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28 Cards in this Set
- Front
- Back
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What are the three forces that cause ulcerations in the foot?
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Friction, pressure, shear forcer
Fricitn is the restance taht nay body meets in moving over another body, the more irregular the surfaces in contact, the greater the increase in friction. So the more irregular the shape of hte foot, the greater the risk of friction nduced tissue breakdown. Pressure is hte force of ne body onto another by its weight,. for a givent wt, the pressure isnversely proporitonal to the area the foot rests on , so increse the area and decresase the pressure Shear force is the combination of frictional and compressive forces. This is believed to be th eforce most responsible for tissue breakdown in the insentsitvie foot. |
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What are the clssfications used inevaluating ulceration of the foot?
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Wagner's was one of the orignal classifications and still the most widely used.
Grade 0 - skin is intact, bu thtere may be some osseous deomity GRAde 1 - localized superficla ulcer. Grade 2 - deep ulcer with extension to tendon, bone, ligament, or jint. Grade 3 - deep abscess with osteomyelits. grade 4 - gangrene of hte toes or the forefoot grade 5- gangrene of the whole foot. Universityu of Texas classfication system - how deep is the ulcer? is it ischemi? and is the wound infecte? |
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What are the risk factors fo rdiabetic foot ulceration?
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peripheral neuropathy whic is probalby the ost signifacant single risk factory.
Deformity and decreased jont motility usually increases the shear force t ohich the foot is sbujectred. Poor glucose control increae the patient risk to neruopathy, decreased wound healing, pVD, and decreaed immun funtcin history of previous ulceration & amputaitjon will caue plantar pressure distribution to be change , therfore increaseing hte risk of amputiationm risk factors are cumulative |
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What are the various treatments for foot ulceration?
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decrease the pressue: this can be done by a vareity of methods.
felted foram dressing: a peic fo felteed foami s cut out ot accomodate the ulcer and is applied ot the foot via rubgber cemnt and is change donce a week. Total contact case: this is a cast made to decrae theamount of force ht efoot is sbuject to, by incraseing the total surfase area. Accomadative orthotics : thews sare very imortant once the ulcer ishealed ot reduce the risk of recurrence surgery: excisonof a bony promince, possible palstic surgery i.e. skin flap grwoht factors & skin substitues: these have nto yet been prove as effect glucose control dressings: 1/4 strength betadines < BID, or NS wet to dry BID, hydrogel, and Aquagel |
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What are the qualities of thediabetic foot that makes it different fromthe norm?
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Decreased vibratory pinprick and light tough
Muscle atrophy and weakness (intrinic muscle ww cock up hallux, platar porminet mt eeads decreased tendon reflex |
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What are the findings in the neuropathic foot
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well nourished tissue
good dorsalis pedis and psoterior tibial pulses decreased or absent senssation, bibration sense and achilles tendon refelx tendency for hammer toes and high foot arch calluses at pressure points charcot deformities foot drop supermposed infectiosn: ulcers, osteomyelits paresthesia, hyperehtesisa, hyhposesthesia, and radicular pian anhydrosis |
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What acause the paitent to develop a neuropathic foot
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vascualr basis vs hpyerglycemia
symmetric neuropathy is more form hyperglycemic, focal lesion s more likely vasuclar hyperglyemia caues incrase activyt of hte polyol pathway in nerves hyperglycmia>icnreased nerve glucos>increases polyol pathway activity>decrases myoinsositol cocnentration>restricoon phosphatidylinosistiol turnover>decrease Na-K-Atpase activety>decrease NCV |
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What are the radiographic featurs of the neuropathic foot
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demineralization
osteolysis charot's joint |
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nmae some other cause sof peropherial neuropathy
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alcoholisim, herniated nucleus pulposu, heavy metals, vitamin defiecnies, collagen diseases, pernicous anemai, malgnanacy, pressure neuropathyu, uremia, porhyria, Hansen's disease, and drugs
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What are variosu tretments for neruopathy
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Hyperglycemia contraol
Sorbinil |
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What is the treatment for painful neuropathy?
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1st - is strict glycemic control
2nd - acetamophen or ibuprofen (avoid narcotis due risk of abuse since neuropahty is chronci) antconvulants may help lancinating and paroxymal pain tricyclic antidepressants topicla capsaicin cream for mild pian neurontin |
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What are hte methods of diagnosis if diabetic peripheral neuropathy?
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Semmes - weinstein monfilaments: 5.07 is where you risk pressure ulcers
vibratory sensation using a 256htz tuning fork at MPJ, midfoot, ankle , and tibial tubercle. pressure-specified sensory device: the loees threshold at which patients developed uslcers of xxx 5.07 xxx |
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What are the risk factors for CAD i nthe diabetic
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Asymptomatic hyperglycemia: this is an independient risk factor for CAD, it has never been proven that tight blood glucose level control decreasses the risk of CAD
lipid abnormalities: diabetics usually vha increased VLDL compared to the normal population and decrese LDL, and diabetic usually develop CAD at lower levels of LDL/VLDL hyperinsulinemia: c causes atherogenesis, low HDL levles, and hypertension |
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What is the treatment for lactic acidosis
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it si focused on the correction of the pH; the patient should be given intravenous bicarbonate to maintain the plsma bicarbonate at 8 to 10 mmol/L and hte pH above 7.1
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What is the treatment for diabetic keoacidosis
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Insulin: given 25 to 50 units bolus IV then give 8 to 10 unis / hr until the ketoacidosis is revered
Fluids: 1-2 fL of isotonoic saline or LR rapdly IV then should be determined by urinoutoput. If plama glucose below 17 mmol/L then add 5% glucose solution to decrease risk of cerebral edema potassium: as needed 3-4 hours after start of treatment. bocarbonated:only need if ph<7.0 |
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What are the complication seen in diabetic ketoacidosis
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erosive gastritis, cerbral edema, hyperkalemia, hypoglycemai, hypokalemia, MI, mucormycosis, RDS, vascular thrombosis
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What are the signs nad symptoms seen in diabetic ketoacdiosis
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anorexa, N/V, incrfeased urin formation, abdominal pain, coma or mental stares changes, kussmalu respiration, leudkcytosiis, labs: >K+,
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Diabetic nephroapthy is clincially defineas?
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by the presenc of persitent prteinuria (.5 g/24 hr) ina patient with diabetes and concomitant retinopathy and elevated blood pressure.
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What is the tretment of deabetic nephropaty?
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Blood pressure ocntrol: delays the pregression fo diabetic nephroapthy and retard the onset of over renal disease
dietary treatment: diet restricted ot .5 to .6 g of preoien/kg of body weigt per day glycmeic control: it is mportan to hav etight glycemic contriol i nthe early stages of hte syndrome, and it is less effecteve at eh late stages aldose reductase angiotensin II medications |
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YOu have a 45 year old NIDDM F with ESRD and a foot infections that has gorwon out MRSA and you want ot put the patient onf Vancomycin. You order a chem 7 and a CBS: NA 140, K 4.5, Cl 101, and CO2 29, BUN 38, CR 3.5, WBC 12.7, Hgb 10.9, Hct 29.9, Plt 150. Pt wt is 59 kg. what does of vancomycin woudl you gvie this paitent
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First yhou find the patient's creatine clearnce so you need to use the formula Clcr(ml/min) = 140 age X wt(kg)/72 X serum CR mg/dl X8.5 (for women)
this pt Clcr is 22 ml/mg whic is decrased so the paitent woudl be starated on 500mg q24-48 hrs; and then doesed according to thetroguh level |
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your patient is in the hospital for minor cellulits and a draing 1st met ulcer, and you're haveing troulbe controlling hsi glucose leve. what re the possible cause of insulin resistnace other than the infection
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inflammation, MI or ischemia, trauma, Sx, emotion strees,s, pregnacy, glucocorticoid,l estrogens (brith control included0, sympatomimetic, nicotinic acid, antibodies to insulin, antibodies to insulin receptoers
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What are the autonomic amifestation seen in diabetes?
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cardiovascular : incrased heart rate, orhtostateic hyptension, decreased cardia outbput; 20-40? of diabetcas are affected
urogential: hestancy poor streeam , feelin foiandequate blader emptying and incontients, icnreased riskfor UTI and posslibly acceleraen end dstage rnal disease (ESRD) GI: it effect the motility, secretions nad apsortion, nausea, postoprandial vomiting, bloating, lsos of appetitie,. One study showe dup to 76% of diabetics had some type of GI problems sweating abnomalities neuroglycopenia and hypoclycemic unaswareness |
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What factors ion the diabetic coudl imped hte healing of an ulceration
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ischemia
poor glycemic ontroll callus formation over the ulcer infection malnutriton peripheral neuropathy ESRD (end stage renal disease) Cardiac abnormailites poor wound care patient non-compliance bony prominence patient no-compliance |
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Whata re the signs of ischemic vascualr disease?
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Dyshidrosis
atrophy of soft tissue absence of hair tendncey to develp fissures on heels and prominence diminshed or absent DP/PT pulses prolonged venous filling time (over 20 sec) rubor of toes aor foot on dependncy blanchign of foot on elevation ankle brachial index of less than .45 mm/hg |
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What are the tow type so f vascualr disease the diabetic suffers form and where do they usually present in the lower extemity?
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macroangiopathy, in po;litea and tibial arteries
microangiopathy i: in the smal artiers of the foot (arterioles and capillareis) and ususaully preced large vessel disease |
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YOu have a 38 year old male going fr surgery tomorrw it local and MAC and the patient must be NPO overnight. His insulin regimen is 25 units NPJ A.M. and 20 units NPH P.M., he gets 8 units REg. A.M. What would his inuslin dose be in the morning and what fluids would you put him on? If he were on an oral agent, how would htat change your management?
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The patient should get half his normal NPH dose in the A.M, and you would hold his regualr insulin to decrese the rik of hypogycemia. the patient should be started on 1/2 D5W & NS at 60 cc an hour at 6AM. If the patient were on a orla agent then the drug should be held.
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Briefly exlain the Somgyi effect ad the Dawn phenomenon
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Somogyi Effet is a rebound hperglyceemia fllowng an episode of hypoglycmeia due to counter regulatory hormone release. THe insulin dose should be decreased, this effect is more common in children.
Dawn phneomenon is an early rise in the mornign paslma glucose that requirees increased amounts of insluin to mainaitn euglycemia nd is indempendient of the Somogyi effect. It is beleved to be cause by the nocutrnal surge of growth hormonerelease, to establish the diffence between the town, aglucose check should be doen at 3 am, since the two have very different treament |
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Briefly explain the symptoms ofhypoglycemia nad its treament
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Symptoms -
excessive secretion pepinphrine: swating , termor, tachycardia, anxiety, and hunger CNS: dizziness, headache, clouidng of vision, blunted mental acuity, loss of fine motor skills, confusion, abnormal behavior, convulsions, coma Treatment: For serious episode : IV bolus of 25 to 50 g glucose as a 50% solutionfollowed by constant infsion of glucose until the patient can eat. Hypoglycemia from sulfonylureas may last for days and it si common for patients to lapse back into coma if glucose nfusions are stopped to soon. |
