Diff Dx: Final - Metabolic Disorders

Front 1

Metabolic alkalosis causes

Back 1

pH > 7.45 due to excessive bases or reductions in acids
1. Excessive vomiting (losing acid content from the stomach)
2. upper GI suctioning
3. diuretic therapy
4. ingestion of large quantity base substance (antacids)

Front 2

Clinical manifestations of metabolic alkalosis

Back 2

Dec respiration = retain CO2 and H
Mm fasiculations (discharge of a-MN) and cramping

Front 3

Metabolic acidosis causes

Back 3

pH < 7.35
1. DKA
2. lactic acidosis (build up of lactic acid)
3. renal failure
4. severe diarrhea
5. drug/chemical toxicities

Front 4

Why may DKA result in metabolic acidosis?

Back 4

Dec in insulin = inc lipolysis and ketone body production
Body tries to compensate and neutralize effects, but uses bicarbonate in the process

Front 5

Why may renal failure result in metabolic acidosis?

Back 5

Kidney unable to rid excess acids or..
Dec production of bicarb

Front 6

What drug/chemical may cause metabolic acidosis?

Back 6

Excessive production of salicylates (aspirin)

The acetominophen (main ingredient in aspirin) is what causes severe diarrhea

Front 7

Primary gout and cause

Back 7

Error in purine metabolism, which causes elevated serum uric acid
Uric acid changes into crystals (urate) and the crystals are depositied into joint or other tissues (ie. kidneys)

Front 8

Gout arthritis

Back 8

When deposits of urate are deposited into joints
ie. first MTP

Front 9

Secondary gout

Back 9

Results of other disorders such as neoplasms, renal dx, DM, hyperlipidemia

Front 10

Who does gout affect?

Back 10

Males 40-50
Post-menopausal women

Front 11

Psuedo-gout

Back 11

Calciumphosphate Dihydrate Crystals (CPPD) affect one joint (often knee)
Can be asssociated with chondrocalcinosis, which is Ca salts in joint cartilage

Front 12

Dx of gout
Clinical manifestations

Back 12

Aspiration of synovial fluid and identifcation of crystals
Accute attack results in intense joint pain, erythema, warmth, extreme tenderness
Often occurs at night and attacks precipiated by trauma, surgery, alcohol consumption, food high in purine

Acute attacks are treated with NSAIDs & the goal is to decrease levels of uric acid with diet and exercise

Front 13

Hemochromotosis - who does it affect?

Back 13

Excessive absorption of iron thru GI
5-10x more likely in males
>50 yo
Accelerated by alcohol consumption and ascorbic acid

Front 14

S/s of hemochromotosis

Back 14

Arthopathy, arthralgias, myalgias
Progressive weakness
Bilateral pitting edema
Vague abdominal pain
Hypogonadolism (lack of menstrual cycle or impotence)
CHF
Hyperpigmentation of skin

Front 15

What does hemochromotosis look like?

Back 15

RA flair up, but biopsy of synovial tissue shows iron deposits

Front 16

Primary causes of osteoporosis

Back 16

Reduction in bone mass per unit volume of bone

Idiotpathic (children/young adults) with normal gonadal fxt
Post-menopausal (most common)
Senile involuntary

Front 17

Secondary causes of osteoporosis

Back 17

Hyperthyroidism and hyperparathyroidism
Hypogonadism
Cushing's dx
DM
Chronic Renal Failure
RA
Malabsoprtion syndrome
Various malignancies
Chronic alcohol dependency

Front 18

Incidence of osteoporosis

Back 18

Most common metabolic bone dx
Affects 25 mil in US
Most common in single white women
Affects 30-45% of white women > 45

Front 19

Risk factors for osteoporosis

Back 19

Age
Sex
Hereditary
Race

Front 20

Why does osteoporosis occur?

Back 20

Bone mass peaks 25-35 yo
Once past this, bone resorption exceeds bone formation which will progress until you have osteopenia (dec in bone mass)

Front 21

Why does menopause cause osteoporosis? How much bone is lost?

Back 21

Dec in estrogen = dec in Ca absorption in intestines
Inc bone resorption to compensate with impaired osteoblastic activity
11% loss in first 5 years, 5% loss over next 20 years

Front 22

Race, body build, and activity level as risk factors of osteoporosis

Back 22

White = lowest bone density and Black = greatest BD
Thin = less cortical bone and greater risk. FAT = more mechanical strain AND inc levels of estrogen (fatsoluble )causes less risk
Inactivity in immobilization is largely associated with dec in bone formation (cyclist = osteoporsis of spine d/t not WB through it and excessive sweating so minerals need to be replaced by resorption from the bone)

Front 23

Smoking as a risk factor for osteoporosis

Back 23

5-10% reduction in bone mass

Front 24

Long term corticosteroid use as a risk factor for osteoporosis

Back 24

Impairs osteblastic activity and increases osteoclastic activity (OUCH)
Fucks up Vit D dependent intetstinal Ca absoprtion (impaired ability to get Ca+ out of vitamin D)

Front 25

Clinical presentation of osteoporosis
Diagnosis?

Back 25

LBP, fractures (often first sign).
Must ahve 30% loss in BMD before observed on X-ray
First diagnosed as osteopenia, then rule out other causes (like hyperthyroidism)

Front 26

Tx for osteoporosis

Back 26

Ca 1000 mg/day pre-menopause and 1500 mg/day post-menopause
Vit D to help absorption of Ca
Calcitonin to dec osteoclastic activity
Fluoride with activates osteoblasts

Front 27

PT implications of osteoporosis?

Back 27

Careful with high intensity ex
Watch mobilizations

Front 28

What is osteomalacia?

Back 28

Softening of bone without loss of bone matrix
Seondary to insufficent mineralization of bone matrix

Front 29

2 primary causes of osteomalacia?

Back 29

Insuffiient Ca absorption from intestines
Inc renal phosphate loss

Front 30

Risk factors for osteomalacia?

Back 30

Dx of small intestines or certain disorders of teh liver
More prevalent in colder climates (secondary to dec sun exposure)

Front 31

Presentation of osteomalacia

Back 31

General achine and fatigue
Proximal myopathies
Bone pain
Inc thoracic kyphosis
Marked bowing of femurs

Front 32

What is Padget's dx and who does it affect?

Back 32

Progressive disorder that is marked by abnormal bone remodeling
Ancestry thru British Islands, Australia, and New Zealand

Front 33

Cause of Padget's dx?
Most common symptom?

Back 33

Bone being broken down thru osteoclasts, remodeled with fibrous tissue that has been broken down
After fibrous tissue, get bone regeneration of sorts thru some osteoblastic activity and that essentially creates the plaques on the bone
Pain due to microfx's and hypervascularity in area

Front 34

What does a pt with Padget's dx complain of?

Back 34

Deep ache at night
HA
Ringing in ears
Vertigo

Front 35

Dx and tx of Padget's dx?

Back 35

Series of changes on radiological exam and see plaques
Treated with anti-inflammatory and calcitonin to help with osteoblastic activity

Front 36

Difference bt mm fasciculations and fibrillations

Back 36

Fasciculations: discharge of an AMN--can usually see these

Fibrillation: indicative of deinnervation--mm depolarizes based on release of ACh--the mm is hypersensitive so any change in gradients can cause a single mm fiber to fire--we cannot usually see these

Front 37

How does lactic acid buildup?

Back 37

Excessive lactic acid is produced during strenuous exercise bc their is insufficient O2 for proper use of glucose, carbs, & water