENDATIONS – Your doctor will advise you if you have deficiency or insufficient vitamin D.  If you have a minor level of vitamin D deficiency we recommend patients buy vitamin D tablets equivalent to 10ug or 12.5ug.  Most are made from vegetables.   If you have been found to be deficient we would recommend you stay on this dose for life as treatment is often needed long-term because the cause of the deficiency, such as dark skin or not enough sunlight, is unlikely to be corrected in the future.  We have observed that it takes at least 6 months taking regular vitamin D for symptoms to resolve and the level of vitamin D to return to normal.  It should be noted that if you have severe deficiency the doctor may recommend that you take a higher dose of vitamin D for a limited time, often equivalent to 25ug for the first 3 months.  Please discuss this with your own doctor.  We recommend that patients buy vitamin D tablets as we are unable to prescribe vitamin D without calcium on the NHS and calcium prescriptions have been associated with increased kidney stones and it is for this reason that we recommend that our patients buy vitamin D.

Maintenance therapy after deficiency has been treated
The dose needed for maintenance maybe lower than that stated.  We advise patients to buy 10ug and take 2 a day.   When the body's stores of vitamin D have been replenished. maintenance treatment is often needed long-term, to prevent further deficiency in the future. This is because it is unlikely that any risk factor for vitamin D deficiency in the first place, will have completely resolved. The dose needed for maintenance may be lower than that needed to treat the deficiency.

Cautions when taking vitamin D supplements
Care is needed with vitamin D supplements in certain situations:
 1. If you are taking certain other medicines that can interact such as  Digoxin (for an irregular         heartbeat – atrial fibrillation),  Thiazide or diuretics (water tablets).                                                   
2. If you have medical conditions such as kidney stones, some types of                                                     kidney disease, liver disease or hormonal disease.
3. Vitamin D should not be taken by people who have high calcium levels.
4. You may need more than the usual dose if taking certain medicines such as Carbamezapine, Phenytoin. HRT or barbiturates. Multivitamins are not suitable for long-term high-dose treatment because the vitamin A which can be harmful in large amounts.

Are there any side-effects from vitamin D supplements?
It is very unusual to get side effects from vitamin D if taken in the prescribed dose. However, very high doses can raise calcium levels in the blood. This would cause symptoms such as thirst, passing a lot of urine, nausea or vomiting.

Prognosis (outlook) in vitamin D deficiency?
The outlook for vitamin D deficiency is usually excellent. Both the vitamin levels and the symptoms generally respond well to treatment. However, it can take time (months) for symptoms to resolve and for bones to recover.  Generally after 6 months of using Vitamin D tablets the patient feels a lot better and symptoms have improved.  This does not mean you need to stop taking the medication.  Vitamin D supplementation is for life.



Monday, December 22, 2014

Classification of oral diseases of HIV- associated immune suppression (ODHIS)


         Present classification systems for HIV – associated oral lesions developed in the early 1990’s which was named as HAART. Patterns of oral conditions keep on changing very frequently. This highlights the need of new system.

Classification of oral diseases of HIV – associated immune suppression (ODHIS)

System should consider:
·         Changes in epidemiology of oral lesions
·         Therapeutics
·         Development of lesions and immune systems
·         Oral lesions to oral disease

Definition of Oral disease:  abnormality characterized by a defined set of signs and symptoms in the oral cavity, extending from the vermilion border of the lip to the oropharynx, with the exception of salivary gland disease

New Classification- Classification of oral diseases of HIV – associated immune suppression (ODHIS)
Group 1 – ODHIS associated with severe immune suppression (CD4<200 cells/mm3)
Group 2 – ODHIS associated with immune suppression (CD4<500 cells/mm3)
Group 3 – ODHIS assumed associated with immune suppression
A) More commonly observed
B) Rarely reported
Group 4 – Therapeutically-induced oral diseases
Group 5 – Emerging oral diseases
Oral diseases do not belong exclusively to one classification Group
Overlap may exist

Use of the New Classification
·         Identifying undiagnosed individuals
·         Provides additional rationale for HIV testing
·         Affects access and type of HIV-related healthcare
·         Provides clinical markers for therapeutic interventions and efficacy

Group 1. ODHIS associated with severe immune suppression (CD4<200 cells/mm3)
1.      Major recurrent aphthous ulcer
2.      Neutropenia-induced ulcers
3.      Necrotizing ulcerative periodontitis
4.      Necrotizing stomatitis
5.      Cytomegalovirus (CMV)
6.      Chronic HSV
7.      Histoplasmosis
8.      Esophageal, pseudomembranous, and hypertrophic candidiasis
9.      Oral hairy leukoplakia
10.   Kaposi’s sarcoma
11.   Idiopathic Necrotizing Stomatitis    

Hyperplastic candidosis

Oesophageal candidosis

Pseudomembranous Candidosis

Kaposi's Sarcoma

Histoplasmosis
Periodontitis
Neccotizing Sialometaplasia
Chronic HSV

Group 2. ODHIS associated with immune suppression (CD4,500 cells/mm3)
1.       Major recurrent aphthous ulcer
2.       Increased frequency, harder to treat, atypical location
3.       Erythematous candidiasis
4.       Salivary gland disease
5.       Drug induced low salivation
6.       Facial palsy
7.       Neuropathies
8.       Hyposalivation
9.       Human papilloma virus (HPV)
10.   Linear gingival erythema
11.   Non-Hodgkin’s lymphoma
12.   Linear Gingival Erythema

Aptheous Ulcer
HPV

Group 3. ODHIS assumed associated with immune suppression
More commonly observed
1.       Angular candidiasis
2.       Herpes labialis
3.       Intra-oral herpes
4.       Minor aphthous ulcers
Rarely reported
1.       Bacillary epithelioid angiomatosis
2.       Tuberculosis
3.       Deep-seated mycosis (except histoplasmosis)
4.       Molluscum contagiosum
5.       Varicella Zoster Virus (VZV)
6.       HSV Labialis
7.       Intra-oral Herpes
8.       Minor Aphthous Ulcers
Angular Chelitis with candidosis

Group 4. Therapeutically-induced oral diseases

Side-effect
·         Melanotic hyperpigmentation
·         Ulcers
·         Hyposalivation
·         Lichenoid drug reaction
·         Neutropenia-induced ulcers
·         Thrombocytopenia
·         Lypodystrophy-associated oral changes
·         Perioral paresthesia
·         Steven Johnson’s?
·         Exfoliative cheilitis?

Resistance-induced disease
·         Different Candida spp and strains
·         HSV

Antiretrovirals and Adverse Reactions

Antiretroviral Drugs
Indinavir
Saquinavir
Amprenavir
Nevirapine
Delavirdine
Efavirenz
Stavudine
Didanosine

Recurrent HSV
Adverse reactions of antiretroviral drugs
Oral ulcers
Stevens Johnson’s
Taste changes
Dryness
Perioral paresthesia
Thrombocytopenia
Ulcers – Medication Induced
Recurrent HSV

Group 5. Emerging oral diseases
1.       Human papilloma virus, several HPV types (may be associated with immune reconstitution)
2.       Erythema migrans
3.       Variants of Non-Hodgkin’s Lymphoma (NHL B-cell types)
4.       Epithelial neoplasms
5.       Aggressive interproximal dental caries
6.       Condyloma Accuminatum
7.       Squamous Cell Carcinoma

Tuesday, September 16, 2014

Embolism

Embolus Definition
A detached intravascular solid, liquid  or gaseous mass that is carried by the blood to a site distant from its origin.

Embolism
Occlusion or obstruction of a vessel by an embolus

Causes and Types of emboli
  • Thrombi: Thromboembolism
  • Microemboli
  • Fragments of atheromatous plaques-Atheroemboli
  • Bone marrow and bone fragments
  • Fat emboli
  • Air/nitrogen emboli
  • Aminiotic fluid
  • Tumour
  • Foreign body emboli: IV catheters
  • Parasitic emboli

Where emboli lodge depend on their size, their origin, and relevant cardiovascular anatomy.
Those arise in the venous system can travel through the right side of the heart to end up in pulmonary circulation.
Those arise in the left side will block the systemic arteries, and the clinical effect will depend on the organ involved, be it brain, kidneys, spleen, or periphery of the limbs.

Categories of Embolism
  • Systemic embolism- Arise in arterial system eg: thromboemboli in arterial system and left heart, atheroemboli, fat, tumor
  • Pulonary embolism- Arise in venous system thrombi in right heart and deep venous thrombosis, all except atheroemboli.
  • Paradoxical-  By right to left shunt- ASD and VSD
  • Retrograde

Pulmonary embolism
Thrombo-emboli often originate in the deep veins and pass in the venous circulation through right side of heart.
The outcome of pulmonary embolism depends on the size of the blood vessel blocked & presence of pre-existing lung diseases.


Massive pulmonary embolism
Massive coiled pulmonary emboli  are impacted in a main pulmonary artery at bifurcation (Saddle embolus).
This leads to acute right heart failure and sudden death. 


Obstruction of medium sized artery
Dual blood supply protects lung from effects of pulmonary arterial embolism.
No infarctions are seen.
There will be local haemorhage but no damage to pulmonary frame work.
Patient may be asymptomatic or breathlessness  or haemoptysis may present

Emboli in small peripheral arteries
Smaller emboli in periphery can lead to infarctions of the lung as there are no collateral supplies to pulmonary arteries in end arteries.
Area affected is often small but may produce symptoms if multiple
Patient has dyspnoea if these are multiple.

If the bronchial blood supply is impaired

Emboli lodging in medium sized arteries can lead to infarctions.
Since the blockage is proximal the infarcted area is large extending as a cone with the base towards the surface and apex at the blocked artery.
Infarcted area is red due to haemorhage  and congestion.
Infarcts are common in lower lobes and are often multiple.

Microscopy
Bloked blood vessel.
Infarcted area shows haemorhage  with loss of nuclear staining.
But still the alveoli can be identified.
The main pulmonary trunk and pulmonary arteries to right and left lungs are seen here opened to reveal a large "saddle" pulmonary thromboembolus. Such an embolus will kill your patient.



Here is another large pulmonary thromboembolus seen in cross section of this lung. The typical source for such thromboemboli is from large veins in the legs and pelvis




This pulmonary thromboembolus is occluding the main pulmonary artery. Persons who are immobilized for weeks are at greatest risk. The patient can experience sudden onset of shortness of breath. Death may occur within minutes.
This pulmonary embolus is adherent to the pulmonary arterial wall. If the patient survives, the thromboembolus will organize and, for the most part, be removed.

A pulmonary infarct is hemorrhagic because of the dual blood supply from the non-occluded bronchial arteries which continue to supply blood, but do not prevent the infarction.

Systemic embolism
Systemic emboli travel in the internal circulation, commonly originating in the left side of the heart.
Arterial emboli, unless very small, nearly always cause infarction. Emboli to the lower limb may produce gangrene of a few toes or of the entire limb.

Sources of emboli
Heart
  1. Ischemic heart disease-mural thrombi, aneurisms,, hypokinetic segments
  2. Arrhythmias
  3. Valvular- Rheumatic hreart
  4. Myocardial - Myocarditis
  5. Intra cardiac lesions-
  6. Myxomas
Arterial System
  • Ulcerated atheromatous plaque
  • Aortic aneurisma
  • Venous shunts in dialysis patients
Sites of lodgement
  • Coronary arteries
  • Cerebral Arteries
  • Renal Arteries
  • Splenic Arteries
  • Retinal arteries
  • Mesentric Arteries
  • Limb arteries
  • Embolous at the bifurcation of the aorta
Cerebral emboli cause death or infarction unless the embolus lodges in an area that receives adequate collateral supply through the circle of Willis.
A special type of systemic embolus comprises the infected material from vegetations on the heart valves in infective endocarditis. These produce septic infarcts and large abscesses in the affected tissues.
Paradoxical embolus: Venous thrombi that pass through a right–to-left congenital cardiac anomaly

 
Bone marrow emboli
Common in patients who suffered major trauma eg. RTA
Attempted cardiac resuscitation  with rib fractures can lead to this.
Any thing that fractures bones can release bone marrow into venous circulation, resulting in pulmonary emboli.
Clinical significance unclear


Embolism of fragments of atheromatous plaques
Ulcerated atheromatous plaques can cause thrombosis on surface of it or cause embolism of fragments
Cholesterol clefts are seen in the embolus

Fat embolism
Fat from marrow cavities of long bones or from soft tissues can also enter the circulation as a result of severe trauma.
‘Fat embolism syndrome’ characterized by respiratory problems, haemorhagic skin rash, and mental deterioration  24-72 hours after the injury.
The syndrome results from mechanical blockage of vessels, chemical injury to vessels of lung producing pulmonary oedema and activation of coagulative pathway to cause DIC.

Causes of fat embolism
·         Severe trauma with fractures of long bones
·         Damage to fatty tissues
·         Diabetes mellitus
·         Pancreatitis
·         Hyperlipidaemia

Laboratory investigations
·         Urine deposit: fat globules
·         Sputum: fat globules
·         Blood picture :DIC and thrombocytopenia

Air embolism
Large quantities of air within the circulation can act as emboli by forming a frothy mass that can block vessels or become trapped in the right heart chambers to impede pumping.
Over 100 ml of air is needed to produce problems. Lesser amounts dissolve in plasma.
Air can either enter the circulation from
Atmosphere: cut injuries of neck and thorax allowing air to be sucked in.
Air forced into the uterine vessels during badly performed abortions and deliveries,
Produced within circulation: decompression sickness in deep sea divers

Acute decompression sickness
N2 or He will dissolve in blood and tissues at high pressures.
As the diver surfaces, the pressure is reduced and gas begins to come out as minute bubbles.
If rapid this causes air embolism (lodge in brain and skeletal muscle).
Platelets adhere to nitrogen bubbles causing DIC.
Pain around joints, skeletal muscle, respiratory distress coma and death.

Treatment of decompression sickness
·         Early stages, by putting the victim in a decompression chamber pressure will dissolve the bubbles where the high pressure will redissolve the bubbles and allow a slow, controlled decompression.
·         The chronic form, Caisson disease, produces multiple areas of ischaemic necrosis in the long bones

Amniotic fluid embolism
Uncommon but life threatening forms of embolisation.
Amniotic  fluid is forced into the circulation as as a result of traring of the placental membranes and rupture of uterine wall or cervical veins.
Emboli are a mixture of fat, hair, mucous, meconeum and squamous cells from the fetus
Commonly lodge in the alveolar capillaries
Clinically, respiratory failure, cerebral convulsions and coma. Often excessive bleeding due to DIC

Tumour emboli
This is an important mechanism of tumour spread.
Unlikely to have immediate CVS effects

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