Glaucoma

D E FI N I T ION

 Optic neuropathy with typical field defect usually associated with ocular

hypertension (intra-ocular pressure, IOP > 21 mmHg).

AE T IOLOGY

Primary causes: 

Acute closed-angle glaucoma (ACAG), primary opened-angle glaucoma

(POAG), chronic closed-angle glaucoma.

Secondary causes:

 Trauma, uveitis, steroids, rubeosis iridis (diabetes, central retinal vein

occlusion).

Congenital:

 Buphthalmos, other inherited ocular disorders.

E P IDEMIOLOGY

Prevalence 1 % in over 40 years, 10 % in over 80 years (POAG).

Third most common cause of blindness worldwide.

H ISTORY

ACAG:

 Painful red eye, vomiting, impaired vision, haloes around lights.

POAG

: Usually asymptomatic, peripheral visual field loss may be noticed.

Congenital: Buphthalmos (ox eye), watering, cloudy cornea.

EXAMINATI ON (BY S L I T-LAMP)

ACAG: Red eye, hazy cornea, loss of red reflex, fixed and dilated pupil, eye tender and hard on

palpation, cupped optic disc, visual field defect (arcuate scotoma), moderately raised IOP.

POAG: Optic disc may be cupped. Usually no signs.

PATHOLOGY/PATHOGENESI 

S Ocular hypertension compresses and stretches the retinal

nerve fibres leaving the optic disc causing scotomas and visual field loss. Ocular

hypertension is caused by # outflow of aqueous humour caused by:

. obstruction to outflow by approximation of iris to cornea closing iridocorneal angle and

trabecular meshwork/canal of Schlemm causing a rapid and severe rise in IOP (ACAG);

. resistance to outflow through trabecular meshwork (POAG); or

. blockage of trabecular meshwork by blood or inflammatory cells.

INVE S T I G A T IONS

Goldmann Applanation Tonometry: Standard examination to measure ocular pressure

(normal 15 mmHg, POAG 22–40 mmHg, ACAG> 60 mmHg).

Pachymetry: Using ultrasound or optical scanning to measure central corneal thickness

(CCT). CCT <590mm are at higher risk of developing glaucoma.

Fundoscopy: To detect pathologically cupped optic disc (cup – disc ratio > 0.6 or an

asymmetry of 0.2). Picture record of optic nerve head is recommended.

Gonioscopy: To assess the iridocorneal angle.

Perimetry (Visual field testing): For arcuate scotoma (early), tunnel vision (late).

MANAGEMENT1

ACAG (medical emergency): IV acetazolamide (500 mg), 4% pilocarpine topically, analgesics,

antiemetics. May require emergency iridotomy.

Long-term (topical hypotensives)2

b-blockers (timolol): # Aqueous humour secretion.

Prostaglandin analogues (Latanoprost): " Flow via uveoscleral drainage.

Carbonic-anhydrase inhibitor (dorzolamide): # Aqueous humour secretion.

Parasympathomimetics: Pilocarpine (constricts pupil, opening up the trabecular meshwork).

Sympathomimetics: Brimonidine (a2-agonist).

1NICE 2009 guidelines are available on the management of glaucoma at: http://www.nice.org.uk.

2The Ocular Hypertension Treatment Study (OHTS) showed that topical hypotensives prevent or delay the

development of glaucoma.

Glaucoma (continued)

Surgery:

Laser treatment: Laser trabeculoplasty for POAG; iridotomy for ACAG.

Conventional: Trabeculectomy, canaloplasty or iridectomy facilitates outflow of aqueous

humour. 5-fluorouracil or mitomycin may be used to reduce scarring.

COMPL I C A T IONS

Congenital: Amblyopia and visual loss.

POAG: Visual loss.

ACAG: Visual loss and anterior synechiae.

P ROGNOS I S

 Poor prognosis for congenital glaucoma caused by amblyopia. Prognosis in

acquired glaucoma depends on early diagnosis and treatment.

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PH.Jafar Jassim 8/19/2020 06:05:00 ص

تابع القراءه

Hyperlipidaemia

D E FI N I T ION 

Elevation of one or more plasma lipid fractions.

AE T IOLOGY

Primary: Some have molecular genetic basis, but most are unknown.

. Familial hypercholesterolaemia: # Functional hepatic LDL receptors.

. Familial hypertriglyceridaemia: Unknown. Autosomal dominant.

. Hypertriglyceridaemia: Lipoprotein lipase or apo-CII deficiency.

. Familial combined hyperlipidaemia: Unknown.

. Remnant hyperlipidaemia: Apo-E2 genotype inheritance, accumulation of LDL remnants.

Secondary: Subdivided depending on the predominant abnormality.

. " Cholesterol: Hypothyroidism, nephrotic syndrome, cholestatic liver disease, anorexia

nervosa.

. " Triglycerides: Diabetes mellitus, drugs (b-blockers, thiazides, oestrogens), alcohol,

obesity, chronic renal disease, hepatocellular diseases.

Physiology: LDL accumulates in intima of systemic arteries, and is taken up by LDL receptor

on macrophage. This forms a foam cell, part of atheromatous plaque. HDL acts as shuttle

in periphery for transport of cholesterol esters back to the liver and is therefore

cardioprotective.

E P IDEMIOLOGY 

50 % of the UK population have a cholesterol level high enough to be

a risk for CHD.

H ISTORY

Asymptomatic.

Symptoms of CVS complications.

Enquire about other CVS risk factors:

. Diabetes

. Family history

. Smoking

. Hypertension

EXAMINA T I ON

 Usually normal. Examine for secondary causes.

Signs of lipid deposits: Around the eyes (xanthelasmas), cornea (arcus), tendons xanthomas

(e.g. extensor tendons of the hands, Achilles tendon, patella tendon), tuberous

xanthomas on knees and elbows, xanthomas in palmar creases (in remnant hyperlipidaemia),

eruptive xanthomas and lipidaemia retinalis (pale retinal vessels) in severe

hypertriglyceridaemia.

Signs of complications: E.g. # peripheral pulses, carotid bruit, other cardiovascular risks –

associated high BP.

INVE S T I G A T IONS

Blood: Fasting lipid profile, exclude secondary causes: glucose, TFT, LFT, U&E.

Cardiovascular risk assessment: Assess using various algorithms, e.g. Framingham risk

equation, QRISK or ASSIGN.1

MANAGEMENT 

Treat secondary causes.

Advice: Exercise, lose weight, stop smoking, control BP, control diabetes, # alcohol, dietary

modification.

1 Framingham risk score is well validated for estimating 10-year cardiovascular risk (http://hp2010.nhlbihin.

net/atpiii/calculator.asp), but it is derived from a North American population. The QRisk and ASSIGN

calculators have been developed for an English or Scottish population and can be assessed online at: http://

www.qrisk.org.uk and http://assign-score.com.

Hyperlipidaemia (continued)

Lipid-lowering drugs: Indicated for:

1) Primary prevention: Patients with multiple risk factors and no atherosclerosis (primary

prevention) when risk for coronary heart disease > 20% in 10 years; and

2) Secondary prevention: Patients with established atherosclerosis, e.g. coronary heart

disease, carotid artery disease and aortic aneurysms (secondary prevention).

. Target: total cholesterol < 4 mmol/L, LDL2 mmol/L

For " total cholesterol or " LDL:

. HMG-CoA reductase inhibitors (‘statins’): Potently lowers mortality and CVS morbidity is

demonstrated in numerous trials. High dose is recommended as first line (e.g. 40 mg

simvastatin).

. Ezetimibe: Inhibits cholesterol absorption in the gut. Can be used if a statin is not tolerated,

or as an adjunctive agent.

For " tyriglycerides:

. Fibrates (e.g. bezafibrate): Stimulates lipoprotein lipase activity via specific transcription

factors.

. Fish oil: Rich in omega-3 marine trigylcerides, but this is not a recommended method of

treating hyperlipidaemia (it can aggravate hypercholesterolaemia.)

Other drugs:

. Anion-exchange resins (e.g. colestyramine, colestipol): Binds bile acids and # reabsorption,

" hepatic cholesterol conversion to bile acids and " LDL receptor expression on

hepatocytes.

. Nicotinic acid: # Hepatic VLDL release, # triglycerides, # cholesterol and " HDL. Use is

limited by side effects (prostaglandin-mediated vasodilation, flushing, dizziness, palpitations).

" Glucose and urate.

COMPL I C A T IONS 

Coronary artery disease, MI, peripheral vascular disease, strokes.

In hypertriglyceridaemia: Pancreatitis and retinal vein thrombosis.

Complication of treatment: Statins are associated with myositis.

P ROGNOS I S

 Depends on early diagnosis, treatment of hyperlipidaemia and control of

other CVS risk factors. There is some evidence that lipid-lowering agents prevent cerebrovascular

accidents.

0 تعليق

PH.Jafar Jassim 8/13/2020 08:00:00 ص

تابع القراءه

Aspirin overdose

D E F I N I T I ON

 Excessive ingestion of aspirin causing toxicity.

AET IOLOGY 

Overdose can occur as a result of deliberate self-harm, suicidal intent or by

accident (e.g. in children). Ingestion of 10–20 g can cause moderate-to-severe toxicity

in adults.

Aspirin (acetylsalicylate) increases respiratory rate and depth by stimulating the CNS respiratory

centre. This hyperventilation produces respiratory alkalosis in the early phase. The

body then compensates by increasing urinary bicarbonate and K

þ

excretion, causing

dehydration and hypokalaemia. Loss of bicarbonate together with the uncoupling of

mitochondrial oxidative phosphorylation by salicylic acid and build up of lactic acid can

lead to metabolic acidosis.

In severe overdoses, CNS depression and respiratory failure can occur.

E P IDEMI OLOGY 

One of the most common drug overdoses.

H ISTORY

Ascertain the key facts:

. How much aspirin?

. When?

. Any other drugs?

. Have you had any alcohol?

The patient may be asymptomatic initially.

Early symptoms: Flushed appearance, fever, sweating, hyperventilation, dizziness, tinnitus,

deafness.

Late symptoms: Lethargy, confusion, convulsions, drowsiness, respiratory depression, coma.

EXAMI N A T ION

 Fever, tachycardia, hyperventilation, epigastric tenderness.

I N V E S T IGATIONS

Blood: Salicylate levels (500–750 mg/L is a moderate overdose; >750 mg/L is a severe

overdose), FBC, U&E (particularly # K

þ

if vomiting), LFT (" AST/ALT), clotting screen

(" PT), glucose and other drug levels (e.g. paracetamol). ABG: May show mixed

metabolic acidosis and respiratory alkalosis.

ECG: May show signs of hypokalaemia – small T waves, U waves.

MANAGEMENT

Acute: Resuscitate with attention to respiratory rate and blood gases. Treat hypovolaemia

(rehydrate), hypokalaemia, hypoglycaemia; vitamin K for hypoprothrombinaemia

(occasionally).

If < 12 h after ingestion: Gastric lavage to empty the stomach, and oral activated charcoal

to bind to and # absorption of the drug.

Moderate cases (500–750 mg/L): Urine alkalinization with IV NaHCO3 (with IV potassium

chloride for hypokalaemia) aims to " salicylate excretion (aim for urine pH 7.5–8.5).

Severe cases (> 750 mg/L) or in severe acidosis: Consider haemodialysis.

In all cases, monitor U&E, glucose (may " or #), temperature, pulse, respiratory rate, BP, urine

output.

COMPL I C A T IONS 

Cerebral and pulmonary oedema (" capillary permeability).

Metabolic disturbances (# K

þ, # or " Na

þ, # or " glucose).

Acute renal failure.

P ROGNOS I S 

If treated early, prognosis is good.

Note: In children < 4 years, even low doses of aspirin are associated with an increased risk of

developing Reye’s syndrome (metabolic acidosis, liver and CNS disturbances). Aspirin can

also trigger an asthma attack in certain individuals.

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PH.Jafar Jassim 8/13/2020 07:55:00 ص

تابع القراءه

Arteriovenous fistulae and malformations

D E FI N I T ION

Arteriovenous fistula: An abnormal communication between an artery and vein that

bypasses the capillary bed.

Arteriovenous malformations: Malformation with normal endothelium.

Haemangioma/Angioma: Malformation with endothelial hyperplasia.

AE T IOLOGY

Congenital: Divided into haemangiomas, (e.g strawberry naevi) and malformations (AVMs).

The latter is divided into low flow or high flow (e.g. hepatic or pulmonary AVM).

Hereditary: AVMs and haemangiomas are associated with many different hereditary

syndromes, e.g. Klippel–Trenaunay, Kasabach–Merritt, Sturge–Weber, von-Hippel–

Lindau and Hereditary Haemorrhagic Telangiectasia (Osler–Weber–Rendu syndrome).

Acquired: Trauma, tumours (e.g. glomus tumour, hypernephroma and sarcomas), infection,

inflammation (e.g. aorto-venocaval fistula) or iatrogenic (e.g. Brescia–Cimino fistula for

haemodialysis or portocaval shunt in portal hypertension).

E P IDEMIOLOGY 

Cutaneous haemangiomas are very common, the others less so.

H ISTORY

 Presentation is variable, depending on the site and size of the AVM and

symptoms may be due to local or systemic effects (see Complications).

Congenital cutaneous haemangiomas are often visible from or soon after birth.

Malformations usually grow with age, puberty or pregnancy.

Those within internal organs may only be detected once complications develop.

Other presentations include varicose veins, limb swelling or pain.

EXAMINA T I ON

 Cutaneous haemangiomas (Campbell de Morgan spots) are usually

scarlet in colour, firm and cannot be emptied of blood on compression.

Internal AVMs may be revealed by an overlying bruit or palpable thrill, possibly with reduced

distal pulses and " pulse pressure.

Signs of complications (see Complications).

INVE S T I G A T IONS

Imaging of AVMs: Depends on the site of the lesion. Modalities used include duplex

scanning, CT or MRI scanning or invasive angiography.

SPECT scan: Quantification of AV shunting uses radiolabelled microspheres that are

introduced into an artery and are too large to pass through capillaries. Those passing

through AVMs are trapped in the lungs and quantified using a gamma camera.

MANAGEMENT

Conservative: Cutaneous haemangiomas usually undergo spontaneous regression at the

end of the first year of life. Internal organ AVMs may not necessitate treatment and can be

monitored.

Interventional radiology: In the case of internal AVMs or fistulae, embolization with metal

coils, tissue adhesive or particles can be performed.

Surgery: Often difficult, but excision (after pre-op embolization) may be possible in the case

of small and accessible AVMs.

Stereotactic radiosurgery: Useful on small AVMs, may take years for full effect.

COM P L IC A T I ONS

Cutaneous: Cosmetic disfigurement, ulceration, bleeding.

Organ-specific: E.g. brain AVMs can cause focal neurological deficits, seizures or stroke;

pulmonary AVMs can cause haemoptysis or parodoxical embolism.

Distal: Ischaemia of peripheral tissues.

Systemic: High-ouput cardiac failure in the case of large AVMs.

PROGNOSIS

 Depends on site and aetiology. 90 % of haemangiomas regress by

5–10 years. 1–4 % annual risk of haemorrhage in cerebral AVMs.

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PH.Jafar Jassim 8/13/2020 07:49:00 ص

تابع القراءه

Anaphylaxis

D E FI N I T ION 

Acute life-threatening multisystem syndrome caused by sudden release of

mast cell- and basophil-derived mediators into the circulation.

AE T IOLOGY

 Can be classified as:

Immunologic: IgE-mediated or immune complex/complement-mediated. Non-immunologic:

mast cell or basophil degranulation without the involvement of antibodies (e.g. reactions

caused by vancomycin, codeine, ACE inhibitors).

Inflammatory mediators such as histamine, tryptase, chymase, histamine-releasing factor,

PAF, prostaglandins and leucotrienes cause bronchospasm, " capillary permeability and

# vascular tone, resulting in tissue oedema.

Common allergens include drugs (e.g. penicillin), radiological contrast agents, latex, insect

stings, egg, peanuts, shellfish and fish. Anaphylaxis may occur following repeated

administration of blood products in patients with selective IgA deficiency (as a result

of formation of anti-IgA antibodies). Anaphylaxis can also be induced by exercise.

E P IDEMIOLOGY 

Relatively common. Anaphylaxis occurs in 1 in 5,000 exposures to

parenteral penicillin or cephalosporins.

1–2 % of patients receiving IV radiocontrast experience a hypersensitivity reaction (often

minor). 0.5–1 % of children suffer from peanut allergy. 1 in 700 patients have selective

IgA deficiency.

H ISTORY 

Acute onset of symptoms on exposure to allergen:

. Wheeze, shortness of breath or sensation of choking.

. Swelling of lips and face.

. Pruritus, rash.

The severity of previous reactions does not predict the severity of future reactions. Patients

may have a history of other allergic hypersensitivity disorders e.g. asthma, allergic rhinitis.

Biphasic reactions occur 1–72 h after the first reaction in up to 20% of patients.

EXAMINA T I ON

 Tachypnoea, wheeze, cyanosis.

Swollen upper airways and eyes, rhinitis, conjunctival injection.

Urticarial rash (erythematous wheals).

Hypotension, tachycardia.

INVE S T I G A T IONS 

The diagnosis of anaphylaxis is made clinically.

Serum tryptase (measured within 15 min–3 h after onset of symptoms), or histamine levels

(measured preferably within 30 min after symptom onset) and urinary metabolites of

histamine (which may remain elevated for several hours after symptom onset) can support

the clinical diagnosis. Normal levels of these mediators do not exclude the possibility of

anaphylaxis.

After the attack:

Allergen skin testing: Identifies allergen. It should be performed by an allergy specialist,

because of the risk of anaphylaxis and the skill required for proper interpretation.

IgE immunoassays: E.g. radioallergosorbent tests (RASTs) to identify food-specific IgE in the

serum.

MANAGEMENT

 Stop any suspected drugs.

Resuscitation according to principles of airway, breathing and circulation.

Secure airway and give 100 % O2. Intubation and transfer to ITU may be necessary so

anaesthetist must be informed early.

Adrenaline IM (0.5 mL of 1:1,000). This can be repeated every 10 min according to response

of pulse and BP.

Antihistamine IV (10mg chlorpheniramine).

Steroids IV (100mg hydrocortisone).

Anaphylaxis (continued)

IV crystalloid or colloid to maintain blood pressure. If hypotensive, lie patient flat with head

tilted down.

Treat bronchospasm with salbutamolipratropium inhaler. Aminophylline IV infusion may

be required.

Advice: Educate on use of adrenaline pen for IM administration. Provide Medicalert bracelet.

Make note in patient’s notes and drug charts. Referral to an allergy specialist for

identification of the culprit allergen and education in allergen avoidance.

COMPL I C A T IONS

 Respiratory failure, shock, death.

P ROGNOS I S

 Good if prompt treatment given.

0 تعليق

PH.Jafar Jassim 8/13/2020 07:40:00 ص

تابع القراءه

Alcohol dependence

D E FI N I T ION

Alcohol dependence is characterized by three or more of:

. Withdrawal on cessation of alcohol.

. Tolerance.

. Compulsion to drink, difficulty controlling termination or the levels of use.

. Persistent desire to cut down or control use.

. Time is spent obtaining, using, or recovering from alcohol.

. Neglect of other interests (social, occupational, or recreational).

. Continued use despite physical and psychological problems.

Recommended limits for , and < are 14 and 21 units/week, respectively. (1 unit¼8 g alcohol –

1 glass wine or 0.5 pint of beer.)

AE T IOLOGY

 Genetic factors suggested by twin studies and family history ( 1 in 3 have

a parent with alcohol-related problem).

Environmental factors include cultural, parental and peer group influences, availability of

alcohol, occupation (e.g. " risk in publicans, doctors, lawyers).

Patients with depressive and anxiety states are at risk.

Alcohol withdrawal: Alcohol enhances inhibitory GABA activity and inhibits excitatory

glutamate neurotransmission. Chronic alcohol exposure results in a compensatory

reduction in GABA receptor function and upregulation of the glutamate NMDA receptors.

Abrupt alcohol cessation leads to overactivation of the excitatory NMDA system

relative to the GABA system.

E P IDEMIOLOGY 

The prevalence of alcohol dependence in primary care populations in the

United States was reported as 2–9% in 2004.

H ISTORY

Alcohol history: A drinking diary is useful to record how much, what, when and with whom

alcohol is taken.

CAGE screening questions:

Cut-down: ‘... felt that you should cut-down on intake?

Annoyed: ‘... felt annoyed by criticism of your drinking?

Guilt: ‘... felt guilty about how much you drink?

Eye-opener:‘... feel that you need a drink when you wake up?

Evaluate for associated comorbidities including smoking, other substance abuse, depression,

anxiety and panic attacks.

Acute intoxication: Amnesia, ataxia, dysarthria, disorientation, palpitations, flushing and

coma.

Symptoms of withdrawal: Nausea, sweating and tremor, restlessness, agitation, visual

hallucination, confusion, seizures.

EXAMINA T I ON

Signs suggestive of chronic alcohol misuse: Dupuytren’s contracture, palmar erythema,

bruising, spider naevi, telangiectasia, facial mooning, bilateral parotid enlargement,

gynaecomastia, smell of alcohol.

Signs ofcomplications: (See Complications below and also Alcoholic hepatitis and Liver failure.)

INVE S T I G A T IONS

Blood: Commonly used markers are MCV ("), GGT ("), transaminases ("). Other less specific

markers include " uric acid, " triglycerides or markers of end organ damage (e.g. bilirubin,

albumin, PT in liver).

Acute overdose: Blood alcohol, glucose, ABG (risk of ketoacidosis or lactic acidosis), U&E,

toxic screen (e.g. barbiturates, paracetamol).

Alcohol dependence (continued)

MANAGEMENT

Acute intoxication: Monitor and support of airway, breathing, circulation. Intubation and

ventilation if severe respiratory depression, IV fluids and careful monitoring of urine

output, blood glucose (as may #), U&E and blood gases.

Withdrawal: IV vitamin B complex (Pabrinex) and reducing doses of chlordiazepoxide. Close

attention to dehydration, electrolyte imbalances and infections. Nutritional support

important as often malnourished. Lactulose and phosphate enemas may help any

encephalopathy.

Advice and intervention: Motivational interviewing techniques, counselling and community-

based services, self-help groups (e.g. AA), alcohol treatment units for those with

established problems, detoxification period is necessary for those physically dependent.

Medical: Acamprosate reduces craving. Naltrexone (opioid receptor antagonist) may be

given to patients who need additional support to maintain abstinence (contraindicated in

patients with underlying liver disease, and liver function tests should be monitored).

Disulfiram (an aldehyde dehydrogenase inhibitor) causes patient to develop vasomotor

symptoms, nausea, abdominal pain when drinking alcohol.

COMPL I C A T IONS

GI: Oesophagitis, Mallory–Weiss tears, varices, gastritis, peptic ulcers, acute or chronic

pancreatitis.

Liver: Fatty change, alcoholic hepatitis, cirrhosis.

Neurological: Acute intoxication.

Withdrawal: Fits, delirium tremens (48–72 h after cessation – coarse tremor, agitation,

fever, tachycardia, confusion, delusions and hallucinations). Chronic complications

include cerebral atrophy and dementia, cerebellar degeneration, optic atrophy, peripheral

neuropathy, myopathy. Indirect effects include hepatic encephalopathy, thiamine

deficiency, causing Wernicke’s encephalopathy1 or Korsakoff’s psychosis.2

Haematological: Anaemia (vitamin B12 or folate deficiency, iron deficiency in patients with

GI bleeding), thrombocytopaenia (due to enlarged spleen in patient with cirrhosis or direct

toxic effect on megakaryocytes), abnormal platelet function.

Respiratory: Depression, inhalation of vomitus.

Cardiac: Hypertension, cardiomyopathy, arrhythmias.

Drug interactions: E.g. oral contraceptive pills (alcohol is a liver enzyme-inhibitor acutely,

but chronic abuse induces liver enzymes.)

Teratogenicity: Foetal alcohol syndrome.

Psychosocial: Depression, anxiety, deliberate self-harm. Domestic, employment and financial

problems.

P ROGNOS I S

 Depends on complications. Alcoholic fatty liver is reversible on abstinence

from alcohol. In general, 5-year survival rates in those with alcoholic cirrhosis who stop

drinking are 60–75%, but < 40% in those who continue.

2 Korsakoff’s psychosis is characterized by profound impairment of retrograde and anterograde memory

with confabulation, as a result of damage to the mammillary bodies and the hippocampus. Irreversible.

1 Wernicke’s encephalopathy is nystagmus, ophthalmoplaegia and ataxia, together with apathy,

disorientation and disturbed memory. Treat urgently with thiamine or may progress to Korsakoff’s

psychosis.

0 تعليق

PH.Jafar Jassim 8/12/2020 12:27:00 ص

تابع القراءه

Retinal vein and artery occlusion

D E FI N I T ION

Retinal artery occlusion (RAO): Occlusion of central or a branch retinal artery.

Retinal vein occlusion (RVO): Occlusion of central or a branch retinal vein.

AE T IOLOGY

RVO:

The most common causes are diabetes mellitus, hypertension and glaucoma.

Changes in blood constituents: " Cell adhesiveness (e.g. diabetes mellitus), hyperviscosity

syndromes (e.g. multiple myeloma, hyperlipidaemia).

Changes in vessel wall: " Intra-ocular pressure (glaucoma), hypertension causing

arteriosclerosis (veins have a common sheath with arteries in the eye and may be

compressed by them), primary inflammation (e.g. vasculitis: primary vasculitides,

Beh¸cet’s syndrome, sarcoidosis).

RAO:

Emboli from carotids arteries (fibrin–platelet or cholesterol emboli) or heart valves (calcific

emboli), thrombosis, arteritis.

E P IDEMIOLOGY Common cause of sudden painless loss of vision (RVO > RAO).

H ISTORY

Sudden painless loss of vision.

RAO may be described as a ‘descending curtain’. It may be temporary (amaurosis fugax) when

the embolus is dislodged.

EXAMINA T I ON # Visual acuity (when macula is affected), visual field loss and relative

afferent pupillary defect (RAPD) may be present in both RAO and RVO. In RAO, visual field

loss is usually a unilateral quadrantanopia.

Fundoscopy:

RVO: Flame haemorrhages, cotton wool spots, swollen optic disc (in central RVO).

RAO: Pale oedematous retina with cherry red spot on the macula, narrow truncated arteries,

emboli may be seen (white – calcium; yellow – cholesterol).

Tonometry: To measure intraocular pressure (" intraocular pressure may be the cause or

complication of central RVO).

Signs of the underlying cause: Hypertension, diabetes mellitus, temporal tenderness

(temporal arteritis).

INVE S T I G A T IONS

Exclude other causes of sudden loss of vision (vitreous haemorrhage, retinal detachment,

giant cell arteritis, ischaemic optic neuropathy).

Tests to identify the cause/risk factors:

RVO: Blood glucose, ESR, exclude hyperviscosity syndromes and vasculitides, lipid profile and

intraocular pressure.

RAO: ESR, carotid doppler ultrasonography, ECG, echocardiogram, lipids.

Fluorescein angiography: Sequential photographs of the fundus are taken following IV

injection of fluorescein to identify areas of leakage and poor perfusion to assess risk of

rubeosis.

MANAGEMENT

RVO: Treat the underlying condition. Laser may be used to # macular oedema, treat ischaemic

areas and prevent neovascularization.

RAO: CO2 rebreathing (may cause arterial dilatation), IV acetazolamide, anterior chamber

paracentesis.

COM P L IC A T I ONS

Loss of vision.

Retinal vein and artery occlusion (continued)

RVO: Macular oedema, neovascularization of the retina and iris (rubeosis) and glaucoma.

RAO: Neovascularization and glaucoma can occur, although uncommon.

P ROGNOS I S

RVO: Cotton wool spots and RAPD (indicators of ischaemic retinal damage) are markers of

poor prognosis.

RAO: Very poor prognosis even with immediate treatment.

0 تعليق

PH.Jafar Jassim 8/05/2020 12:36:00 ص

تابع القراءه

يجب أن يتمتع بالثقافة الطبية حتى وإن لم يكن يكن طبيباً  ، والتي تعتبر الثقافة والمعرفة تعتبر عصباً لحياة الإنسان ، وصحة المجتمع الذي يعيش فيه ، وفي هذا المقال سوف تتذكر مجموعة معلومات عامة تختص في مجال الطب.

 من أهمّ الغدد في جسم الإنسان: الغدة الجنبدرقية ، والنخامية ، والدرقية ، والجنسية ، والمعدة ، والكظرية ، والعرقية ، والبنكرياس ، 

واللعابية. 

ينقل القمل للإنسان مرض اسمه التيفوس. 

الغدد الليمفاوية تعمل على تصفية الدم وتطهيره. يطلق عملية غسيل الكلى. 

يعدّ الكبد العضو الوحيد في جسم الإنسان الذي يعود للنمو بعد اقتطاع جزء منه. 

في العام 1989 م تمتت عملية زراعة الكبد في شيكاغو الأمريكية. 

مرض انفصام الشخصية اسمه مرض الشيزوفرينيا. فصيلة الدم

 o + تسمّى باسم فصيلة الدم الكريمة. 

تعرف الذبحة الصدرية بأنّها عبارة عن ألم حاد وقصير الوقت يحدث في الصدر وذلك بسبب إصابة الشريان التاجي. 

فيتامين الوحيد الذي يكسبه الجسم من أشعة الشمس هو فيتامين د. 

يبلغ وزن مخضر الإنسان البالغ من 3 إلى 2 كغم. 

الغدة التي تصبّ جميع محتوياتها بشكل مباشر في الدم هي الغدد الصماء. 

يؤدي نقص فيتامين أ للإصابة بمرض العشى الليليّ. 

من أعراض مرض البلاجرا: الغثيان ، والاكتئاب ، والصداع ، والإسهال ، والتهاب الجلد. 

يعتبر الطبيب العربي مجدي يعقوب من أشهر جراحي القلب على مستوى العالم ، وفردريك بانتينج مكتشف الإنسولين ، والطبيب العربي ابن زهر مكتشف جرثومة الجرب ، وسالك مكتشف مصل شلل الأطفال. يقصد بمرض السرطان الانقسام غير العادي لخلايا الجسم دون توقّف. 

وظيفة كريات الدم البيضاء هي الدفاع عن الجسم ضد الأمراض والجراثيم. 

تقع الغدة الدرقية في الرقبة. 

مادة الميلانين هي المسؤولة عن تلوين جسم الإنسان. 

تعدّ العضلات أثقل من العظام. 

يبلغ عدد فقرات العمود الفقري ثلاثاً وثلاثين فقرة. 

يعتبر مخ ّالمرأة أقل وزناً من مخّ الرجل. يبلغ عدد عظام الجمجمة اثنتين وعشرين عظمة. 

يبلغ حجم الهواء الذي يستنشقه الإنسان في كل عام خمسة ملايين لتر.

يبلغ عدد ضربات قلب الحوت ضربة واحدة في الدقيقة الواحدة. 

يبلغ عدد خلايا الجسم في الإنسان ستين ترليون خلية. 

يبلغ عدد الخلايا العصبية الذي يملكها الإنسان ثمانية وعشرين بليون خلية. 

المسؤول عن التذوق هي الحليمات الذوقية في اللسان. 

تعتبر عضلة الفخذ أكبر عضلة في الجسم ، وعضلة الركاب في الأذن الوسطى أصغر عضلة ، وعضلة الفكين أقوى عضلة. 

ضم المعدة تتكون من المخاط ، ولو لم تكن كذلك له ضمت نفسها .

1 تعليق

PH.Jafar Jassim 7/29/2020 12:19:00 ص

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