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FM ch 4,5,6,15
| Question | Answer |
|---|---|
| What is the most common endocrine disorder? | Diabetes mellitus (DM) |
| Approximately how many Americans have diabetes according to the slide? | Over 30 million Americans, or about 1 in 10. |
| Approximately how many U.S. adults have prediabetes? | One-third of U.S. adults. |
| Diabetes is a leading cause of what three major complications? | Blindness, renal failure, and lower-limb amputation. |
| What causes Type 1 DM? | Autoimmune destruction of pancreatic beta cells → absolute insulin deficiency. |
| What is the usual age of onset for Type 1 DM? | Under 20 years. |
| Does Type 1 DM require insulin? | Yes. |
| Approximately what percentage of diabetes cases are Type 1? | Less than 10%. |
| What are the two major abnormalities in Type 2 DM? | Insulin resistance + impaired insulin secretion. |
| What is the usual onset of Type 2 DM? | Over 40 years, although it is increasingly occurring in youth. |
| Approximately what percentage of diabetes cases are Type 2? | Greater than 90%. |
| How is Type 2 DM managed? | Diet, exercise, oral agents, and sometimes insulin. |
| What fasting glucose range indicates prediabetes on the slide? | 100–125 mg/dL. |
| What conditions often accompany prediabetes? | Hypertension and dyslipidemia. |
| What is most effective during the prediabetes stage? | Lifestyle changes. |
| What is the pathogenesis sequence of diabetes? | Insulin loss/resistance → glucose remains extracellular → hepatic glucose release → fat/protein catabolism. |
| What are the 3 major metabolic problems in Type 1 DM, and what can they lead to? | Decreased glucose use Increased fat mobilization → ketones + acidosis Impaired protein use → muscle breakdown |
| Why is Type 2 DM less likely to cause ketoacidosis, and what risk remains? | Type 2 patients retain some insulin function, which helps them avoid ketoacidosis, but they remain at high risk for hyperglycemia complications. |
| What are the cardinal signs/symptoms of diabetes? | Polyuria, polydipsia, polyphagia (Type 1), weight loss (Type 1), blurred vision, ketonuria, weakness/fatigue. |
| What are the major cardiovascular complications of diabetes? | 1.5–4× increased risk of CAD, stroke, and MI; diabetic cardiomyopathy; “silent ischemia” due to neuropathy. CVD accounts for 2/3 of diabetic deaths. |
| What are the major retinopathy and nephropathy complications of diabetes? | After 20 years, nearly all Type 1 and ~60% of Type 2 patients have retinopathy. Diabetes is the leading cause of end-stage renal disease in the U.S. |
| Why are people with diabetes more susceptible to infection? | Elevated glucose fosters bacterial growth + impaired circulation reduces WBC mobilization → higher rates of skin, urinary, and vaginal infections. |
| What hand/shoulder disorders are especially associated with diabetes? | CTS, Dupuytren's contracture, trigger finger, and adhesive capsulitis occur 4× more often; >30% of Type 1 or Type 2 patients have hand or shoulder disease. |
| What is Limited Joint Mobility (LJM) in diabetes? | Painless stiffness + flexion contractures of the finger joints → “prayer sign.” It correlates with disease duration and insulin therapy. |
| What is characteristic of adhesive capsulitis in diabetes? | Global tightness with equal external/internal rotation limitation; aggressive early therapy restores functional motion. |
| What is DISH, and how is it associated with diabetes? | Diffuse idiopathic skeletal hyperostosis = osteophytes bridging vertebrae. Most common in Type 2 DM, with the thoracic spine most involved. |
| What should I know about osteoporosis in diabetes? | May develop within 5 years of DM onset, is more severe in Type 1, and microfractures may go unrecognized because of sensory loss. |
| What are the 3 types of diabetic neuropathy and their major features? | S most common; tingling, burning sensory loss h&f → Charcot's joint + ulcer M weakness, atrophy, bil prox wkns /diabetic amyotrophy → claw toe, flatfoot, arch collap A affect hrt, GI, blad, thermoreg → lack of HR varia exer intol, postural hypotension |
| What exercise precaution is important with cardiovascular autonomic neuropathy? | Stress testing is recommended before exercise. |
| What PTA screening test identifies diabetic patients at risk for foot ulcers and amputation? | Semmes-Weinstein monofilament testing. |
| Why is diabetic foot care so important? | Foot problems are a leading cause of hospital admission in diabetes; diabetes is the most common reason for lower-limb amputation, and half of cases are preventable with proper foot care. |
| How are diabetic foot ulcers prevented? | Offloading/pressure reduction is essential. Proper footwear reduces ulcer recurrence from 80% → 20%, and total-contact inserts + metatarsal pads redistribute plantar stress. |
| What treatments are listed for diabetic wounds? | Debridement, infection control, protective dressings, revascularization, growth factors, infrared light therapy, and cool laser revascularization. |
| What foot-care education should a PTA give a patient with diabetes? | Daily foot inspection using a mirror for all surfaces + proper cleaning + lubrication + safe callus removal + immediately report warmth, erythema, or skin changes. |
| What are the ABC treatment goals for diabetes? | A1c <7%; BP <130/80 mmHg; LDL <100 mg/dL; HDL >50 mg/dL; triglycerides <150 mg/dL. |
| How is Type 1 DM treated? | Insulin is required through multiple daily injections or a pump. “Brittle diabetes” = wide glucose swings. Tight control delays complications. |
| How is Type 2 DM treated, and what lifestyle program reduced new diabetes cases by 58%? | Diet + exercise first → oral hypoglycemics → insulin if needed. A low-fat, low-calorie diet + 30 min exercise 5×/week reduced new diabetes cases by 58%. |
| What emerging therapies are being investigated for Type 1 DM? | Islet-cell transplantation, artificial pancreas, stem-cell research, gene therapy, and vaccine development. |
| How do I recognize and treat hypoglycemia? | Blood glucose ≤70 mg/dL; rapid onset (min); pallor, sweating, tachycar, shaky, confus, convulsion; normal breath. Treat immediately with fast-acting carbs such as juice, honey, or glucose tablets. Hospitalize if glucose <50 mg/dL, alt mental status persis |
| What is the lipogenic effect of repeated insulin injections, and how is it prevented? | Repeated injections at the same site → subcutaneous thickening → decreased insulin absorption. Rotate injection sites and avoid injecting into muscles used during exercise. |
| What is the DKA triad and what are its major signs? | Hyperglycemia + acidosis + ketosis. Signs: acetone breath, dehydration, polyuria, stupor. Mortality 5–10%; immediate medical care is essential. |
| How do hypoglycemia and hyperglycemia differ? | Hypoglycemia: rapid/minutes, pallor + sweating, normal breath, glucose <70 mg/dL. Hyperglycemia: gradual/days, flushed + dehydrated, fruity/acetone breath, glucose ≥250 mg/dL. |
| According to the slide, what should be given if you cannot tell whether a patient has hypo- or hyperglycemia? | Fruit juice — the slide states it is safe for both. |
| What are the major benefits of exercise in diabetes? | Improves insulin sensitivity for 12–72 hours, lowers blood glucose, reduces CVD risk, and improves lipid profiles. |
| What is the overall difference between hypothyroidism and hyperthyroidism? | Hypothyroidism = slowed metabolism. Hyperthyroidism = accelerated metabolism. |
| Compare neurological/mental symptoms of hypo- vs. hyperthyroidism | Hypo: depression, anxiety, lethargy, fatigue, headache, slowed speech/mental function, impaired short-term memory. Hyper: tremors, hyperkinesis, nervousness, increased DTRs, emotional lability, insomnia, weakness, muscle atrophy. |
| Compare musculoskeletal/related findings of hypo- vs. hyperthyroidism. | Hypo: proximal weakness, CTS, trigger points, myalgia, increased bone density, cold intolerance, paresthesias. Hyper: chronic periarthritis, heat intolerance, flushed skin, hyperpigmentation, increased hair loss. |
| Compare cardiovascular findings of hypo- vs. hyperthyroidism. | Hypo: dyspnea, bradycardia, CHF, respiratory muscle weakness, decreased peripheral circulation, angina, increased cholesterol. Hyper: tachycardia, palpitations, increased respiratory rate, increased BP, arrhythmias. |
| Compare GI/metabolic findings of hypo- vs. hyperthyroidism. | Hypo: anorexia, constipation, weight gain, decreased absorption of food/glucose. Hyper: hypermetabolism, increased appetite, increased peristalsis, nausea, vomiting, diarrhea, dysphagia. |
| Compare reproductive findings of hypo- vs. hyperthyroidism. | Hypo: infertility, irregular menstrual cycle, increased menstrual bleeding. Hyper: polyuria, infertility, increased first-trimester miscarriage, amenorrhea. |
| What are the key facts and classic symptoms of Graves' disease? | Most common form, autoimmune; women affected 4:1, usually ages 20–40. Excess thyroid hormone → generalized hypermetab symptoms: goiter, nervousness, heat intolerance, weight loss despite increased appetite, sweating, tremor, palpitations, exophthalmos. |
| What neuromuscular problems occur with Graves' disease? | Proximal muscle weakness/myopathy, chronic periarthritis, and calcific tendinitis → often progresses to adhesive capsulitis. |
| How is hyperthyroidism treated according to the slide? | Antithyroid drugs, radioactive iodine (RAI), or surgery. RAI is first-line for adults ≥18 and causes hypothyroidism in ≥50% within 1 year. |
| What bony prominences are at risk in SUPINE? | Occiput, spine of scapula, vertebral spinous processes, elbows/olecranon, sacrum, coccyx, heels, medial malleolus. |
| What bony prominences are at risk in PRONE? | Forehead, ears, anterior acromion process, sternum, anterior head of humerus, patella, dorsum of feet. |
| What bony prominences are at risk in SIDELYING? | Ears, lateral acromion process, greater trochanter, lateral epicondyle of humerus, head of fibula, lateral malleolus, opposite medial malleolus, posterior iliac crest. |
| What bony prominences are at risk in SITTING? | Ischial tuberosities; sacrum/coccyx if slouched; spine of scapula against backrest; heels if unsupported; elbows on armrests. |
| What is key to preventing pressure injuries at these sites? | Regular assessment and repositioning. |
| What 3 things are evaluated when assessing a burn? | Depth, size, location. Depth depends on temperature/radiation + exposure duration; size = % total body surface area; burn classification is based on skin layers affected. |
| Compare the depth, appearance/pain, and healing of a SUPERFICIAL burn. | Outer epidermis; red + slight edema; heals without peeling/evidence of scar; 2–5 days. |
| Compare the depth, appearance/pain, and healing of a SUPERFICIAL PARTIAL-THICKNESS burn. | Epidermis + upper dermis; extremely painful + blisters; minimal/no scarring; 5–21 days. |
| Compare the depth, appearance/pain, and healing of a DEEP PARTIAL-THICKNESS burn. | Complete epidermal destruction + majority of dermis; discoloration, broken blisters, edema; nerve-ending damage → moderate pain; hypertrophic/keloid scarring may occur; 21–35 days without infection. |
| Compare the depth, appearance/pain, and healing of a FULL-THICKNESS burn. | Complete epidermis + dermis destruction with partial subcutaneous damage; eschar + minimal pain; requires grafts and is susceptible to infection; healing weeks to months. |
| What characterizes a SUBDURAL burn according to the slide? | Complete destruction of epidermis, dermis, and subcutaneous layer; may involve muscle/bone; requires surgery; extensive healing time. |
| What is systemic sclerosis and who is most affected? | Fibrosis of skin, joints, blood vessels, and internal organs; women affected 2–3× more than men. |
| Compare limited vs. diffuse cutaneous systemic sclerosis. | Limited (75–80%): distal extremities/face, slow progression, CREST common, ~70% prognosis at 10 years. Diffuse (15–20%): widespread skin thickening, rapid progression, early heart/lung/GI involvement, 40–60% prognosis at 10 years. |
| What are the 3 clinical stages of systemic sclerosis? | Edematous: bilateral non-pitting edema of fingers/hands → Sclerotic: tight, waxy, bound-down skin → Atrophic: skin atrophy + ulcerations at flexion sites. |
| What should I know about Raynaud's phenomenon in systemic sclerosis? | Often first manifestation; blanching → cyanosis → erythema of fingers/toes triggered by cold or stress; present in ~95% of diffuse SSc cases. |
| What structural skin changes occur with aging? | Thinning stratum corneum + fewer melanocytes + reduced elastin/collagen + decreased subcutaneous fat → translucent, paper-thin skin. |
| What functional integumentary changes occur with aging? | Impaired thermoregulation + diminished pain perception + weakened inflammatory response → increased susceptibility to hypothermia and hyperthermia. |
| Why does aging increase the risk of vitamin D deficiency and osteoporosis? | At age 65, 7-dehydrocholesterol levels are only ~25% of youthful levels → contributes to vitamin D deficiency + osteoporosis. |
| What is osteomyelitis, what commonly causes it, and who is at risk? | Bacterial bone inflammation, most often S. aureus; may become chronic if untreated. Risks: children, older adults, IV drug abusers, immunocompromised people, and those with implants. |
| What are the 2 routes of infection in osteomyelitis? | Exogenous: direct inoculation. Hematogenous: bloodstream spread from distant infection. |
| What is the pathogenesis sequence of osteomyelitis? | Bacterial seeding → abscess & sequestrum → involucrum & chronic infection. |
| Why is necrotic bone problematic in osteomyelitis? | It becomes an isolated reservoir for infection with reduced blood flow and resistance to systemic antibiotics. |
| Compare osteomyelitis manifestations in adults, children, and chronic disease. | Adul: bone p, warmth, swelling, fever; vert involvement may cause radiculopathy/paral Child: fever, pain, edema, erythema; “sausage toe” in diabetic pedal osteomyelitis. Chro: local pain/swelling, otherwise asymptoma; poor prognosis even with surgery. |
| How is osteomyelitis diagnosed and treated according to the slide? | Diagnosed by bone biopsy; treated with sequential IV + high-dose antibiotic therapy. |
| What should I know about infection and prosthetic joint failure? | Infection is the second most common cause of prosthetic joint failure after mechanical loosening. |
| What is the chain of transmission in order? | Pathogen → reservoir → portal of exit → mode of transmission → portal of entry. Breaking the chain at any link controls transmission. |
| What are the 5 routes of transmission? | Contact: direct/indirect. Airborne: <5 microns, suspended in air. Droplet: >5 microns, falls within 3 ft. Vehicle: common inanimate source — water, food, blood, objects. Vector-borne: insects/animals. |
| What factors increase host susceptibility to infection? | Age, nutrition, concurrent disease, invasive devices (catheters/IV lines), immunosuppressive therapy, poor hand hygiene. |
| How common are HAIs according to the slide? | Affect 1 in 31 hospitalized patients; slide reports 68,700 HAIs in 2015 and >72,000 associated U.S. hospital deaths. |
| Compare standard vs. transmission-based precautions. | Standard: ALL patients → hand hygiene, PPE, respiratory etiquette. Transmission-based: documented/suspected infection → contact, airborne, or droplet precautions. |
| What are the major strategies for controlling transmission? | Handwashing; alcohol-based rubs when hands aren't visibly soiled; immunization; prophylactic antibiotics for high-risk exposures; environmental controls such as water treatment, food safety, and vector control. |
| What facts should I remember about hand hygiene? | Handwashing = easiest/most effective prevention; a single hand can carry 200 million organisms. Alcohol rubs are more effective than soap when hands aren't visibly soiled. Wash before + after every patient contact. |
| What immunizations are emphasized for healthcare workers? | HBV, MMR, varicella, tetanus/Tdap, diphtheria, and annual influenza. |
| What are the key infection-control takeaways for a PTA? | Hand hygiene first; standard precautions always; stay immunized; observe/report early infection signs—especially atypical presentations in older adults. Immediately report changes in mental status, fever, or wound appearance. |
| What is fibromyalgia and what are its key features? | Chron p affect 6+ million Amer, more common than RA , ~90% women. Widespread pain/tenderness in ≥11/18 tender points + diffuse aching/burning pain, non-restorative sleep, morning fatigue/stiffness, cognitive dysfunction, IBS, and ANS dysfunction. |
| What ANS-related dysfunction is listed with fibromyalgia? | Abnormal blood flow during exercise + diaphragm dysfunction. |
| Abnormal blood flow during exercise + diaphragm dysfunction. | Prescriptive exercise; progress very slowly, starting at 3–5 min if needed. Reaching 30 min/day may take weeks–months; use small daily increments. |
| What exercise is recommended for fibromyalgia? | Aerobic exercise improves pain, sleep, and metabolic rate. Aquatic therapy at 84–90°F is ideal because of low axial load + progressive conditioning. |
| What manual-therapy precautions apply to fibromyalgia? | Avoid “no pain, no gain” because allodynia is real. Soft-tissue techniques should be gentle/slow with discomfort 1–5/10. Cross-friction massage is contraindicated. Ultrasound + interferential current may reduce pain when combined with manual therapy. |
| What is autoimmunity? | The immune system mistakes self-tissue as foreign. >56 autoimmune diseases are mentioned; genetic, hormonal, and environmental factors contribute, and women are disproportionately affected. |
| What is SLE and what is its hallmark? | Systemic lupus erythematosus = chronic inflammatory disorder that can affect any organ system. Hallmark = autoantibody/ANA production → immune complexes deposited in skin, joints, kidneys. |
| What are the major clinical manifestations of SLE? | Butterfly rash across nose/cheeks; migratory symmetric non-erosive arthritis; pleuritis, pericarditis, nephritis; CNS headache, psychosis, cognitive decline. |
| What are the major PTA implications for SLE? | Balance rest/activity; prescribe exercise to maintain strength without stressing inflamed joints; monitor for avascular necrosis of femoral head; watch renal signs (edema, weight gain, HTN); teach Raynaud's precautions; screen/report cognitive changes. |
| Why should excessive bed rest be avoided in SLE? | It worsens fatigue, promotes muscle atrophy, and accelerates osteoporosis. |
| What defines CFS and who is commonly affected? | Unexplained fatigue lasting ≥6 months, not relieved by rest and worsened by minimal physical activity. Women = 75%+ of cases; mean onset 29–35 years. |
| What are the key clinical features of CFS? | Profound fatigue + post-exertional malaise; “brain fog” affecting memory/concentration; neurally mediated hypotension → dizziness on standing; sleep disturbance, morning stiffness, widespread pain. |
| What is the PTA role for CFS according to the slide? | Graded ex ther + cognitive behavioral therapy are listed as evidence-based interventions. Begin low-level intermittent activity, as little as 3–5 min, and carefully monitor perceived exertion; fatigue increase >1 unit on a 1–5 scale signals overexertion. |
| Compare the immune effects of moderate vs. intense/prolonged exercise. | Mod: enhances immunity → boosts neutrophil/macrophage, increases NK cells, anti-inflam benefit, counters stress-induced immune supp Intense: suppr immunity → decr lymphocytes + NK-cell activ for 2–4 hr, open “immune window” for viral invas, incre DNA oxi |
| What is the key PTA implication for exercise immunology? | After severe exercise, the immune system requires 6–24 hr to recover in a healthy younger population. Exercise that seems mild to a healthy adult may be strenuous for a deconditioned older patient. |
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