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Flashcards in Clin Path Final Deck (296)
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1
Q

What are rheumatic diseases?

A

Chronic systemic processes and affected patients often have musculoskeletal complaints that are not resolving with chiropractic care.

2
Q

What is Adult Reumatoid Arthritis?

A

Systemic inflammatory disease that predominantly manifests in the synovial membrane of diarthrodial joints

3
Q

What does the chronic inflammatory process of RA induce?

A

Changes in the cellular composition and the gene expression profile of the synovial membrane

4
Q

What are some are some intra -articular effects that RA causes?

A

hyperplasia of synovial fibroblasts and structural damage of cartilage, bone, and ligaments.

5
Q

What are some extra-articular effects of RA?

A

affecting a variety of organs occurs in the majority of patients and is a significant factor in morbidity and mortality of people with RA.

6
Q

Is the serverity of RA narrow or wide spectrumed? And what does this mean?

A

The severity of RA encompasses a wide spectrum; ranging from self-limiting disease to chronic progressive disease, causing varying degrees of joint destruction and clinically evident extra-articular organ involvement

7
Q

what % of the general population experiences RA?

A

1-2% of the general population

8
Q

Does RA affect all ethnic groups?

A

Yes, it affects all ethnic groups

9
Q

Does RA affect males or females more often?

A

Females > males by 3:1

10
Q

At what age does RA usually occur?

A

Occurs at any age; usual age of onset is 20-40 years old (4t h/5th decades)

11
Q

what are some classic presentations of RA patients?

A

1) Morning stiffness lasting at least 30 minutes (1 hour?), for 6 weeks (?) 2) Arthritis {symmetric polyarthritis) especially of proximal small joints of the hands and feet 3) Rheumatoid nodules

12
Q

what % of RA patients have serum rheumatoid factor?

A

85.00%

13
Q

Do negative serum rheumatoid factor patients always remain negative?

A

No, Some initially RF-negative patients convert to RF-positive as the condition progresses

14
Q

how sensitive and specific is serum rheumatoid factor for RA?

A

75-85% sensitive, 60-65% specific

15
Q

What is anti=cyclic citrullinated peptid (anti-ccp0 and what is it used for?

A

it tests for defectts in Immunoglobin G antibodies to cyclic citrullinated peptide. Used in conjunction with RF it enhances the sensitivity and specificity of an earlier and accurate diagnosis so aggressive treatment can be rendered early before a lot of damage occurs

16
Q

how sensitive and specific is serum rheumatoid factor for RA?

A

Anti-CCP: 60% sensitive, 98-99% specific

17
Q

What speed of onset for RA?

A

Onset is usually slow

18
Q

what systemic changes are seen with RA?

A

Accompanied by low-grade fevers, malaise, fatigue, weight loss

19
Q

what are some skin manifestions seen with RA?

A

Rheumatoid nodules and Rashes

20
Q

what are some ocular manifestions seen with RA?

A

Keratoconjunctivitis

21
Q

what are some respiratory manifestions seen with RA?

A

Pleural effusion

22
Q

what are some cardiac manifestions seen with RA?

A

Pericarditis and pericardial effusion

23
Q

what are some GI manifestions seen with RA?

A

Gastritis and PUD due to NSAIDS

24
Q

what are some Neurologic manifestions seen with RA? (3)

A

Cervical spine instability , Peripheral nerve entrapment, Mononeuritis due to vasculitis

25
Q

what are some Hematologic manifestions seen with RA?

A

1) Normocytic (sometimes microcytic) -hypochromic anemia with low ferritin is very common; difficult to distinguish it from iron deficiency 2) WBC count is usually normal or slightly elevated, leukocytosis indicative of acute onset; sometimes leukopenia with splenomegaly 3)Platelet count may be slightly elevated in proportion to level of inflammation

26
Q

What are some serology findings with RA?

A

Increased ESR/CRP that can be used to monitor course

27
Q

What are some essentials of diagnosis for RA? 95)

A

1) Usually insidious onset with morning stiffness and pain in affected joints 2) Symmetric polyarthritis with predilection for small joints of the hands and feet; deformities common with progressive disease 3) Radiographic findings; juxta-articular osteoporosis, joint erosions, and joint space narrowing 4) Rheumatoid factor and antibodies to cyclic citrullinated peptides, (anti-CCP) are present in 70-80% 5) Extra-articular manifestations: subcutaneous nodules, pleural effusion; pericarditis, lymphadenopathy, splenomegaly with leukopenia and vasculitis

28
Q

What is SLE?

A

a chronic inflammatory disease in which there is production of auto-antibodies to components of the cells of various structures like joints, kidneys, serous surfaces and vessel walls.

29
Q

Does SLE affect males or females more?

A

Female to male is 5:1

30
Q

What age does SLE usually occur?

A

Young to middle-aged women (15-40 years)

31
Q

What ethnicity is more common to be affected by SLE?

A

African- american 1:250 vs caucasain 1:1000

32
Q

What are some very common systemic clinical features of SLE? (4)

A

1) Fever 2) Anorexia 3) Weight loss 4) Malaise

33
Q

what are some epithelial features of sle? (4)

A

Skin rash where exposed to sunlight; face, neck, upper chest: 1) Malar rash 2)Discoid rash 3) Photosensitivity of the skin rashes 4)Oral ulceration

34
Q

What is the arthritis assosciated with SLE like?

A

Any joint may be involved, but especially small joints of the hands, wrists, and knees; characterized by tenderness, swelling, or effusion; observed in 90% of SL E patients

35
Q

What lung manifestations can SLE cause?

A

Pleuritis

36
Q

What heart manifestations can SLE cause?

A

Pericarditis and pericardial effusion

37
Q

What neurologic manifestations can SLE cause?

A

seizures or psychosis with medications or other metabolic causes ruled out

38
Q

What renal manifestations can SLE cause?

A

Persistent proteinuria >0.5mg/day (>3+ reagent strip) or Cellular casts; red, hemoglobin, granular, tubular, or mixed

39
Q

What hematological manifestations can SLE cause?(4)

A

• Hemolytic anemia (normocytic/normochromic; 60-70%) or • Leukopenia (<100,000/mm3, 30%)

40
Q

What serology tests can be used for SLE?

A
  • ANA (95-100%)
  • Anti-native DNA (-50%) or
  • Anti-SM (11) (-20%)
41
Q

What are the 11 criteria that are used to diagnose SLE?

A

1) malar Rash 2) discoid rash 3) photosensitivity 4) oral ulceration 5) arthritis 6) pleuritis or pericarditis 7) seizures or psychosis 8) proteinuria or cellular casts 9) hematology changes 10) ANA 11) anti-native DNA or Anti-SM

42
Q

How many of the 11 criteria need to occur in order for SLE patients to be considered in clinical trials?

A

four or more (of the 11 criteria are required to be displayed)

43
Q

What are essentials of diagnosis for SLE? (7)

A
  • Occurs mainly in young women
  • Rash over areas exposed to sunlight
  • Joint symptoms in 90% of patients.
  • Multiple system involvement
  • Anemia, leukopenia, thrombocytopenia
  • Glomerulonephritis, central nervous system disease, and complications of antiphospholipid antibodies are major sources of disease morbidity
  • Serologic findings: ANA (100%), anti-native DNA, antibodies (-2/3), and low serum complement levels (particularly during disease flares)
44
Q

What is systemic sclerosis?

A

A tissue hardening disease where dense connective tissue replacement happens in dermis of skin, submucosa of esophagus and parts of GI, heart, lungs, kidneys.

45
Q

what population and age does systemic sclerosis occur most often in?

A

Middle-aged (3rd - 5th decade) women (2-3x)

46
Q

How many forms of systemic sclerosis are there?

A

2 forms: limited and diffuse

47
Q

what are the clinical features of limited systemic sclerosis (CREST syndrome)? (5)

A

1) Calcinosis cutis (Calcium deposits form under the skin on the fingers or other areas of the body) 2) Raynaud’s phenomenon (spasm of blood vessels in the fingers or toes in response to cold or stress) 3) Esophageal dysfunction (represents esophageal dysmotility, which can cause difficulty in swallowing; part of Gl hypomobility) 4) Sclerodactyly (tightening of the skin causing the fingers to bend) 5) Telangiectasia (dilated vessels on the skin of the fingers, face, or inside of the mouth)

48
Q

what are the clinical features of diffuse systemic sclerosis? (3)

A

1) Skin involvement includes trunk and proximal extremities 2) More widespread organ involvement including kidney, lung, heart 3) Gl hypomobility as seen in Limited form

49
Q

what are some hematological findings for systemic sclerosis?

A

Mild anemias are possible (hemolytic and factor deficiency; iron and vitamin B12

50
Q

what are some urinalysis findings for systemic sclerosis?

A

Proteinuria when renal involvement is present

51
Q

what are some serological findings for systemic sclerosis?

A

1) ANA (80-95%) 2) Anti-scleroderma antibody (Scl-70) - 30% of diffuse clinical presentation and 20% with crest 3) Anti-centromere antibody present in 50% of CREST

52
Q

What 2 other tests can be helpful with diagnosing systemic sclerosis?

A

Barium wallow and skin biopsy

53
Q

What are th essentials of diagnosis of systemic sclerosis?

A
  • Limited disease (80%): thickening of skin confined to the face,~neck, and distal extremities
  • Diffuse disease (20%): widespread thickening of skin, including truncal involvement, with ares of increased pigmentation and depigmentation
  • Raynaud phenomenon and ANA are present in virtually all patients
  • Systemic features of gastroesophageal reflux, hypomotility of Gl gract, pulmonary fibrosis, pulmonary hypertension, and renal involvement
54
Q

What are the 2 types of idiopathic inflammatory myopathies?

A

Polymyositis and dermatomyositis

55
Q

what are idiopathic inflammatory myopathies?

A

Two pathologically distinct diseases with very similar muscular involvement that are the most frequent primary myopathies observed in adults with the most common symptom of muscle weakness

56
Q

what gender, ethnicity and age do idiopathic inflmmatory myopathies occur most often in?

A

Women afflicted twice as much as men; onset usually between 5-6th decade of life; greater incidence in blacks (especially polymyositis)

57
Q

What does polymyositis affect only?

A

Muscular involvement only

58
Q

What muscle groups are usually affected in polymyositis?

A

Proximal upper and lower extremity and neck flexor muscle group weakness: 1) Leg weakness usuall precedes upper extremity involvement 2) patients have difficulty rising from a chiar or climbing stairs

59
Q

is pain and tenderness the usual chief complaint for polymyocitis?

A

no, rarely the chief complaint (pain and tenderness usually occurs around 25% of the time)

60
Q

How often does dysphagia occur with polymyositis?

A

25.00%

61
Q

what is a late sign of polymyositis?

A

Muscle atrophy and contracture

62
Q

What does dermatomysoitis involve?

A

Muscle involvement as seen in polymyositis plus dermatologic manifestations of a rash over the butterfly area of the face (similar to SLE), neck, shoulders, and upper chest and back (shawl sign)

63
Q

What orbital symptoms occurs with dermatomyositis?

A

Periorbital edema’with purplish coloration over the upper eyelids

64
Q

what occurs in the hands with dermatomysoitis?

A

Hands have scaly patches on dorsum of PIP and MCP joints (Gottron’s sign); papules over the knuckles; erythema under the nails

65
Q

What lab findings occur with idiopathic inflammatory myopathies? (5)

A

1) Absence of anemia, elevated ESR, or RF 2) ANA in most patients 3) Anti-Jo-1 in Antisynthetase Syndrome patients o Elevated CK (and Aldolase) is the best test 4) EMG helpful but not specific for the condition 5) Muscle biopsy of involved muscles most specific laboratory finding

66
Q

how many patients (especially with dermatomysoitis) experience occult malifnancies?

A

25.00%

67
Q

what recommended evaluations should be included for idiopathic inflammatory myopathies?

A

1) CBC 2) expanded biochemical profile 3) SPEP 4) Urinanalysis 5) Age-and risk appropriate screening tests

68
Q

What are the essentials of diagnosis for idiopathic inflammatory myopathies? (4)

A

1) Bilateral proximal muscle weakness 2) Characteristic cutaneous manifestation in dermatomyositis (Gottron papules, heliotrope rash)3) Diagnostic tests: elevated creatine kinase, muscle biopsy, EMG, MRI 4) Increased risk of malignancy, particularly in dermatomyositis

69
Q

What is Mixed connective tissue disease (MCTD)?

A

Disorder that contains elements of SLE, PSS, and inflammatory myopathy

70
Q

What are some clinical features of MCTD?

A

1) Arthritis (90-95%) 2) Raynaud’s phenomenon (80-90%) 3) Abnormal esophageal motility (70%) 4) Fever (30%)

71
Q

What are the laboratory findings of MCTD?

A

ANA (95%) and Anti-RNP; if positive, disease will likely evolve to SLE

72
Q

What is Sjogren syndrome?

A

Autoimmune mediated chronic dysfunction of exocrine glands in many areas of the body

73
Q

what gender and age does Sjogren’s occur most often in?

A

90% of patients with Sjorgren’s are women with average of age onset; 50 years; 2-5% of female population over 55 years old have Sjogren’s (second in incidence to rheumatoid arthritis)

74
Q

What are the clinical features of Sjogren Syndrome (4)

A

1) Keratoconjunctivitis 2) Xerostomia 3) Enlarged parotid glands 4) Loss of ability to taste and smell 5) Desiccation of nose, throat, larynx, bronchi, vagina, and skin

75
Q

what are some extraglandular multiple systemic complaints that can occur with sjogren Syndrome? (7)

A
o Dysphagia 
o Vasculitis 
o Pleuritis 
o Obstructive lung disease 
o Neuropsychiatric dysfunction (peripheral neuropathies) 
o Pancreatitis 
o Nephritis
76
Q

what is primary Sjogren (aka SICCA SYNDROME)?

A

Involves salivary, lacrimal, and labial glands, and possible multi-organ involvement

77
Q

What is secondary sjogren?

A

o Incorporates most components of primary Sjogren’s plus components of RA or SLE; not always called secondary

78
Q

What are the lab findings like for Sjogren syndrome? (5 serological, 3 hematological)

A

1) Hematology - Mild anemia with leukopenia and eosinophilia

2) Serology
o ANA (95%)
o Anti-SSA (65%)** (presence tends to correlate with extraglandular manifestations)
o Anti-SSB (65%)** (presence tends to correlate with extraglandular manifestations)
o RF(75%)
o Polyclonal hypergammaglobulinemia

79
Q

What are the essentials of diagnosis for Sjogren’s? (4)

A
  • Women are 90% of patients; the average age is 50 years
  • Dryness of eyes and dry mouth (sicca components) are the most common features; they occur alone or in association with rheumatoid arthritis or other connective tissue diseases
  • Rheumatoid factor and other autoantibodies common
  • Increased incidence of lymphoma
80
Q

what do polymyalgia rheumatica (PMR) and Giant Cell Arteritis (GCA) have in common?

A

Both representat a spectrum of the same disease and both affect the same patient population (>50 years)

81
Q

What is polymyalgia rheumatica aka PMR characerized by? (2)

A

1) Pain and stiffness in proximal limb girdle joints (shoulders and hips), and lower back 2)Pain and stiffness in proximal limb girdle joints (shoulders and hips), and lower back

82
Q

What systemic changes are often seen with PMR?

A

Often accompanied by fever, malaise, weight loss

83
Q

How often does PMR occur without GCA?

A

2/3 of patients have PMR without coexisting GCA

84
Q

what does PMR often respond quickly to?

A

low dose prenisone

85
Q

what lab evaluation is done for PMR?

A

1) Rapid (elevated) ESR 2) Possible anemia 3) Positive artery biopsy if coexists with GCA

86
Q

What is temporal arteritis aka giant cell arteritis?

A

Granulomatous inflammation disrupting internal elastic membrane in medium and large sized arteries

87
Q

What are the lab findings like for giant cell arteritis aka temporal arteritis?

A

50% will be anemica. Most consitant finding is elevated ESR. Temporal artery biopsy is also done.

88
Q

What branches are frequenty affected by giant cell arteritis?

A

branches of the aorta including temporal artery

89
Q

what are some clinical signs of giant cell arteritis?

A
  • Headaches +/- tender or nodular temporal arteries
  • Probable visual disturbances; blindness if not treated in a timely fashion
  • Weight loss; jaw claudication; myalgias and arthralgias
90
Q

What are some laboratory findings for giant cell arteritis?

A
  • Anemia (50%) + leukocytosis
  • Elevated ESR is most consistent finding most commonly in excess of 100 mm/hr, but some patients have a normal ESR
  • Temporal artery biopsy
91
Q

What are the essentials of diagnosis for PMR and GCA?

A

o Age over 50 years
o GCA is characterized by visual abnormalities, and a markedly elevated ESR
o The hallmark of PMR is pain and stiffness in shoulders and hips lasting for several weeks without other explanation

92
Q

What are the seropositive arthropathies?(9)

A

RA, Sjogren’s, Polymyalgia Rheumatica, Giant Cell arteritis, Mixed Connective Tissue Disease, Iodiopathic inflammatory myopathies (Polymyositis and dermatomyositis), Scleroderma, Systemic Lupus Erythematosus

93
Q

What are the seronegative arthropathies? (5)

A

Ankylosing Spondylitis, Psoriatic arthritis, Reactive arthritis, Enteropathic Arthritis (colic Arthritis, arthritis associated with inflammatory bowel disease) and Gouty Arthritis

94
Q

What is ankylosing sponylitis?

A

a chronic systemic inflammatory disorder of the axial skeleton and large peripheral joints. SI is the hallmark feature.

95
Q

What is another name for AS?

A

Marie-Strumpell Disease

96
Q

What is the hallmark future of AS?

A

Sacroiliitis is the hallmark feature

97
Q

What histocompatibility antigen is AS associated with?

A

antigen HLA-B27

98
Q

What gender, ethnicity and age does AS mostly occur in?

A

Male predominant, Caucasian predominates over African-American and Usual age of onset between 20-40 years old

99
Q

What clinical findings are found with AS? (6)

A

1) Bouts of low back pain may begin in late adolescence or early adulthood 2) Pain and stiffness worse with periods of inactivity 3) Progressive loss of back ranges of motion; progresses cephalado 4) May lead to radicular pain syndromes 5) May involve peripheral joints 6) Common to have inflammatory eye involvement.

100
Q

What laboratory findings are there for AS?

A

1) (+)HLA-B27 (>90%)
• With the incidence of AS being 1:1000 plus the percentage of normal individuals with a (+)HLA-B27 (8% healthy Caucasians, 2% blacks), most people who have a (+)HLA-B27 do not have AS
• A negative HLA-B27 is evidence against the diagnosis of AS (unless there is overwhelming clinical and radiologic evidence in favor of the diagnosis)
2) Elevated ESR with active disease (80-90%) 3) Mild anemia (25%)

101
Q

What are the essentials of diagnosis for AS? (5)

A

1) Chronic low backache in young adults, generally worst in the morning
2) Progressive limitation of back motion and of chest expansion
3) Transient (50%) or persistent (25%) peripheral arthritis o Anterior uveitis in 20-25%
4) Diagnostic radiographic changes in sacroiliac joints
5) HLA-B27 testing is most helpful when there is an indeterminate probability of disease

102
Q

What is Psoriatic arthritis?

A

inflammatory arthropathy that combines clinical features of RA and Seronegative spondyloarthropathies.

103
Q

In what population does psoriatic arthritis occur?

A

Occurs in 5-7% of individuals with psoriasis

104
Q

What clinical findings are found with psoriatic arthritis? (5)

A
  1. Symmetric polyarthritis resembling RA but with fewer joints
  2. Oligoarthritis that is very destructive to affected joints
  3. DIP joint arthritis; monoarticular early; high incidence of nail pitting and onycholysis
  4. Arthritis mutilans; marked osteolysis
  5. Axial disease (spondylytic form); sacroiliitis and spinal joints
105
Q

What are the essentials of diagnosis for psoriatic arthritis? (4)

A

1) Psoriasis precedes onset of arthritis in 80% of cases
2) Arthritis usually asymmetric, with “sausage” appearance of fingers andtoes but a polyarthritis that resembles rheumatoid arthritis also occurs
3) Sacroiliac joint involvement common; ankylosis of the SI joints may occur
4) Radiographic findings: osteolysis, pencil-in-cup deformity,; relative lack of osteoporosis, bony ankylosis; asymmetric SI and atypical syndesmophytes

106
Q

What is reactive arthritis and what is it aka?

A

aka reiters syndrome. Arthritis with specific nonarthicular manifestations that appear shortly after certain infections (shigella, salmonella and campylobacter) of genitourinary or GI tract.

107
Q

Who will usually get reactive arthritis?

A

Predominantly observe in young men and higher incidence in caucasians

108
Q

What are some clinical findings for reactive arthritis?

A

Urethritis, Arthritis, conjuctivitis and mucocutaneous lesions

109
Q

What does urethritis entail for reactive arthritis?

A

Usually occurs first (dysuria and mucopululent discharge) if the dysenteric form causitive organisms are shigella, Salmonella, Campylobacter, Yersinia

110
Q

What does arthritis entail for reactive arthritis?

A

Arthritis follows 1-4 weeks after infection; asymmetric usually affecting largerweight-bearing joints

1) Knees
2) Ankles
3) Small joints of feet, hands, wrists
4) Elbow
5) Possibly sacroiliac joints (50% incidence of low back pain)
6) Joints appear similar to a septic joint but are sterile

111
Q

What does Conjuctivitis entail for reactive arthritis?

A

Conjunctivitis (or iritis) which occurs at same time or a few days after onset of antecedent infection

112
Q

What does mucocutaneous lesions entail for reactive arthritis?

A

Mucocutaneous lesions may form around the mouth and eyes, and there is a classic maculopapular rash that occurs on the feet called keratoderma blennorrhagicum

113
Q

What are the lab findings for Reactive Arthritis?

A

1) (+)HLA-B27 in -85% of the patients

2) Elevated ESR - 70% 3) Anemia, leukocytosis, and thrombocytosis -30%

114
Q

What are the essentials of diagnosis for Reactive Arthritis? (3)

A

o 50-80% of patients are HLA-B27 positive
o Oligoarthritis, conjunctivitis, urethritis, and mouth ulcers most commonfeatureso Usually follow dysentery or a sexually transmitted infection

115
Q

What is acute Rheumatic fever?

A

A systemic immune respone to infectious pharyngitis with group A beta-hemolytic streptococcus and causes focal granulomatous reaction with vasculitis, hence an inflammatory reaction in various tissues, necrosis of collagen.

116
Q

What are the lab findings for acute rheumatic fever?

A

ESR is usually elevated. Anti streptolysin-O or anti-DNAseB will develop 7-10 days after infection and be highest 3 weeks after infection and will not be detectable after 12 months. Throat cultures usually negative when ARF is suspected.

117
Q

What is Adult rheumatoid arthritis?

A

A systemic inflammatory disease that predominantly manifests in the synovial membrane of diarthroidal joints. This will develop in a genetically predisoped person, but exogenous triggers have not been identified. The inflammatory process causes changes in cellular composition and gene expression of the synovial membrane leading to hyperplasia of synovial fibroblasts and structural damage of cartilage, bone and ligaments.

118
Q

What are the Lab findings for adult RA?

A

Best test is Anti-CCP which has 60% sensitivity and a 98-99% specificity. ESR or CRP can be used to monitor the course. RF is only 75-85% sensitive and 60-65% specific. RF is seen with a lot of other conditions. Hematology- microcytic- hypochromic anemia with low ferritin and this makes the anemia hard to distinguish from iron deficiency anemia.

119
Q

What are serongegative spondyloarthorpathies?

A

Diseases without RF.

120
Q

What is enteropathic arthritis aka colic arthritis?

A

peripheral and or spondylitic arthritis that develops in 20% of patients with inflammatory bowel disease. Most commonly seen with chrons and ulcerative colitis.

121
Q

What are some clinical findings of Enteropathic arthritis?

A

1) Peripheral arthritis
• Non-deforming asymmetric oligoarticular of large joints Clinical course of the arthritis parallels course of the IBD
• Onset of arthritis is usually months to years after onset of IBD
• Occasionally onset of arthritis is very early and occupies the patient’s attention such that they ignore the early bowel symptoms
2) Spondylitic form
• Clinically and radiologically similar to ankylosing spondylitis
• Arthritis follows a course independent of the course of the bowel disease3) Post-jejunoileal bypass surgery
• Symmetric inflammatory polyarthritis of small or large joints; incidence is 15% of patients who have this surgery

122
Q

What is whipple’s disease?

A

o An uncommon gastrointestinal abnormality caused by an infection with the bacillus Tropheryma whippeiii which causes chronic diarrhea, malabsorption, abdominal distention, and weight loss

123
Q

How many whipple’s disease patients will experience enteropathic arthritis?

A

2/3 of these patients develop a mild large-joint polyarthritis which precedes the gastrointestinal manifestations

124
Q

What laboratory findings are there for enterpathic

A

1) (+)HLA-B27 in approximately 50% of patients with spondyliticinvolvement
2) Elevated ESR
3) (+)RF (+)ANA in Jl bypass patients

125
Q

What is gouty arthritis?

A

Recurrent arthritis of peripheral joints that results from deposition, in and about the joints and tendons, pf crystals of monsodium urate from supersaturated hyperuricemic body fluids. This arthritis can become chronic and deforming.

126
Q

What gender, and age does gouty arthritis occur in?

A
  • 90% males

* Occurs after age of 30 years (females catch up in incidence post-menopause)

127
Q

What are the common causes of sustained hyperuricemia? (3)

A

1) Decreased renal clearance of urate (chronic diuretic therapy and primary renal diseases in which there is a decreased GFR
2) Increased purine synthesis: primary abnormality of unknown cause, increased nucleoprotein turnover in hematologic conditions
3) Dietary considerations: following overindulgence in rich foods, especially if alcoholic beverages are also consumed

128
Q

What are the clinical features of gouty arthritis? (5)

A

1) First acute attack usually occurs at night in the MP joint of the big toe (podagra); possibly the feet, ankles, knees
2) Joint is swollen, exquisitely tender, with the overlying skin tense and dusky red
3) Rapid reduction of pain and inflammation with use of NSAIDS
4) Often accompanied by a fever
5) Tophi in the ears, hands, feet, olecranons, prepatellar bursas after several acute attacks

129
Q

When do the monosodium urate crystals typically deposit?

A

When no motion occurs: depositis in synovial fluid at night so therefore pain in the morning. Does not affect blood b/c blood is constantly moving

130
Q

What are the laboratory findings for gouty arthritis? (4)

A
  • Hyperuricemiao Present in >90% of patients during first attack (often need serial determinations)o 25% incidence of normal uric acid levels if only a single determination
  • Leukocytosis
  • Elevated ESR
  • Monosodium urate crystals in synovial joint fluid or from tophi
131
Q

What are the essentials of diagnosis for Gouty arthritis? (5)

A
  • Acute onset, typically nocturnal and usually monarticular, often involving the first MTP joint
  • Polyarticular involvement more common in patients with long-standing disease
  • Identification of urate crystals in joint fluid or tophi is diagnostic
  • Dramatic therapeutic response to NSAIDs
  • With chTonicity, urate deposits in subcutaneous tissue, bone, cartilage, joints, and other tissues
132
Q

What are the different types of infectious arthritis? (4)

A

Nongonococcal Septic arthirtis, Gonococcal septic arthritis, Lyme disease, Acute rheumatic fever

133
Q

What is infectious arthritis?

A

arthritis resulting from infection of synovial tissue with pyogenic bacteria or less commonly other infectious agents.

134
Q

What is nongonococcal septic arthritis and who does it usually affect?

A

A type of infectious arthritis commonly seen in IV drug abusers, immunocompromised, joints damaged by things like RA, recent prosthetic or arthroscopic surgical procedures.

135
Q

What are the clinical findings of nongonococcal septic arthritis?

A

• Sudden acute pain, swelling, and heat at the infected joint; possible (80% of the time) chills and fever
• Infected joints are most often monoarticular
1) Knee (most common)
2) Hips
3) Wrists
4) Shoulders
5) Ankles

136
Q

What are the laboratory findings for nongonococcal septic arthritis? (4)

A

1)Synovial fluid analysis
2) High WBCs; neutrophils
3) Infectious agents cultured
o Staphylococcus aureuso Group A and B Streptococcus
o Escherichia coli
o Pseudomonas aeruginosa
4) Routine laboratory findings are variable and not very sensitive or specific:
o Leukocytosis
o Increased ESR

137
Q

What would be seen with imaging in nongonococcal septic arthritis?

A
  • Plain fiim radiographs insensitive early in the infection

* Progresses to bony erosions, joint space narrowing, osteomyelitis, periostitis.

138
Q

Whare the essential of diagnosis for nongonococcal septic arthritis? (4)

A
  • Acute onset of inflammatory monoarticular arthritis, most often in large weight-bearing joints and wrists
  • Previous joint damage or injection drug abuse common risk factors
  • Infection with causative organisms commonly found elsewhere in body
  • Joint effusions are usually large, with WBC counts commonly > 50K/mcL
139
Q

What is gonococcal septic arthritis and who does it usually affect?

A

a type of infectious arthritis commonly seen in women 2-3 times more than males (rarely after 40 years old), also seen in homosexual males.

140
Q

What are the clinical findings of gonococcal septic arthritis?

A

1) Up to four days of a migratory polyarthralgia including wrists, knees, ankles, elbows, followed by one of two patterns• Tenosynovitis of wrist, fingers, ankles or toes (60%)• Purulent monarthritis of knee, wrist, ankle, or elbow (40%)
2) Pustules on palms of hands or soles of feet
3) Possible Fever

141
Q

What are the laboratory findings of gonococcal septic arthritis (2)

A

1) Synovial fluid analysis
• High neutrophils
• Possible positive Gram stain and culture
2) Blood, urethral, throat, and rectal cultures may be of help

142
Q

What would be seen with imaging for gonococcal septic arthritis?

A

Imaging reveals soft tissue swelling at best

143
Q

What are the essentials of diagnosis for gonococcal septic arthritis? (7)

A
  • Prodromal migratory polyarthralgias
  • Tenosynovitis most common sign
  • Purulent monarthritis in 50%
  • Characteristic skin lesions
  • Most common in young women during menses or pregnancy
  • Symptoms of urethritis frequently absent
  • Dramatic response to antibiotics
144
Q

What is lyme disease?

A

a potentially multisystem inflammatory disease that can occur in anyone bitten by Ixodes tick that spreads the infection of the spirochete borrelia burgdorferi.

145
Q

How long does the tick need to be feedings for it to have a significant likleyhood of infection?

A

at least 24-36 hours but a decreased lieklihood of infection if feedings <72hours

146
Q

How many clinical stages occurs with lyme dusease and most other spirochete diseases?

A

3

147
Q

What occurs in stage 1 of Lyme Disease?

A

After a 3-32 day incubation period (7-10 day average), a classic rash callederythema migrans (EM; 80-90% incidence) forms and lasts 3-4 weeks

148
Q

What usually accompanies the erythema migrans?

A

Accompanied by flu-like fever, chills, fatigue, malaise, headache, myalgias, and(50% incidence) arthralgias

149
Q

What occurs in stage 2 of Lyme Disease?

A

Early disseminated infection (weeks - months after inoculation; hematogenous and lymphatic spread)

150
Q

What bodily systems are affected by stage 2 of Lyme disease? (5)

A

Constiutional, Skin, CNS, Musculoskeltal system and cardiac

151
Q

What are the constituational symptoms exhibited in Stage 2 of Lyme disease? (3)

A

Malaise, fatigue and fever

152
Q

What are the Skin symptoms exhibited in Stage 2 of Lyme disease?

A

Smaller papular lesions not a bite site

153
Q

What are the CNS symptoms exhibited in Stage 2 of Lyme disease? (5)

A

o Aseptic meningitis o Encephalitis o Bell’s palsy o Headacheo Mood swings, irritability, personality changes

154
Q

What are the Musculoskeletal symptoms exhibited in Stage 2 of Lyme disease?

A

o Migratory pains in joints, musclesftendons)

155
Q

What are the cardiac symptoms exhibited in Stage 2 of Lyme disease? (4)

A

o Myocarditiso Pericarditiso Arrhythmiaso Heart block

156
Q

When does Stage 3 (latepersistent infection) of Lyme Disease usually occur and does it have to be preceded by stages 1 and 2?

A

Occurs months to years after initial infection, and may not be preceded byapparent Stages 1 and 2

157
Q

What bodily systems are affected by stage 3 of Lyme disease? (3)

A

Musculoskeletal, neurologic and skin

158
Q

What are the Musculoskeletal symptoms exhibited in Stage 2 of Lyme disease? (2)

A

1) Joint and periarticular pain similar to or perhaps fibromyalgia 2) Chronic/recurrent large joint arthritis 3) Chronic (and possibly debilitating) synovitis

159
Q

What are the Neurologic symptoms exhibited in Stage 2 of Lyme disease? (1)

A

o Subacute encephalopathy• Memory loss, modd changes, sleep disturbances• Axonal polyneuropathies

160
Q

What are the Skin symptoms exhibited in Stage 2 of Lyme disease? (1)

A

o Acrodermatitis chronicum atrophicans

161
Q

What is the national surveillance definition for lyme disease?

A

A person with exposure to a potential tick habitat (within the 30 days just prior to developing erythema migrans) with:1. Erythema migrans diagnosed by a physician2. At least one late manifestation of the disease3. Laboratory confirmation

162
Q

What are the non specific lab findings for stage 1 of Lyme disease? (4)

A

Non-specific lab changes in Stage 1 include:• Mildly elevated ESR (-50%)• Mildly elevated liver enzymes (~30%)• Mild anemia with mild leukocytosis (-10%)• Microscopic hematuria (“10%)

163
Q

What are the specific lab findings for stage 1 of Lyme disease? (2)

A

Detection of Antibodies to the Borrelia spirochete• SCREEN detection of TOTAL ANTIBODY via IP A or ELISA method• CONFIRMATION detection oflgM and IgG via Western Blot; done on all positive or equivocal positive ELISA (many diseases can cause false positive ELISA)

164
Q

What is an ELISA test?

A

Used to detect antibodies

165
Q

What are the essentials of diagnosis for Lyme Disease? (4)

A

1) Erythema migrans 2) Headache or stiff neck3) Arthralgias, arthritis, and myalgias; arthritis is often chronic and recurrent4) Wide geographic distribution, with most US cases in NE, mid-Atlantic, upper Midwest, and Pacific coastal regions

166
Q

What is acute Rheumatic fever (ARF)?

A

Systemic immune response following 0.3% of cases of infectious pharyngitis withgroup A beta-hemolytic Streptococcus

167
Q

What does acute Rheumatic fever cause?

A

Causes focal perivascular granulomatous reaction with vasculitis; hence aninflammatory reaction in various tissues; necrosis of collagen

168
Q

In what age group does ARF occur?

A

Host factors: 5-15 years old

169
Q

What clinical findings are seen with ARF?

A

Onset of signs and symptoms commence 2-3 (range 1-5) weeks after infection

170
Q

How is ARF diagnosed?

A

Diagnosis is based on a combination of Jones criteria (two major criteria, or one major and two minor criteria

171
Q

What are the systemic sympoms that make up the major criteria for diagnosing ARF?

A

1) Carditis, 2) Erthema marginatum and subcutaneus nodules 3) Sydenham’s chorea 4) Polyarthritis

172
Q

What conditions are part of the major criteria of carditis for ARF?

A

• Pericarditis• Cardiomegaly• Congestive failure• Mitral or aortic regurgitation murmurs• ECG changes• Altered heart sounds• Arrhythmias

173
Q

What are erythema marginatum?

A

EM are rapidly enlarging macules that change into rings with a clear center

174
Q

What are subcutaneous nodules specific to ARF?

A

Subcutaneous nodules are small (< 2cm) and firm andare attached to fascia or tendon overlying bonyprominences; lasts for days or weeks, and recur

175
Q

What are sydenham’s chorea?

A

Involuntary movement disorder of the face, tongue, and upper extremities

176
Q

What is polyarthritis in regards to ARF?

A

Migratory in nature involving large joints

177
Q

What are the minor criteria for ARF?

A

o Fevero Polyarthralgias o Reversible prolonged PR interval • o” Rapid sedimentation rate or positive CRP ‘ o Evidence of antecedent fi-hemolytic strep infection

178
Q

What are the laboratory findings for ARF?

A

o ESR/CRP (see above)o Antistreptolysin-0 test (ASO) or Anti-DNAse B- Develops within 7-10 days after onset of infection; highest titer by 3rd week of ARF; diminishes slowly to none detectable by 12 monthso Throat cultures are often negative once ARF is suspected; A positive throat culture does not rule in ARF, nor does a negative culture rule out ARF

179
Q

What are the essentials of diagnosis for ARF?

A

• Uncommon in the US; more common in developing countries• Peak incidence ages 5-15 years• Diagnosis based on Jones criteria and confirmation of streptococcal infection• May involve mitral and other valves acutely, rarely leading to heart failure

180
Q

What is Serum Thyrotropin Assay?

A

TSH

181
Q

Where is TSH secreated from and what does it respond to?

A

Secreted by the anterior pituitary in response to altered TRH, T4 and T3

182
Q

What kind of serum test is Serum Thryrotropin assay?

A

a single serum test to screen for the status of thyroid function

183
Q

What does increased TSH suggest?

A

Increased TSH suggests hypothyroidism

184
Q

What does normal TSH suggest?

A

Normal TSH suggests euthyroid; no follow up tests are indicated

185
Q

What does decreased TSH suggest and what is it confirmed by?

A

Decreased TSH suggests hyperthyroidism (or rare hypopituitary); confirmed with standard FT4, TT4. FT4I, T3, etc.

186
Q

What is free thyroine (FT4)?

A

Assay of the non-protein bound, physiologically active portion of T4

187
Q

Is the FT4 affected by many non-thyroidal influences?

A

No, Not affected by many of the non-thyroidal influences that can alter the TT4

188
Q

Is FT4 a good indicator of thyroid function?

A

Yes, Measurement of FT4 is a better indicator of thyroid function

189
Q

What is Total serum thryoxine (TT4)?

A

TT4 is a measure of total circulating levels of T4. TT4 is profoundly affected by altered levels of carrier proteins (especially TBG). Usually >99% of circulating T4 is protein bound to albumin, pre-albumin, and TBG and Protein bound T4 is not physiologically active

190
Q

Can non thyroidal illnesses cause altered TT4 assay results?

A

Yes, Certain non-thyroidal illnesses, physiologic and pharmacologic challenges result in altered TBG production and hence altered TT4 assay results, yet the patient is euthyroid (normal thyroid function)

191
Q

What is Free T4 index (FT4I)?

A

Calculated (not directly assayed) value reflecting the level of circulating free {non-protein bound, physiologically active) thyroxine

192
Q

What does the free T4 index use for calculations?

A

Calculation utilizes the TT4 assay and THBR

193
Q

What is the Free T4 index intended for?

A

This value takes into account altered levels of TBG production and, therefore, better reflects the functional status of the thyroid gland than does the TT4 assay.

194
Q

What is T3RU (T 3 resin uptake)?

A

Estimate of the number of unbound (unsaturated) thyroid hormone-binding sites on serum protein (primarily TBG) using an Indirect estimate of T4 when there is normal amounts of thyroid-binding proteins

195
Q

Is T3RU used routinely to gauge

A

THBR is not routinely used as a separate test to gauge thyroid function

196
Q

What is Free T3?

A

Direct assay of the very minute level of circulating free triiodothyronine

197
Q

What is the Free T3 (FT3) good for diagnosing?

A

Clinical value in diagnosing hyperthyroidism in women who are pregnant or taking estrogen

198
Q

How does T3RU allow for calculation of FT4I?

A

Used in combination with TT4 assay to calculate the FT4I

199
Q

What is serum triiodothryonine assay (TT3)?

A

Measure of the total amount of circulating T3, Similar to T4, >99% of T3 circulates bound to carrier proteins

200
Q

What does serum TT3 mean?

A

TT3 elevated in hyperthyroidism due to both increased T4 production and T3 thyrotoxicosis

201
Q

What are TT3 levels affected by?

A

TT3 levels are affected by alterations in protein (TBG, albumin, pre-albumin) levels

202
Q

What is hypothyroidism

A

•Clinical manifestations caused by hypometabolism due to lack of action of thyroid hormones on target tissues

203
Q

what are some constitutional symptoms of hypothyroidism?

A

fatigue, Lethargy, cold intolerance, decreased appetite

204
Q

what are some constitutional signs of hypothyroidism?

A

weight gain

205
Q

what are some cardiovascular symptoms of hypothyroidism?

A

Soft tissue swelling

206
Q

what are some cardiovascular signs of hypothyroidism?

A

bradycardia, diastolic hypertension, soft heart sounds and edema

207
Q

what are some pulmonary symptoms of hypothyroidism?

A

Snoring

208
Q

what are some pulmonary signs of hypothyroidism?

A

sleep apnea, hypoventilation, dyspnea on exertion

209
Q

what are some GI symptoms of hypothyroidism?

A

constipation, abdominal ditension

210
Q

what are some GI signs of hypothyroidism?

A

Ileus

211
Q

what are some GU symptoms of hypothyroidism?

A

Menorrhagia or amenorrhea

212
Q

what are some GU signs of hypothyroidism?

A

Galactorrhea

213
Q

what are some musculoskeletal symptoms of hypothyroidism?

A

Muscle stiffness, muscles cramps, arthalgias, myalgias

214
Q

what are some musculoskeletal signs of hypothyroidism?

A

Weakness, carpal tunnel syndrome

215
Q

what are some neuro-psychiatric symptoms of hypothyroidism?

A

Slowed mentation, memory impairment, anxiety, depression, headache, paresthesias

216
Q

what are some neuro-psychiatric signs of hypothyroidism?

A

Hyporeflexia, ataxia, dementia, psychosis, coma

217
Q

what are some dermatologic symptoms of hypothyroidism?

A

Dry skin

218
Q

what are some dermatologic signs of hypothyroidism?

A

Swelling, pallor, yellow hue

219
Q

what are some otolargyngological symptoms of hypothyroidism?

A

Hoarseness, decreased hearing

220
Q

what are some otolargyngological signs of hypothyroidism?

A

Middle ear effusion

221
Q

What signs and symptoms are most common for hypothyroidism? Specific or non specific?

A

Most common signs and symptoms are nonspecific and easily attributable to other disease, agining or life stresses and the mnifestations occur gradually.

222
Q

what are the causes of hypothyroidism? (5)

A

1.Autoimmunethyroidits(Hashimoto’ sthyroiditis) 2.Thyroprivicorpost-abiative 3.Goitrous(iodinedeficiency) 4.Neonatal(Cretinism ) 5.Central(Secondar yorsuprathyroid)

223
Q

Which cause of hypothyroidism requires use of anti-thyroid antibody testing?

A

autoimmune thyroid thyroiditis (hasthimoto’s thyroiditis)

224
Q

With hypothyroidism what happens to thyrotropin (TSH) levels?

A

increased

225
Q

With hypothyroidism what happens to total thyroxine (TT4 or FT4I) levels?

A

Decreased

226
Q

With hypothyroidism what happens to Free T4 levels?

A

Decreased

227
Q

With hypothyroidism what happens to total and free T3 levels?

A

Decreased

228
Q

With hypothyroidism what happens to antithryoglobulin antibody?

A

Increased (70% in Hashimoto’s)

229
Q

With hypothyroidism what happens to antithyroperoxidase (Anti-TPO) antibody?

A

Increased (95% in Hashimoto’s)

230
Q

What kind of anemia is seen with hypothyroidism?

A

Macrocytic anemia (decreased RBC count, Hbg, Hct but increased MCV)

231
Q

What happens to total and ldL cholesterol, triglyceride and Lipoportein A in hypothyroidism?

A

increased

232
Q

What happens to serum glucose and sodium in hypothyroidism?

A

Low

233
Q

what happens to liver enzymes and CK in hypothyroidism?

A

Increased

234
Q

What are the essentials of diagnosis for hypothyroidism?

A

•Weakness, fatigu, cold intolerance, constipation, weight change, depression, menorrhagia, hoarseness •Dryskin, bradycardia, delayed return of deep tendon reflexes •Anemia, hyponatremia, hyperlipidemia •FT4 level is usually low •TSH elevated in primary hypothyroidism

235
Q

What is thyrotoxicosis (hyperthyroidism)?

A

•Metabolic and widespread organ system manifestations of elevated thyroid hormone concentrations

236
Q

What are some constitutional symtpoms for thyrotoxicosis?

A

nervousness, restlessness, heat intolerance, fatigue, increased appetitie, insomni

237
Q

What are some constitutional signs for thyrotoxicosis?

A

Weight loss

238
Q

What are some cardiovascular symptoms for thyrotoxicosis?

A

palpitations, chest pain

239
Q

What are some cardiovascular signs for thyrotoxicosis?

A

tachycardia, atrial arrhythmias, systolic hypertension

240
Q

What are some pulmonary symtpoms for thyrotoxicosis?

A

dyspnea (exertional

241
Q

What are some pulmonary signs for thyrotoxicosis?

A

none

242
Q

What are some GI symtpoms for thyrotoxicosis?

A

Hyperdefection (diarrea), abdominal pain

243
Q

What are some GI signs for thyrotoxicosis?

A

borborygmi (stomach rumble)

244
Q

What are some GU symtpoms for thyrotoxicosis?

A

Frequent urination, decreased libido, amenorrhea or impotence

245
Q

What are some GU signs for thyrotoxicosis?

A

Gynecomastia

246
Q

What are some Musculoskeletal symtpoms for thyrotoxicosis?

A

Proximal muscle weakness (thighs), muscle cramps

247
Q

What are some musculoskeletal signs for thyrotoxicosis?

A

osteopenia

248
Q

What are some neuro-psychiatric symtpoms for thyrotoxicosis?

A

Tremor, anxiety, depression

249
Q

What are some neuro-psychiatric signs for thyrotoxicosis?

A

delirium, psychosis

250
Q

What are some Ophthalmologic symtpoms for thyrotoxicosis?

A

Sense of irritation, gritiness, sensitiviy to light, double vision, sense of pressure in the eyes

251
Q

What are some Ophthalmologic signs for thyrotoxicosis?

A

Exophthalmos, conjunctival redness

252
Q

What are some Dermatologic signs for thyrotoxicosis?

A

increased sweating and oiliness, pruritus

253
Q

What are some dermatologic signs for thyrotoxicosis?

A

Velvety moist skin, urticaria, acne

254
Q

What are the 5 causes of hyperthyroidism?

A

1.Autoimmune (Grave’s Disease)2.Subacute (deQuervain) thyroiditis 3.Toxic nodule(s) 4.Drug-induced (thyrotoxicosisfactitia ) 5.T 3 thyrotoxicosis

255
Q

What cause of hyperthyroidism requires use of anti-thyroid antibody testing?

A

autoimmune (Grave’s disease)

256
Q

With hyperthyroidism what happens to thyrotropin (TSH) levels?

A

Decreased

257
Q

With hyperthyroidism what happens to Total thyroxine (TT4) levels?

A

Increased

258
Q

With hyperthyroidism what happens to Free T4 levels?

A

Increased

259
Q

With hyperthyroidism what happens to Total and free T3 levels?

A

Increased

260
Q

With hyperthyroidism what happens to thyroid ceceptor antibodies (TRAb, Thyroid stimulating Immunoglobulins - TSI) levels?

A

Positive in Graves (65%)

261
Q

With hyperthyroidism what happens to hemoglobin levels?

A

Usually normal; possible anemia

262
Q

With hyperthyroidism what happens to total and LDL cholesterol levels?

A

Decreased

263
Q

With hyperthyroidism what happens to calcium, alkaline phosphatase levels?

A

Increased

264
Q

What are the essentials of diagnosis for hyperthyroidism?

A

•Sweating, weight loss or gain, anxiety, palpitations,loose stools,heat intolerance, irritability, fatigue, weakness, menstrual irregularity •Tachycardia; warm, moist skin, stare, tremor •In Grave’s disease:goiter often with bruit, ophthalmopathy •Suppressed TSH in primary hyperthyroidism, increased T4, FT4, T3, FT3

265
Q

What thyroid tests are used for screening?

A

TSH and FT4

266
Q

What thyroid tests are used for hypothyrodisim?

A

TSH, FT4, antithyroid antibodies

267
Q

What thyroid tests are used for hyperthyroidism?

A

TSH, FT4, FT3, antithyroid antibodies

268
Q

What are some absolute indications for thyroid testing in euthyroid patients? (6)

A

1) Newborns 2) Goiter 3) History of head/neck radiation 4) Past or present treatment with thryoid medications; replacement or suppression 5) Graves’ eye disease 6) Atrial fibrillation or flutter

269
Q

What are some relative indications for thyroid testing in euthyroid patients? (3)

A

1) History of nonthyroidal autoimmune disease 2) Unexplained major weight loss or gain 3) Females over 50 years

270
Q

What is osteoarthritis?

A

The most common joint disease which can occur in anyone regarless of age, race, or geographic location. 90% of population will have some evidence by the age of 40.

271
Q

What are the lab findings for OA?

A

Imaging is key to Dx. NO signs of inflammation. Labs can be used to rule in or out other types of arthritis.

272
Q

What is fibromyalgia?

A

A chronic musculoskeletal pain syndrome of widespread pain distribution and multiple painful pints to palpation.

273
Q

What are the lab findings like for fibromyalgia?

A

Just used to rule in or out other diseases.

274
Q

Conversion of Vitamin D is under direct influence of what?

A

PTH.

275
Q

When should you check intact PTH and total serum calcium?

A

When radiographically you suspect bone density loss.

276
Q

When you have low and high amounts of serum calcium how can you tell if it is from malignancy, or hyper or hypo parathyrodism?

A

Hypoparathyroidism- if low calcium and low PTH. Malignancy- if high calcium and low PTH. Hyperparathyroidism- high calcium and high PTH.

277
Q

Colecalciferol is converted to what where?

A

25-hydroxy vitamin D in the liver.

278
Q

25-hydroxy vitamin D is converted to what and where?

A

1,25-dihydroxy vitamin D in the kidneys.

279
Q

What is Pagets disease and it is aka?

A

aka osteitis deformans. A chronic disorder of unknown origin that displayes abnormally softened bones and enlarged bone material as a result of highly vascularized weakened , heavy calcified bone with coarsely thickened lamellae and trabeculae.

280
Q

What are the lab findings like with pagets disease?

A

Markedly increased levels of alkaline phosphatase (will give you one of the highest levels), increased urinary hydroxyproline.

281
Q

What is primary hyperparathyroidism?

A

Over secretion of PTH

282
Q

What are the lab findings for hyperparathyroidism?

A

Serum chem: hypercalcemia (intermittent early and sustained later), hypophosphatemia, increased alkaline phosphatase. Urine: hypercalciuria.

283
Q

What is secondary hyperparathyroidism?

A

Hypocalcemia due to renal disease and partial resistance of the metabolic action of PTH and this low levels of serum calcium will increase PTH production.

284
Q

What are the lab findings for secondary hyperparathyroidism?

A

Hypocalcemia, hyperphosphatemia, increased alk phos, increased PTH, increased osteocalcin, increased Dpd, Increased NTX, alterned renal function studies.

285
Q

What is euthyroid?

A

Normal functioning thyroid.

286
Q

What thyroid hormone is physically active?

A

T3.

287
Q

Where is the largest amounts of T3 made at?

A

at the cellular level from T4 via an enzymatic process removing one of the iodine molecules from T4.

288
Q

What happens to T3 if T4 is over or underproduced?

A

T3 will be similarly increased or decreased besides in the one disease where the thyroid selectily overproduces just T3.

289
Q

How are most thyroid hormones released?

A

Bound to a protein called thyroid binding globulin (TBG).

290
Q

Will thyroid hormones be physically active while bound to TBG?

A

No.

291
Q

What thyroid hormone posseses the most physically active form?

A

The free portion (not bound to tbg.

292
Q

What is the best test used to evaluate thyroid funciton?

A

TSH since everyone has there own levels of normal FT4, and they can be higher and lower than other people. Increased TSH suggests hypothyroidism and decreased TSH suggests hyperthyroidism.

293
Q

What is graves and what is hashimotos?

A

Graves- hyperthyroidism. Hashimotos- Hypothyroidism.

294
Q

What are the lab test results for hypothyroidism?

A

Increased: TSH, total and LDL cholestrol, AST, CK, LDH. Decreased: TT4, THBR, FT4, Total and free T3, hemoglobin.

295
Q

What are the lab test results for hyperthyroidism?

A

Increased: TT4, THBR, FT4, Total and free T3, calcium. Decreased: TSH, Total and LDL cholesterol.

296
Q

What is hyper- and what is hypo- adrenocortical problems called?

A

Hyper- Cushings. Hypo- addisons.