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DM complications
Clinical Medicine II
| Question | Answer |
|---|---|
| Why is the incidence of DM ^ | d/t obesity and sedentary life style |
| What is 80% COD in pt’s w/ DM | premature vascular dz |
| Effects of chronic ^ glucose | damages capillaries, “end organ” damage, leading to atherosclerosis > MI, CAD, PVD, CHF |
| What are acute diabetic complications | hypoglycemia, DKA, |
| Macrovascular DM complcations | CHD, Cerevbrovasbular dz, PAD |
| Microvascular DM complications | retinopathy, nephropathy, neuropathy: sensory and Autonomic |
| What PEs are included w/ DMs | Ht, Wt, BMI, BP, (orthos?), fundoscopic, thyroid, foot exam |
| What does the foot exam entail | inspection, palpation, pulses, patellar and Achilles reflexes, propiroception, vibration, monofilament sensation |
| Labs for DMs | A1c, FLP, LFTs, SCr and GFR, UA + albumin to creatinine ratio, TSH-T1DM, |
| Frequency for Primary care visit, FPG, A1c, Lipids, UA, | 2, 4-6, 2-4, 1, every visit |
| What is the major cause of morbidity and mortality in individual w/ DM | Coronary Vascular Dz (CVD) |
| Coexisting conditions contributing to CVD | HTN, dyslipids, smoking, obesity, obstructive sleep apnea |
| Goal HTN to decrease vascular complications | 125-130/80 |
| Which number is more important | want DBP <80, systolic CAN be higher… |
| What measured BP is associated w/ ^ cardiovascular events in diabetes | >115/75 |
| What causes in underlying nephropathy in T1DM | HTN |
| What significantly reduces nonfatal and fatal strokes | reducing BP |
| How do we tx HTN | by individualizing pt’s and their therapy d/t characteristics and RFs |
| Non-pharm tx for HTN | diet, exercise, wt loss, alcohol consumption |
| What should lipid levels be | LDL <100, HDL >50, TGs < 150 |
| Tx for dyslipidemia | lifestyle modifications, dec cholesterol and sat fats, ^ n-3FAs, fiber, plant stanol/sterols, wt loss and ^ Physical activity |
| What is an acceptable lipid goal for DMs | 30-40% of baseline |
| What is LDL goal for DM2 pts w/ CVD | < 70mg/dl |
| What pharm therapy is added in DM pts with lipidemia | ASA 75-162mg/day |
| RFs for CVD risk | dyslipdemia, HTN, smoking, FH of premature CVD, micro-macro-albuminuria, ED |
| Leading casue of blindness in the U.S | diabetic retinopathy |
| Signs for diabetic retinopathy | black spots over vision |
| Cause of DR | chronic hyperglycemia: exacerbated by HTN, dyslipid, preggo |
| Sxs of DR | blurry vision, gradual blind spots, vision loss |
| Difference b/w proliferative and non-proliferative DR | proliferative: hasn’t started new blood vessels yet |
| DM macular edema | swelling of retina d/t leaky capillaries, accumulates in retinal layers |
| Mild Classifications of Diabetic macular edema | mild: some retinal thick, hard exudates in post pole, but DISTANT from center of the macula |
| Moderate classifications | retinal thinckening or hard exudates approaching the center of macula |
| Severe classifications | retinal thickening or hard exudates INVOLVING the macula |
| TX for DR | best if caught early, laser photocoagulation, vitrectomy, intraocular injections, Tight BP control, ASA |
| Is ASA CI in DR | no |
| F/U and evaluation for DR and DME for T1DM and T2DM | 1: 3-5 years after dx and yearly once pt is 10 and older 2: at time of dx |
| How should the eye exam be performed | with a dilated pupillary exam by a specialist, |
| Exacerbating factors of DN | HTN, atherosclerosis, poor BG control, pregnancy |
| How does diabetic nephropathy ↑ | d/t hyperfiltration, micro and macroprotenuria causing a ↓ GFR |
| How long until end stage renal dz with DN | 10 years or so |
| What classifies as macroproteinuria | albumin >300mg, total proein >550 |
| Screening for nephrophathy | 2: at dx 1: w/I 5 years of dx,puberty, then annually |
| Which DM is more likely for DN | type 1 |
| What is nl proteinuria | <30ug/mg? of creatinine |
| Dx of DN | neuro exam: pin prick, temp, ankle DTR, be aware of potential autonaumic problems |
| How does diabetic peripheral neuropathy (DPN) occur | capillary damage d/t high blood glucose, ↓ perfusion of distal tissues, death to peripheral nerves |
| MC cause of hospital admissions for diabetics | foot ulcerations |
| Screening for diabetic neuropathy | 2: at dx 1: 5 yrs later same w/ autonaumic signs |
| What indicates large fiber loss | loss of light touch and proprioception |
| What indicates small fiber loss | loss of pain and temperature |
| What is the MC type | a combinations of both alrge and small fibers |
| Sxs of DPN | numbness, tingling, prickling, aching, burning, lanciting, unusual sensitivity |
| Signs of DPN | ↓ vibratory perception and proprioception, ↓ DTR, ↓ hot, cold, |
| Motor syndromes of Diabetic neuropathy | wrist, foot drop, lateral rectus paralysis, proximal motor weakness, thigh pain, ↓ DTR |
| MC motor neuropathy | distal muscle wasting of the forefoot |
| Two types of ulcerations with motor neuropathy | claw toes, equinus contracture |
| What is autonomic Diabetic neurpathy | gastroparesis, D/C, Urinary retiention: UTI and pyelo, incontinence, impotence |
| AC autonomic DN | orthostatic HOTN, dysrhythmias, tachy, exercise intolerance, MI, painless MI |
| Cranial mononeuropathy | acute onset, usually unilateral occulomotor n. palsys, often do MRI MRA to r/o other causes |
| When do we see peripheral neuropathy | frequently once they are severe and past the dx of it |
| Clinical guidelines for DPN | 0-1: No S/S, 2a: + for sxs, ↑ pains burning, shoot, pins’& needles, abscent sensation to several modalities and ↓ DTR, 2b: no sxs of numbness or pain, but reduced thermal sensitivity, 3: foot lesions and deformaties |
| Tx of type 2a DPN | stable glycemic control and sxs tx, referral: neurologist, diabeticologist? |
| Tx of type 2b DPN | Educate, foot care, glycemic control, can lead to ulcers more quickly d/t no pain/sensation |
| Tx of type 3 DPN | surgery, ambutation if needed, educations |
| Who do we refer for preventative care and survelliance | smokers and charcot foot |
| Screening for PAD | cladification, pedal pulse, ankle/bracial test |
| Ischemia of the limbs resulting in infx | gangrene, d/t neuropathy and elderly |
| Why don’t diabetic sores heal as fast | ↓ blood and neuro supply |
| Assessment during foot examination | skin color changes, swelling, sores, ingrown toenails, cracks and cuts, |
| How do sores form on the feet | ↓ autonomic neuopathy and vascular supply, ↓ sweating so ↑ dryness and skin fissures |
| 4types of contributing factors to foot dz | Autonomic neuropathy, Biomechanical alterations, PAD |
| progressive musculoskeletal condition characterized by joint dislocation, fractures and deformities. It results in progressive destruction of bone and soft tissue of weight-bearing joints, most commonly in the foot and ankle | charcot foot |
| what can initiate charcot foot | minor trauma, like twisting the foot |
| sxs of charcot foot | dislocation of joint, swelling in foot and ankle, subluxation |
| tx of charcot | joint stabilization, non wt bearing for 8 weeks and surgery? |
| Two causes of charcot foot | neurotraumatic and neurovascular |
| ↓ sensation + repatetive trauma | joint and bone collapse of neurotraumatic charcot foot |
| Loss of sympathetic vascular tone leads to increased blood flow to the joint, causing an imbalance in bone metabolism. Over time the joint becomes osteopenic | neurovascular theory |
| Classifications of charcot | fore, mid (MC), and hind foot |
| one may see extensive resorption of bone ends, osteoporosis, and no spurs or fragments are present | atrophic charcot |
| xrays show no osteoporosis. Fractures and dislocations of bones and disorganization of joints are noticeable | hypertrophic charcot foot |
| compliccation of charcot | rocker-foot, little to no tx, hard to walk |
| Ulcer classifications | 0-5 0: intact skin (impending ulcer) 1: superficial, 2: deep to tendon bone or ligament 3: osteomyelitis 4: gangrene of toes or forefoot 5: gangrene of entire foot |
| Name for ulcer clasifications | wagner’s classifications |
| How does ED occur w/ DM | damaged BVs ↓ BF to penis, damaged nerves, |
| What does ↓ erection show a sign of | early sign of atherosclerosis |
Created by:
becker15
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