Pathologies related to the foot and ankle Flashcards

1
Q

Diabetes mellitus; Overview/Etiology
aka Diabetes

A

*Chronic systemic disorder characterized by hyperglycemia and abnormal metabolism

*Primary
types I
-Auto-immunity affecting the pancreas that produces insulin
-Deficiency of insulin production and secretion

type II
*Excessive dietary sugar and other simple carbohydrates limits effect of insulin
*May be influenced by auto-immunity

*Insulin
-Released from the Pancreas
-Lowers blood sugar
-Stores fats

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2
Q

Diabetes mellitus; Incidence/Prevalence

A

*1/3 of Americans are pre-diabetic; a huge number… (US pop. > 330 million)

*~ 1/10 Americans with diabetes
-MOST common endocrine/metabolic disorder
-Type II MORE common (> 90%) than type I
-Occurring in younger and younger individuals
—MORE sedentary lifestyles
—-Increasing obesity

Risk Factors- see next slide

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3
Q

Diabetes mellitus, other conditions

A

*SAD- layered with sugars and simple carbohydrates

*≥ 2 hrs. of screen time/day as a part of a sedentary lifestyle

*Daily carbonated beverage- MORE sugar

*Fast food > 2x/wk.- MORE sugar

*Unmanaged stress and lack of regular sleep
–Inhibits insulin production

–Increased cortisol production that produces MORE sugars

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4
Q

diabetes Mellitus; Pathogenesis- PSA

A

*Type I- inability to produce and secrete adequate insulin to use glucose

*Type II- inadequate response of insulin receptors to insulin

ing insulin production

-ing fat storage and SYSTEMIC INFLAMMATION

-As the cycle continues you limit the effect of insulin, so the body makes even MORE insulin

-MORE fat storage and SYSTEMIC INFLAMMATION

-Insulin production finally stops or nearly stops bc Pancreatic cells that make insulin are exhausted

-Obesity and diabetes develop

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5
Q

Diabetes Mellitus; PT Implications
Clinical Manifestations and S&S with both types

A

*Cardinal S&S

-Frequent urination (polyuria)… why?

Extreme thirst (polydipsia)

-Decreased skin turgor

-Blurry vision due to sugar damaging blood vessels
-Weakness/fatigue… why?

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6
Q

Diabetes Mellitus; PT Implications
Clinical Manifestations and S&S with both types

A

*May progress to 3 types of neuropathies

  1. Sensory
    -Large ill-defined areas of non-segmental paresthesia and hyposensitivity or numbness of involved terminal nn

-Joint destruction because repeated microtrauma is not felt- Charcot foot- see next slide

-Less aware of a heart attack they are already MORE prone to

-Motor- weakness of mm. innervated by the involved terminal nn.

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7
Q

Diabetes Mellitus; PT Implications
Clinical Manifestations and S&S with both types

A

-May progress to 3 types of neuropathies
*Autonomic- affects function of multiple systems, particularly cardiovascular system
–Diminished pulses
–Necrosis, especially distally, i.e., wounds, amputations
–Poor healing
–Stroke
–Cardiac dz

–Excess hunger because cells can’t use glucose with ineffective insulin… so more eating… obesity

–Other severe complications for all types

–Leading cause of kidney dz and blindness

–Cognitive dysfunction leading to Alzheimer’s, referred to as type III diabetes

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8
Q

Diabetes Mellitus;
PT Implications
Clinical manifestations and S&S

A

Hx
*Observation
Charcot foot
Dry mouth
Cognitive decline
Fruity and long deep breaths with type 1

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9
Q

Diabetes Mellitus; PT Implications
Clinical manifestations and S&S

A

S*can and Biomechanical Exam
-Age-related Joint Change S&S in ½ of diabetics

-Resisted/MMT- possible weaknesses

-Neuro
Diminished sensation
Terminal n. pattern
Also assess 2 pt. discrimination and monofilament sensation

*+ Dural mobility tests

-Weaknesses of involved terminal nn.

-Myotomes WNL; why?

-Palpation of diminished pulses

*Urgent referral to MD

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10
Q

Diabetes Mellitus; PT Implications
Due to SYSTEMIC INFLAMMATION and impaired circulation

A

-HIGHER prevalence of Carpal Tunnel Syndrome, Dupuytren’s contracture, Trigger finger, and Adhesive Capsulitis

-HIGHEST prevalence of DISH (enthesis ossification) in those with Diabetes
Delayed healing

-Disorganized and excessive scar tissue

-Nociplastic pain

-SYSTEMIC INFLAMMATION

-Just to name a few…

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11
Q

Diabetes mellitus; SYSTEMIC INFLAMMATION is primary contributor to

A

-Diabetes
-HTN
-High triglycerides
-Low HDL

-Being overweight
>2/5 = metabolic syndrome

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12
Q

Diabetes Mellitus; PT Implications

A

*Contraindications to Grade V JMs

-Due to increase in osteoclastic activity, Osteoporosis develops in first 5 years of dx

-Hardening of aa and their walls associated with Diabetes

*Type II can be controlled and reversed with proper diet, exercise, and/or medications

*Exercise- “a balancing act”

-Check with MD initially

-No restrictions if glucose levels monitored and managed well

-3 10-minute bouts of cardiovascular activity better for sugar levels than 1 30-minute bout; why?

-Wait to exercise 1-2 hrs. after a meal; why?

-May need to decrease insulin prior to exercise; why?

-May need extra carbs to build glucose “stores” after exercise

-Keep snacks handy in case of hypoglycemia

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13
Q

Diabetes mellitus

A

*PT Implications
-Education

-Wear accommodating shoes and socks
-Examine feet regularly for skin breakdown
-Avoid alcohol and cortisone shots, high sugars in both

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14
Q

overview and incidence/ prevalence of gout

A

*Overview- metabolic disorder with elevated levels of uric acid and deposition of urate crystals

*Incidence/Prevalence
-1st MTP is MOST common site
-MOST common crystallopathy in the US
-Primarily in middle-aged biological males

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15
Q

Risk factor and etiology of Gout

A

*Risk Factors
-Family hx

-Decreased renal function with aging

-Conditions increasing uric acid production, i.e., leukemia, lymphoma, psoriasis, or RBC disorder

-Conditions limiting excretion of uric acid, i.e., alcoholism, HTN, obesity, and renal and thyroid disorders

-High fructose of SAD

-High nitrogen in organ meats, trout, shellfish, sardines, etc.

*Etiology
-Primary- Genetic

-Secondary to another disorder

-Idiopathic or unknown

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16
Q

Gout;Pathogenesis

A

-Uric acid typically forms from breaking down cellular waste in the bloodstream

-Kidneys unable to process higher amount of uric acid

-So MORE uric acid remains in circulation and migrates, primarily to joints

-Sparks an inflammatory response leading to tissue changes

-Necrosis of original tissue

-Proliferation of fibrous secondary tissue

17
Q

Gout; PT Implications
Clinical Manifestations and S&S

A

-Symptoms develop after ~ 10-20 yrs. of hyperuricemia… so it’s been going on for a while…

-Typically, monoarticular.. which means?

-Rather sudden onset of severe joint pain, often at night or morning

-Episodic with increasing frequency and severity based pm risk factors

-May develop cellulitis or infection

-May have constitutional symptoms if multiple joints involved

18
Q

Gout; PT Implications

A

-Education on causes and risk

-Patients often develop subsequent orthopedic conditions in and around gouty area

-Clinical manifestations and S&S

-Hx

-Observation

-Redness
-Swelling

-Temperature- warmth, possibly fever

-Scan and Biomechanical findings like age-related joint changes

-Urgent referral to MD

19
Q

osteomyelitis

A

*Overview
-Inflammation of bone due to microorganism
-Destructive infection

*Incidence/Prevalence
-Uncommon in wealthier countries… but resurgence with longevity and IV drug use
-MOST common in tarsal and metatarsal bones (43%) followed by tibia and femur
-Also, may occur in vertebra- see thoracic notes

*Risk Factors
-Immunosuppression
-Chronic illness like Diabetes
-IV drug use
-Joint replacement

20
Q

osteomyelitis; Etiology and Pathogenesis

A

-Complex and poorly understood

-Microorganisms, typically Staphylococcus aureus

-Preferentially binds to cartilage

-Metaphysis of bone is very porous… spreads quickly

21
Q

osteomyelitis; PT Implications
Clinical Manifestations and S&S

A

-Gradual onset of deep and achy P!/stiffness is MOST common presenting symptom

-Infection S&S

-Localized and PROGRESSIVE P! that limits motion and WBing, may become constant

-May develop constitutional symptoms

22
Q

osteomyelitis; PT Implications
Clinical Manifestations and S&S

A

Hx
Observation
-Asymmetrical gait
-Red and swollen

-Temperature- warmth, possibly fever

-Scan and Biomechanical Exam findings like age-related joint changes

-Urgent referral to MD

23
Q

Osteochondritis dissecans

A

-Refer to knee lecture plus:

-Incidence/Prevalence- MOST common in medial femoral condyle and talus

24
Q

Osteochondritis dissecans;PT Implications
Clinical manifestations and S&S

A

-S&S of hypermobility/instability of involved ligament but with persistent age-related joint like changes

*Scan
-ROM- limited and painful, particularly with DF; why?

-Resisted/MMT- may be weak and painful, particular at end range DF

-Compression likely (+) and distraction relieving

-Biomechanical Exam

-Stability tests (+)

TTP over talar dome

Urgent referral to MD