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ClinMed II > Test 3: Pathologies of the foot and ankle > Flashcards

Test 3: Pathologies of the foot and ankle Flashcards

1
Q

what is diabetes

A

chronic systemic disorder characterized by hyperglycemia and abnormal metabolism

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2
Q

primary types of diabetes

A

type I: auto immune; affects pancreas insulin production/secretion

type II: excessive dietary sugar and other simple carbs lead to lack of insulin; possible auto immune influences; cant process sugar due to damage of body

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3
Q

what is insulin/ its function

A

released from pancreas

lowers blood sugar

stores fat

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4
Q

how many americans are pre diabetic/diabetic

A

1/3 have pre diabetes

1/10 americans have diabetes

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5
Q

incidence/prevalence of diabetes

A

most common endocrine/metabolic disorder

type II more common (90%)

increasing obesity/sedentary lifestyle

happening in younger and younger individuals

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6
Q

risk factors for diabetes

A

family hx
obese
older age
physical inactivity
previous gestational diabetes
other conditions with insulin resistance
hx vascular disease
hypertension
low HDL cholesterol (good)
smoking

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7
Q

contributors to diabetes

A

SAD; high sugars/carbs

over 2 hrs screen time/day

daily carbonated beverages

fast food >2x/wk

unmanaged stress/lack of regular sleep (inhibits insulin production and increased cortisol that produces more sugars)

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8
Q

pathogenesis of type I diabetes

A

inability to produce and secrete adequate insulin to use glucise

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9
Q

pathogenesis of type II diabetes

A

inadequate response of insulin receptors to insulin

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10
Q

explain the cycle of diabetes and fat storage

A

sugars cause insulin production

fat is stored and systemic inflammation occurs

eventually effect of insulin is limited so body makes more

when more is made, more fat is stored and more inflammation

eventually insulin production stops bc pancreas cells are exhausted

obesity and diabetes develop

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11
Q

S&S of diabetes

A

frequent urination (polyuria)
dry mouth
extreme thirst (polydipsia)
decreased skin turgor
blurry vision due to sugar damaging blood vessels
weak/fatigued
excess hunger (body cant use insulin)

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12
Q

what are the 3 types of neuropathies diabetes can lead to

A

sensory
motor weakness of mm innervated by peripheral nn
autonomic

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13
Q

what is sensory neuropathy

A

non segmental paraesthesia and hyposensitivity or numbness if involved peripheral n

joint destruction bc repeated microtrauma isn’t felt (charcot foot)

less aware of a heart attack they are already more prone to

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14
Q

what is motor neuropathy

A

weakness of mm innervated by the involved peripheral n

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15
Q

what is an autonomic neuropathy

A

affects multiple systems, particularly cardiovascular

diminished pulses
necrosis
poor healing
stroke
cardiac dz

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16
Q

what are possible severe complications to diabetes

A

leading cause of kidney disease and blindness

cognitive dysfunction leading to alzheimers referred to as type III diabetes

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17
Q

what S&S of diabates can you observe in the clinic

A

charcot foot
dry mouth
cognitive decline
fruity and long/deep breaths with type I

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18
Q

what scan/BM exam fininds might you find with someone who has diabetes

A

ARJC S&S in 1/2 diabetics

possible weakness

diminished sensation (assess 2pt discrimination)

+ dural mobility

myotomes WNL

diminished pulses

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19
Q

referral for diabetes

A

urgent referral to MD

20
Q

what are the implications for PT with pts with diabetes

A

higher prevalence of
-carpal tunnel
-Dupuytren’s contracture
-trigger finger
-adhesive capsulitis
-HIGHEST prevalence of DISH

delayed healing
disorganized/excessive scar tissue
nociplastic pain

21
Q

why may osteoporosis develop in those with diabetes

A

due to increased osteoclastic activity

usually develops in first 5 years

22
Q

explain what it means that exercise with diabetes is a “balancing act”

A

check in with MD initially

no restrictions if glucose is managed well

3-10 bouts of CV activity better for sugar levels than 1 30 min session (exercise is good for lowering blood sugar)

wait 1-2 hours after a meal (eating lowers blood sugar, so if you eat and exercise and both lower sugar you could then become hypoglycemic)

may need to decrease insulin prior to exercise (same thing, dont want to drop sugar too low)

may need extra carbs to build glucose stores

keep snacks handy

23
Q

signs of hypoglycemia

A

HA
dizzy
low energy
tachycardia
shaky
difficulty focusing

24
Q

signs of hyperglycemia

A

thirst
N&V
dehydration S&S
dulled senses
weak pulse
abdominal pain

25
Q

education for diabetic pts (dressing/obs/avoid)

A

wear accomodating shoes and socks

examine feet regularly for skin breakdown

avoid alcohol and cortisone shots (high sugars in both)

26
Q

systemic inflammation is a primary contributor to what conditions

A

diabetes
HTN
high triglycerides
low HDL
being overweight

> 2/5 = metabolic syndrome

27
Q

what is gout

A

metabolic disorder with elevated levels or uric acid and deposition of urate crystals

28
Q

incidence/prevalence of gout

A

1st MTP is most common site

most common crystallopathy in the US

primarily in middle aged males

29
Q

risk factors for gout

A

family hx

decreased renal functioning

conditions that increase uric acid production

conditions that limit excretion of uric acid

high fructose from SAD

high nitrogen in organ meats, trout, shellfish, and sardines

30
Q

what are examples of conditions that increase uric acid production

A

leukemia

lymphoma

psoriasis

RBC disorder

31
Q

conditions that limit uric acid excretion

A

alcoholism

HTN

obesity

renal and thyroid disorders

32
Q

etiology of uric acid

A

genetic is primary

secondary to another disorder

idiopathic or unknown

33
Q

pathogenesis of gout

A

uric acid typically forms from breaking down cellular waste in blood

kindeys are unable to process higher amounts of uric acid

more uric acid remains in circulaiton and migrates primarily to joints

sparks inflammatory response leading to tissue change

34
Q

what tissue changes may take place with gout

A

necrosis of original tissue

proliferation of fibrous secondary tissue

35
Q

S&S of gout

A

symptoms develop 10-20 years after hyperuricemia

typically monoarticular (one joint)

rather sudden onset of severe joint pain

episodic with increasing frequency/severity

may develop cellulitis

may have constitutional S&S if multiple joints involved

36
Q

PT implications of gout

A

edu pt on risk factors

pts often develop subsequent orthopedic conditions in and around gout area

37
Q

clinical S&S that could indicate gout for PT

A

Hx

observation of redness/swelling

warm temp

scan/BE similar to ARJC findings but sudden

38
Q

referral for gout

A

urgent

39
Q

what is osteomyelitis

A

inflammation of a bone due to microorganism

destructive infection

40
Q

incidence/prevalence of osteomyeltitis

A

uncommon in wealthier cultures

resurgence with longevity and IV drug use

most common in tarsal and metatarsal bones (43%) followed by tibia and femur

also can occur in vertebra

41
Q

risk factors for osteomyelitis

A

immunosupression
chronic illness like diabetes
IV drug use
joint replacement

42
Q

etiology and pathogenesis of osteomyelitis

A

complex and poorly understood

microorganisms typically staphlococcus aureus

preferential to cartilage

metaphysis of bone is very porous so it spreads quickly

43
Q

clinical manifestations of osteomyelitis

A

gradual onset of deep and achy pain and stiffness = most common presenting symptom

infection S&S

localized and progressive pain that limits motion and WBing

may develop constitutional S&S

44
Q

what S&S might you see in a PT clinic for osteomyelitis in the foot

A

Hx
asymmetrical gait
red/hot/swollen

scan/BE like ARJC

45
Q

referral for osteomyelitis

A

urgent referral to MD

ClinMed II (12 decks)

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