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A: Microaneurysms are the out pouching of capillary walls due to pericyte loss cheap cardizem online american express blood pressure 300180, appears as small red dots safe cardizem 60mg heart attack 18 year old male. Microaneurysm is always along the vessel wall purchase cardizem discount blood pressure medication exercise, it may be confused with haemorrhage buy cardizem amex arrhythmia 18 years old. A: These are lipid and protein residues of serous leakage from the vessels, yellowish in colour and irregular in outline with sharply defned margin. A: As follows: • Control of diabetes mellitus, stop smoking and control of hypertension (if any). Diabetic maculopathy is one of the common causes of loss of vision in patient with non-proliferative retinopathy. Maculopathy Preproliferative Proliferative retinopathy Proliferative retinopathy retinopathy (Severe vitreous haemorrhage) Q:How to treat such a case? Plus • There are multiple photocoagulation scars (appears like exudate, with areas of small brown or yellowish spot of variable size and shape). My diagnosis is Proliferative diabetic retinopathy, treated with photocoagulation. A: Unknown, probably there is production of angiogenic factors from the area of ischaemic retina. These new vessels are very fragile and leaking, liable to rupture causing haemorrhage (intraret- inal, preretinal or vitreous). Serous protein leakage from these vessels stimulates connective tissue reaction called retinitis proliferans. Q:What are the indications of laser photocoagulation therapy in diabetic retinopathy? Presentation of a Case: • There are multiple areas of black pigmentation like bone spicules with variable size and shape, some in criss-cross pattern, at the periphery of fundus. A: It is a progressive degenerative disease of retina with pigmentary epithelium in a bone spicule pattern. A: As follows: • Isolated or congenital: Bardet–Biedl syndrome (previously called Laurence–Moon–Biedl syndrome). A: As follows: raise the upper eye lid, see the following— • Divergent squint (eyeball is fxed in downward and outward position). Nuclear lesion (causes are: infarction, haemorrhage, neoplasm and multiple sclerosis). Unruptured aneurysm of posterior communicating artery (there is painful ophthalmoplegia). Bilateral ptosis Bilateral ptosis Bilateral ptosis (senile) Bilateral ptosis (congenital) (myasthenia gravis) (ocular myopathy) Q:How to differentiate between ptosis of myopathy and ptosis due to other cause? A: It is a hereditary disorder, inherited as autosomal dominant or sporadic, common in young, charac- terized by bilateral ptosis with complete ophthalmoplegia. A: As follows: • Neck: Lymph nodes, scar, thyromegaly, aneurysm (carotid and aortic). Horner’s syndrome (left) Horner’s syndrome (bilateral) Q:What is Horner’s syndrome? A: It is a syndrome due to lesion in the sympathetic pathway characterized by: • Partial ptosis. A: Upper eye lead is controlled by Levator palpebrae superioris which is supplied by 3rd nerve. A: It originates from the sympathetic nucleus in hypothalamus and passes through the brain stem to the lateral horn of C8 and T1 segment of spinal cord. From there, pre-ganglionic fbres emerge and pass to sympathetic ganglia (usually superior cervical ganglia).
Treatment of nephrotic syndrome consists of treatment of the underlying dis- ease order cardizem 60 mg with mastercard heart attack 2014, if present buy cardizem 120 mg cheap blood pressure 130/80, as well as management of t he edema and at t empt s t o limit t he pro- gr ession of the r en al d isease discount cardizem 180mg mastercard hypertension va disability. For ed ema purchase cardizem with american express prehypertension and viagra, all pat ient s r equ ir e st r ict salt restriction, but most patients will also need diuretics. Becau se bot h t h iazide an d loop diuret ics are highly protein bound, t here is reduced delivery to the kidney, and often very large doses are required t o manage the edema. Dietary protein restriction usually is recommended for patients with moderate proteinuria and chronic kidney disease, and is thought to protect against t he progression of glomerular scarring. Besides the edema, patients with nephrotic syndrome have other consequences of renal protein wasting. Pat ient s wit h evidence of t hrombus format ion require ant icoagu lat ion, oft en for life. It is possible to measure this in a random urine sample rather than a timed collection, because a ratio of albumin (in milligrams) to creatinine (in grams) of 30 to 300 usually cor- relates with the total excretion described. When albuminuria exceeds 300 mg/ d, it is det ect able on ordinary urine dipst icks (macroalbuminuria), and the pat ient is said to have overt nephropathy. Aft er t he development of microalbuminuria, most pat ient s will remain asymp- tomatic, but the glomerulopathy will continue to progress over the subsequent 5 to 10 years until overt nephropathy develops. At this point, many patients have some edema, and nearly all pat ient s have developed hypert ension. T h e presence of hyper- tension will markedly accelerate the decline of renal function. The development of nephropathy and proteinuria is very significant because they are associated with a much higher risk for cardiovascular disease, which is the leading cause of death in patients with diabetes. Thus, the development of microalbuminuria in diabetic patients is ext remely import ant because of t he progressive disease it heralds. Tight glycemic control wit h a goal hemoglobin A less t han 7 %h as b een sh own t o 1c slow or prevent t he progression of renal disease in pat ient s wit h microalbuminuria Once macroalbuminuria has developed, however, it is not clear whether improved glycem ic con t r ol affect s the cou r se of r en al d isease. In ad d it ion, as r en al fu n ct ion declines, insulin requirements typically fall, and some oral medications such as sul- fonylureas an d met formin can be dangerou s in advan ced ren al in sufficien cy. Strict blood pressure control wit h a goal less t han 140/ 90 mm H g in all pat ient s wit h diabetes is essent ial to slow progression. Many guidelines recommend lower goal blood pr essu r es of less t h an 130/ 80 m m H g in pat ien t s wit h d iab et ic n eph r op - athy and proteinuria > 500 mg/ d. If additional blood pressure control is needed, nondihydropyridine calcium channel blockers, bet a-blockers, or diuretics may be added. In addition, because cardiovascular disease is the major killer of patients with diabetes, aggressive risk factor reduction should be attempted, including smok- ing cessat ion and reduct ion of hypercholesterolemia. She has no other medical problems and says t hat at her last opht halmologic appoint ment she was told that t he dia- betes had started to affect her eyes. Physical examination is normal except for hard exudates and dot hemor- rhages on funduscopic examination, and diminished sensation up to the mid-shin bilaterally. H ave the patient return in 6 weeks and check a repeat urine analysis at that time. Change the glyburide to glipizide and have the patient return for follow- up in 6 weeks.
Salt restriction buy cardizem toronto prehypertension not overweight, loop diuretics purchase cardizem 180 mg on line blood pressure medication and juice, and bed rest are effective at reducing these symptoms purchase cardizem now prehypertension systolic normal diastolic. It is essential that the clinician know what the therapeutic objective is purchase cardizem 120 mg on line 4, so that one can monitor and guide therapy. Some responses are clinical, such as the patient’s abdominal pain, or temperature, or pulmonary examination. Obviously, the student must work on being more skilled in eliciting the data in an unbiased and standardized manner. The student must be prepared to know what to do if the measured marker does not respond according to what is expected. Is the next step to retreat, or to repeat the metastatic workup, or to follow up with another more specific test? Ap p ro a ch t o Re a d in g The clinical problem– oriented approach to reading is different from the classic “s y s t e m a t i c ” r e s e a r c h o f a d i s e a s e. P a t i e n t s r a r e l y p r e s e n t w i t h a c l e a r d i a g n o s i s ; hence, the student must become skilled in applying the textbook information to the clinical setting. In ot her words, t he student should read with t he goal of answering specific quest ions. One way of att acking this problem is t o develop st andard “approaches” t o common -clinical problems. With no other information to go on, the student would note that this woman has a clinical diagnosis of pancreatitis. Using the “most common cause” informa- tion, the student would make an educated guess that the patient has gallstones, because being female and pregnant are risk factors. If, instead, cholelithiasis is removed from the equation of this scenario, a phrase may be added such as: “T h e ult rasonogram of the gallbladder sh ows no st ones. Now, the student would use the phrase “patients without gallstones who have pancreatitis most likely abuse alcohol. This question is difficult because the next step may be more diagnostic informa- tion, or staging, or therapy. It may be more challenging than “the most likely diag- nosis,” because there may be insufficient information to make a diagnosis and the next step may be to pursue more diagnostic information. Another possibility is that there is enough information for a probable diagnosis, and the next step is to st age t he disease. H ence, from clin ical dat a, a ju dgment n eed s t o be r en d er ed r egar din g h ow far alon g on e is on the road of: Make a diagnosis ã Stage the disease ã Treatment based on stage ã Fo ll o w res po ns e Frequent ly, the st udent is “t aught ” t o regurgit at e the same informat ion that someone has written about a part icular disease, but is not skilled at giving t he next st ep. T his t alent is learned opt imally at t he bedside, in a support ive environment, wit h freedom to make educated guesses, and with const ruct ive feedback. Make the diagnosis:“ B a s e d o n the i n f o r m a t i o n I h a v e, I b e l i e v e t h a t M r. S m i t h h a s stable angina because he has retrosternal chest pain when he walks three blocks, but it is relieved within minutes by rest and with sublingual nitroglycerin. Stage the disease:“ I d o n ’t b e l i e ve t h a t t h i s i s s e ve r e d i s e a s e b e c a u s e h e d o e s n o t have pain lasting for more than 5 minutes, angina at rest, or congestive heart failure. Treatment based on stage:“ T h e r e f o r e, m y n e x t s t e p i s t o t r e a t w i t h a s p i r i n, b e t a - blockers, and sublingual nitroglycerin as needed, as well as lifestyle changes. Fo l lo w res po ns e : “I wan t t o follow the t r eat m en t by assessin g h is p ain ( I will ask him about the degree of exercise he is able to perform without chest pain), performing a cardiac stress test, and reassessing him after the test is done. The next step depends upon the clinical state of the patient (if unst able, the next st ep is t h erapeut ic), the potential severity of the disease (the next step may be staging), or the uncertainty of the diagnosis (t h e next step is diagnost ic). This question goes further than making the diagnosis, but also requires the student to understand the underlying mechanism for the process. The student is advised to learn the mechanisms for each disease process, and not merely memorize a constellation of symptoms.
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