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Semiology > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is the normal degradation of connective tissue

A

connective tissue constantly repairs and remodels, degradation is mediated by enzymes, tunrover is initiated by cytokines

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2
Q

How is the Screening in musculoskeletal system performed? Welcher Abkürzung geht man nach?

A

GALS - global assessment of locomotor system, Gait Arms Legs Spine

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3
Q

What areas does muscular or mechanical neck pain involve and where does it radiate to?

A

It involves trapeziuss, C7 spinous processes, paracervical musculature and it radiates to occiput (back of head)

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4
Q

How is muscular or mechanical pain treated?

A

analgesic drug (relieves pain), physiotherapy and ergonomics

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5
Q

Nerve root entrapment of C5 leads to what sensory changes, reflex losses and weaknesses?

A

Lateral arm, biceps, shoulder abduction and elbow flexion

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6
Q

Nerve root entrapment of C6 leads to what sensory changes, reflex losses and weaknesses?

A

Lateral forearm & thumb and index finger, biceps and supinator, elbow flexion and wrist extension

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7
Q

Nerve root entrapment of C7 leads to what sensory changes, reflex losses and weaknesses?

A

Middle finger, triceps, elbow extension

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8
Q

Nerve root entrapment of C8 leads to what sensory changes, reflex losses and weaknesses?

A

medial forearm & little and ring fingers, none, finger flexion

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9
Q

Nerve root entrapment of T1 leads to what sensory changes, reflex losses and weaknesses?

A

Medial upper arm, none, finger ab- and adduction

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10
Q

Where does rotator cuff (supraspinatus) tendonosis occur?

A

trauma (30%), elderly, RA

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11
Q

clinical findings of calcific tendonosis and bursitis

A

calcium pyrophosphate deposits in tendon, acute or chronic recurrent shoulder pain/ restriction of movements, shedding crytsals into bursa leading to acute pain

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12
Q

Epicondylitis defintion, where does it occur mostly?

A

inflammation of epicondyle, often in athelets: Teniis elbow or golfer’s elbow

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13
Q

Define Carpal tunnel syndrome

A

median nerve compression, idiopathic (cause unknown), thickened ligaments, tendon sheats, bone enlargement

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14
Q

What is Anemia?

A

expression of an underlying disease or disorder, Lack of oxygen in tissues (!) due to deficiency of haemoglobin

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15
Q

How does tissue hypoxia in anemia occur?

A

due to decreased conc of Hb/ht MAINLY and erythrocytes

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16
Q

Name compensatory mechanisms of tissue hypoxia due to anemia

A

high erythropoietin production, high heart rate, high stroke volume, vasodilation, high DPG in red cell

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17
Q

At what amount of haemoglobin does normal compensatory mechanisms fail?

A

<50-60 g/l

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18
Q

Name some of the most important symptoms in Anemia

A

CNS= fatigue, even fainting/ Heart= chest pain, angina, heart attack/ shortness of breath / yellowing skin and eyes, red eyes if severe/ spleen enlargement

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19
Q

What is the mean corpuscular volume or MCV of Normocytic anemia?

A

80-100

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20
Q

What is the mean corpuscular volume or MCV of Macrocytic anemia?

A

> 100

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21
Q

What is the mean corpuscular volume or MCV of Microcytic anemia?

A

<80

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22
Q

Inflammation increases IL-6, which in turn increases the release of a subtance that inhibits iron transport. WHat is this substance called

A

Hepcidin

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23
Q

Name labaratory findings of intravascular hemolysis

A

Hemoglobinemia, Hemoglobinuria, Hemosiderinuria, Methemalbuminemia

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24
Q

What is Leukocytosis

A

increased leukocytes in peripheral blood

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25
Q

when does it count as eosinophilia?

A

when above 0.5 x 10E-9/l

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26
Q

does eosinophil rise the older the patient ?

A

no, it’s highest when neonate at falls gradually when older

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27
Q

What are secondary eosinophilia causes?

A

Allergic disorders (Asthma), dermatological disorders, drugs (AB), infectious diseases (parasitic infections), GI disorders, vasculitides, rheumatological disease, respiratory disease, neoplasm (lymphomas, acute lymphoblastic leukaemia), miscellaenous disease

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28
Q

What are primary eosinophilia causes?

A

haemotolical neoplasms with clonal eosinophilia, myeloid and lymphoid neoplasm, chronic or atypical leukaemia

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29
Q

Which is correct?

A) Polyclonal - malignant, Clonal - reactive
B) Polyclonal - reactive, Clonal - malignant

A

B)

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30
Q

What are reactive lymphocytosis causes?

A

infectious disease auch as EBV, noon infectious causes auch as auto-immune cond. like RA, smoking, post splenectomy

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31
Q

What are clonal (malignant) lymphocytosis causes ?

A

premalignatn causes auch as monoclonal B lymphocytosis, and various lymphoproliferative malignancies auch as chronic lymphoctic leukemia and lymphomas

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32
Q

Name the count of mild neutropenia

A

1.5-1.0 x 10E-9/l

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33
Q

Name the count of moderate neutropenia

A

1.0-0.5x10E-9/l

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34
Q

Name the count of severe neutropenia

A

<0.5x10E-9/l

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35
Q

Name causes of Neuropenia

A

inherited or acquired. acquired examples are vit b12 or folate deficiency, infections, drug-induced, bone marrow infiltration, viral infections auch as HIV; Hepatitis B,C and EBV und CMV another cause may be increased peripheral dystruction due to hypersplenism, immune-mediated, drug induced or associated with collagen vascular disease (felty syndrome or SLE)

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36
Q

What abnormalities are found in primary polycythemia?

A

Polycythaemia vera, mutations in erythropoietin receptor and high-oygen affinity haemoglobins

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37
Q

What are abnormalities found in secondary polycythemia?

A

chronic lung disease, morbid obesity, heavy smoking and renal disease or renal cell carcinoma

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38
Q

Define Polycythemia vera (PV)

A

alteration in pluripotent progenitor cell leading to excessive proliferation of erythoid, myeloid and megakaryocytic progenitor cells (mutations in JAK2 in 95%)

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39
Q

What size of a lymph node classifies as Lymphadenopathy?

A

a node greater than 1 cm

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40
Q

name reason why lymph nodes enlarge

A

1) there is an increase in number of benign lymphocytes and macrophages in response to antigens
2) infiltration inflammatory cells (lymphadenitis)
3) proliferation of malignant lymphocytes or macrophages
4) infiltration by metastatic malignant cells
5) infiltration of lymph nodes by lipid /metabolite- laden macrophages (lipid storage disease)

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41
Q

which lymphadenopathy has the highest risk of malignancy with estimated 90% of older than 40 and 25% in younger than 40?

A

Supraclavicular Lymphadenopathy

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42
Q

abnormalities of which structures are assumed when the node is ride sided in supraclavicular lymphadenopathy?

A

cancer in mediastinum, lungs or esophagus

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43
Q

abnormalities of which structures are assumed when the node is left sided (Virchwo’s) in supraclavicular lymphadenopathy?

A

testes, ovaries, kidneys, pancreas, stomach, gallbladder or prostate

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44
Q

What does a paraumbilical node (Sister Joseph’s) indicate?

A

abdominal or pelvic neoplasm

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45
Q

What characteristic of durance excludes a low grade lymphoma?

A

nodes that either last less than 2 weeks or longer than one year with now size progression

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46
Q

Name malignant lymphadenopathies

A

lymphoma hodgkin and non-hodgkin, leukemia, Kaposi’s sarcoma, metastases

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47
Q

Name autoimmune lymphadenopathies

A

SLE, RA, Sjogren’s syndrome, Still’s disease, dermatomyositis, kawasaki’s disease, sarcoidosis

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48
Q

What are labaratory investigations of Lymphadenopathies?

A

FBC, ESR, LDH, CRP, as well as serology of liver and renal function, calcium, protein electrtophoresis, virology, serology, autoimmune screen

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49
Q

How is the assumptions of a possible malignant lymph node handled?

A

BIOPSY

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50
Q

Only in which exception are glucocorticoids used in lymphadenopathies? And why are they usually not used?

A

in life threatening pharyngeal obstruction by the lymph tissue in waldeyer’s ring and usuall ynot used because they obscure diagnosis and delay healing when infected

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51
Q

what are the main causes for anemia?

A

Iron Deficiency 29%, Chronic Disease 27%

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52
Q

Name 3 inherited anemias

A

Diamond- Blackfan Syndrome, Idiopathic Aplastic Anemia, Fanconi’s anemia

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53
Q

What is Diamon-Blackfan Syndrome

A

autosomal recessive disease, pure red cell aplasia associated with short stature, web neck, shield chest, cleft lip and triphalangeal thumb

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54
Q

idiopathic aplastic anemia

A

acquired failure of hematopoetic stem cell results in pancytopenia (low RBC,WBC and platelets)

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55
Q

fanconi’s anemia

A

autosomal recdssive disorder, results in pancytopenia and associated with pigmentary, skeletal, renal and developmental abnormality

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56
Q

What is common finding of skin in anemia (eyes as well)

A

pale, pale conjunctiva, yellowish turning eyes

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57
Q

What is a disease found in oral area in iron deficiency?

A

Angular cheilitis

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58
Q

What are pathologic findings of nails in iron deficiency?

A

Koilonychia spoon nails

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59
Q

what is Pagophagia

A

eating disorder involving compulsive consumption of ice and or iced drinks

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60
Q

what are the main causes for anemia?

A

Iron Deficiency 29%, Chronic Disease 27%

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61
Q

Name 3 inherited anemias

A

Diamond- Blackfan Syndrome, Idiopathic Aplastic Anemia, Fanconi’s anemia

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62
Q

What is Diamon-Blackfan Syndrome

A

autosomal recessive disease, pure red cell aplasia associated with short stature, web neck, shield chest, cleft lip and triphalangeal thumb

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63
Q

Why can severe hemolysis be life-threatening?

A

due to hypoxia, arrythmia, thrombus, blockage of renal tubules as well as function of kidneys leading

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64
Q

fanconi’s anemia

A

autosomal recdssive disorder, results in pancytopenia and associated with pigmentary, skeletal, renal and developmental abnormality

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65
Q

What is common finding of skin in anemia (eyes as well)

A

pale, pale conjunctiva, yellowish turning eyes

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66
Q

What is a disease found in oral area in iron deficiency?

A

Angular cheilitis

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67
Q

What are pathologic findings of nails in iron deficiency?

A

Koilonychia spoon nails

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68
Q

what is Pagophagia

A

eating disorder involving compulsive consumption of ice and or iced drinks

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69
Q

What are characteristics of Anaemia of Chronic Disease? (ACD)

A

2nd most common form of anemia, most frequent among hospitalized patients, normocytic normochromic can progress to microcytic hypochromic

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70
Q

Define Hemolysis

A

it is the destruction or removal of red blood cells from the circulation

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71
Q

What are clinical findings of Hemolytic anemia?

A

Jaundice of skin and sclera, dark urine (hemoglobinuria), Splenomegaly, hepatomegaly, cholelithiasis

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72
Q

Name anemias with cytopenia (low mature blood cells) syndromes

A

haematology malignancy auch as

myelodysplastic syndrome, acute leukemia or lymphoma as well as myeloma

autoimmune, connective tissue disorder

solid tumors (iron deficiency)

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73
Q

Name Hereditary Anemias

A

hereditary spherocytosis, hereditary elliptocytosis, G6PD deficiency, pyruvate kinase deficiency, thalassemia

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74
Q

What has to be considered in Bone Marrow examination

A

maturation of erythroid and myeloid lineages, ratio of myeloid and erythroid series, presence of leukemic- lymphoid or other tumor cells, presence of megakaryocytes, abundance of iron stores (ring sideroblasts)

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75
Q

Name secondary warm antibodies diseases

A

Lymphoproliferative disease (lymphoma), autoimmune diseases SLE, colitis ulcerosa), acute leukaemia, solid malignancy (ovarian carcinoma)

Generally: Lymphoproliferative disorders, autoimmune disorders, viral or bacterial infections, vaccinations, solid organ transplants

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76
Q

Name secondary cold anitbodies diseases

A

Lymphoproliferative disease (M. Waldenstrom, lymphoma), infection (mycoplasma, EBV)

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77
Q

Name characteristics of warm autoimmune hemolytic anemia

A

most common AIHA (70%), lgG1 or igG3, +/- complements, max reactivity 37°C, usually idiopathic, children younger than 4 or adults older than 40

78
Q

name charactersitics of Cold Agglutinin Disease

A

lgM antibody, less than 37°C, auto-anti I antigen, usually chronic

79
Q

Name 3 haemotology malignancies

A

Myelofibrosis, Chronic Myeloid Leukemia, Lymphomas

80
Q

Name 3 Non-hematological disorders

A

liver disease (cirrhosis), infections (malaria, leishmaniasis), autoimmune disorders (SLE)

81
Q

Name anemias with cytopenia (low mature blood cells) syndromes

A

haemtology malignancy auch as

myelodysplastic syndrome, acute leukemia or lymphoma as well as myeloma

autoimmune, connective tissue disorder

solid tumors (iron deficiency)

82
Q

Name the MOST IMPORTANT laboratory investigations of anemia

A

FBC ( MCV, reticulocyte count), Blood smear examination (LDH)

83
Q

What has to be considered in Bone Marrow examination

A

maturation of erythroid and myeloid lineages, ratio of myeloid and erythroid series, presence of leukemic- lymphoid or other tumor cells, presence of megakaryocytes, abudnance of iron stores (ring sideroblasts)

84
Q

Which nodes are unlikely to be reactive

A

epitrochlear nodes

85
Q

Name characteristics of Rotator cuff (supraspinatus) tendonosis

A

common cause shoulder pain, trauma in 30%, worse by arm abduction and elevation, passive elevation less painful, severe pain, analgesics, physio, injections (corticoids)

86
Q

Name characteristics of Calcific tendonosis and bursitis

A

calcium pyrophosphate deposits in tendon, visible on x-ray, acute or chronic recurrent shoulder pain & restriction of movement, shedding crystals into bursa: acute pain, gout and septic arthritis

87
Q

Name characteristics of Carpal tunnel syndrome

A

median nerve compression in carpal tunnel, idiopathic, thickened ligaments, tendon sheaths, bone enlargement, numbness, tingling, pain in median nerve distribution which might radiate to forearm

88
Q

What is the Tinel’s sign?

A

Tapping of the median nerve causes sensation of tingling or pins and needles

89
Q

What is the Phalen’s test?

A

Holding wrist in flexion and feeling a sensation is a positive test

90
Q

What is the Dupuytren’s contracture?

A

a painless, palpable fibrosis of the palmar aponeurosis, fibroblast invade the dermis due to abnormal signaling, occurs in caucasians, diabetes, alcohol overuse, cirrhosis

91
Q

Name characteristics of Back (lumbar) pain

A

common cause of disability, red flags are: before 20 years or after 50years, persistent and a serious cause is suspected, worse at night, worse in morning, associated with systemic illness, fever or weight loss, neurological symptoms or signs

92
Q

What are characteristics of Lumbar disc prolapse

A

Muscle spasm and scoliosis, positive straight- leg raising test, signs of cauda equina syndrome

93
Q

Name characteristics of Ant. knee pain

A

common id adolescence, no cause found, settles in time

94
Q

Torn meniscus characteristics

A

usually injury (sports), immediate lateral or medial pain with or without swelling, treated with ice, MRI to see

95
Q

Torn cruciate ligaments characteristics

A

often with meniscal tear, urgent orthopedic referral

96
Q

Where does Knee join effusion occur and what are its characteristics

A

inflammatory arthritis, septic arthritis, gout/pseudogout, patellar tap sign, blood test auch as WBC and inflam. markers and aspiration for WBC and gram stain

97
Q

What are characteristics of Chronic pain syndromes (Fibromyalgia)

A

pain for longer than 3 months in trigger points above and below waist, sleep disturbances (abnormalities of serotonin, substance P, cortisol)

98
Q

What is treatment of Chronic pain syndromes

A

multidisciplinary approach, cognitive behavioural, analgesics, antidepressants (SSRIs)

99
Q

What are common symptoms of Osteoarthritis even if it sometimes is asymptomatic?

A

joint-pain, short lived morning stiffness, functional limitations

100
Q

Name characteristics of Nodal Osteroarthritis

A

mainly distal interphalangeal joints, one at a time over years, often female around menopause, painful onset with or without enthesitis, impaired gripping

Heberden’s nodes - DIP
Bouchard’s nodes - PIP

101
Q

How is OA investigated and managed?

A

xray
physical: exercises for strength and stability, insoles, walking stick
treated with local heat or ice packs, NSAID gels, COX2, before paracetamol, intra-articular corticosteroids, surgery with replacement arthroplasty

102
Q

What are characteristics of Rheumatoid arthritis?

A

autoantibodies to Fc portein to lgG and citrullinated cyclic peptide, persistent synovitis, chronic symmetrical polyarthritis and systemic inflammation, more common in women

103
Q

What are typical clinical features of Rheumatoid arthritis?

A

slowly progressive, symmetrical, peripheral inflammatory polyarthritis, mostly small joints of hand and feet, muscle wasting and fatigue

104
Q

What are non articular manifestations of RA?

A

Scleritis, Sjögren’s syndrome, Pericarditis, Amyloidosis, Feltys syndrome, Carpal tunnel, anaemia, pleural effusion, alveolitis, coromary artery disease, rheumatoid nodules

105
Q

What are investigations of RA

A

blood count: normochromic, normocytic, inflam markers, serology (RF 60-70%, ACPA present earlier, ANA 30%), MRI for synovitis or early erosions, aspiration of joint if septic arthritis suspected, MSUS ultrasound

106
Q

How is RA managed?

A

NSAIDs and analgesics to control, if synovitis DMARDs, physiotherapy,steroids, if not getting better: TNF alpha therapy or rituximab

107
Q

What are DMARDs used for?

A

reduce inflammation -> reduction of joint swelling, fall in plasma acute phase reactants, slow joint erosions and irreversible damage, slow acting agents, partial or transient effect, most are contraindicated in pregnancy

108
Q

What diet can often lead to gout or hyperuricemia? Are men or women more prone to get the disease?

A

Men more prone

purine rich foods, high saturated fats, fructose containing drinks, sweets, alcohol

109
Q

what are causes of hyperuricemia due to decreased uric acid clearance?

A

CKD, ketoacidosis, hyperparathyroidism, hypothyroidism, sarcoidosis

110
Q

What are clinical features of Gout?

A

Hyperuricemia, acute attack (redness of first MTP), chronic gout, chronic polyarticular gount, tophaceous (smooth white deposits (tophi), can ulcerate), renal urate stones

111
Q

What are Gout investigations

A

joint fluid microscopy(needle shaped crystals), serum uric acid (usually raised)

112
Q

How is Gout treated

A

NSAIDs, corticosteroids with or without colchicine, as well as urate reducing treatment: allopurinol, febuxostat

113
Q

What are characteristics of Pseudogout?

A

Chondrocalcinosis -> Calcium pyrophosphate deposits -> acute synovitis, elderly women, knee or wirst, sometimes: haemochromatosis, hyperparathyroidism, wilson’s disease, gout, rhomboidal crystals in joint fluid

114
Q

How is Pseudogout treated?

A

NSAID or colchicine

115
Q

What are characteristics of Septic arthritis

A

Staphylococcus aureus, hot red swollen and held immobile muscle spasm, less than 20% are polyarticular

116
Q

How is septic arthritis investigated?

A

increased WBC and inflam markers in blood, joint aspirate from gram stain, culture and microscopy

117
Q

How is septic arthritis treated?

A

IV Antibiotics

118
Q

Which of the following is often familial cause with type 1 HLA antigen (B27) and has a negative RF

A)Rheumatoid arthritis
B) Spondyloarthritis
C) Septic arthritis

A

B)

119
Q

What are characteristics of Ankylosing spondylitis

A

predominantly male, enthesitis, high incidence of HLA-B27

120
Q

Enthesitis mechanism

A

lymphocyte and plasma cell infiltration -> local bone erosion at attachments of ligaments -> new bone formation (syndesmophyte)

121
Q

What are clinical features of Ankylosing spondylitis

A

episodic inflammation of sacroiliac joints, positive Schober’s test, loss of spinal curves, Uveitis (ant), costochondritis, peripheral joints: assymetrical, usually large joints

122
Q

How is Ankylosing spondylitis treated

A

NSAIDs, DMARDs, antiTNFa auch as infliximab, etanercept, adalimumab, certolizumab, golimumab, secukinumab

123
Q

What is Psoriatic arthritis

A

10% of people with Psoriasis also develop arthritis mostly affecting joints

124
Q

What are clinical manifestations of Psoriatic arthritis

A

Mono or oligoarthritis, polyarthritis, sacroiliitis, DIP arthritis with or without nail dystrophy, osteolysis

125
Q

What are characteristics of Reactive arthritis

A

sterile synovitis, following an infection

spondyloarthritis after acute dysentery or sexually acquired infection (urethritis, cervicitis)

126
Q

Causes of Reactive arthritis?

A

Salmonella, Shigella, Yersinia enterocolitica, Chlamydia trachomatis, Ureaplasm urealyticum, bacterial antigens or DNA found in inflamed synovium

127
Q

What are clinical findings of Reactive arthritis?

A

acute, asymmetrical, lower-limb arthritis or enthesitis, sacroiliitis or spondylarthritis, sterile conjunctivitis or uveitis, skin lesions (circinate balantis, keratoderma blennorrhagicam, nail dystrophy)

128
Q

How is Reactive arthritis treated?

A

antibiotics for infection

129
Q

What are characteristics of Enteropathic arthritis

A

10-15% of patients with ulcerative colitis and Crohn’s disease, asymmetrical arthritis, lower limbs with or without sacroiliitis, arthritis may proceed to bowel disease

130
Q

Is SLE more common in men or in women?

A

women

131
Q

How are ANAs formed?

A

ANAs are made to antigens of molecules involved in cellular functions

with continued pressure from self-antigens immune response switches from low affinity, highly cross reactive lgM antibodies to high affinity lgG antibodies and lastly to antibodies directed towards are more limited epitopes on self-antigens

idiotypes of anytbodies stimulate autoreactive T cells to expand, helping unique clones of B cells to expand

final result = specific ANA production leading to clinical manifestations

132
Q

What are clinical features of SLE

A

fever, malaise,

joints (more than 90%) affected such as arthralgia, arthritis and myalgia (50%)

Skin 85%: Erythema (butterfly rash), photosensitivity, alopecia, scarring

Lungs (50%), pleural effusion, pneumonitis

Cardiovascular: Pericarditis, Myocarditis, aortic valve lesions, libeman- sacks endocarditis

Renal: lupus nephritis, nephrotic syndrome

Nervous system: depression, epilepsy, polyneuropathy, aseptic meningitis, vasculitis, thrombosis

133
Q

How is SLE managed?

A

avoid sunlight, manage CVD risk factors, NSAIDs, hydroxychloroquine for skin and joints, corticoids for nephritis and cytopenia and biologic agents against B cells auch as Belimumab and Rituximab

134
Q

What does Belimumab do?

A

monoclonal antibody that inhibits soluble form of B-cell survival factor (BlyS or BAFF), BLyS elevated in SLE and promotes memory B cells

135
Q

What does Rituximab do

A

a monoclonal antibody that depletes B cells

136
Q

What are characteristics of Antiphospholipid syndrome

A

Thrombosis, miscarriages, AB: anticardiolipin, lupus anticoagulant, anti- beta 2- glucoprotein 1

137
Q

What do the clinical manifestation sin Antiphospholipid syndrome result from?

A

result from aPL effects on coagulation auch as procoagulant actions of AB upon protein C, annexin V, platelets and fibrinolysis

once aPL present, second hit required to develop syndrome

138
Q

What are clinical features and lab features of Antiphospholipid syndrome

A

Thrombosis, ischemic strokes, miscarriages, thrombocytopenia, livedo reticularis

139
Q

Where does Systemic sclerosis occur more commonly?

A

Women

140
Q

What is Raynaud’s phenomenom and where does it commonly occur?

A

decreased blood flow to fingers -> arterial spasms (white to blue to red), pain and numbness

141
Q

What is limited cutaneous Systemic sclerosis

A

CREST, Raynaud’s, skin involvement of hands, face, feet and forearms, painful digital ulcers, telangiectasia, GI tract malabsorption, pulmonary hypertension

142
Q

What is Diffuse cutaneous Systemic Sclerosis

A

Raynaud’s, diffuse swelling and stiffness of fingers, skin thickening, esophageal involvement, renal, pulmonary fibrosis with or without pulmonary hypertension, myocardial fibrosis

143
Q

What are Scleroderma investigations?

A

Ht/Hb (chronic anemia), Cre, Urine microscopy

Autoantibodies: LcSSc: anti-centromere
DcSSc: anti-Scl-70 highly specific, anti-RNA-polymerase

RF might be positive, ANA

144
Q

What can you die from in Scleroderma

A

Pulmonary fibrosis, renal crisis, cardiac arrythmia

145
Q

What is Polymyositis?

A

inflammation of striated muscle (proximal muscle weakness and wasting)

146
Q

What is Dermatomyositis?

A

inflammation of striated muscle with skin involvement, characteristic rash:

Heliotrope purple rash periorbital
Gottron’s papules purple red patches on finger

147
Q

What are investigations of PM and DM

A

muscle enzymes and inflam markers (high CK, LDH, AST,ESR,CRP)

autoanitbodies auch as ANA,RF, myositis-sepcific (anti-Jo1)

Electromyography

Muscle biopsy

SCREENING

148
Q

How is PM treated?

A

corticoids as well as corticoid sparing agents

149
Q

How is resistant or recurrent PM treated?

A

Rituximab, cyclosporine, cyclophosphamide

150
Q

Name characteristic of the large vessel vasculitits: Polymyalgia rheumatica

A

older than 50years, sudden onset of pain and stiffness (shoulders, neck, hips, lumbar spine), worse in morning, ESR (extremely elevated) and CRP investigated , may coexist with giant cell arteritis

151
Q

Name characteristics of the large vessel vasculitis: Giant cell arteritis

A

“temproal arterits”, older than 50y, headaches, scalp or temple tenderness, jaw claudication, tenderness and swelling of temproal a., sudden painless loss of eye vision

152
Q

What are investigations of Giant cell arteritis?

A

Normocytic, normochromic anemia

very high ESR above 100

temporal artery biopsy (larger than 1cm)
cellular infiltrates auch as CD4+, macrophages,giant cells)
granulomatous inflammation

153
Q

Name characteristics of Takayasu arteritis (large vessel vasculitis)

A

disease of aortic arch syndrome
vascultitis of aortic arch
absent peripheral pulses
hypertension

154
Q

Name characteristics of Polyarteritis Nodosa (medium vessel vasculitis)

A

middle aged men, associated with hepatitis B, necrosis of vessel walls and microaneurysm formation

155
Q

Clinical aspects of Polyarteritis nodosa

A 
Neurological (mononeuritis multiplex)
abdominal (pain, bleeding)
renal: hematuria, acute or chronic renal failure
cardiac: coronary artery disease
skin: livedo reticularis
Lung almost never!
156
Q

Name characteristics of a Medium vessel vasculitis called Kawasaki’s disease

A

affects children younger than 5, fever, conjuctivitis, dryness and redness of lips and oral cavity, cervical lymphadenopathy, rash, redness and oedema of palms and soles

157
Q

What are complications of Kawasaki’s disease

A

coronary aneurysms

158
Q

What are ANCA positive diseases

A

wegener’s granulomatosis, churg strauss granulomatosis, microscopic polyangiitis -> Pulmonary diseases

159
Q

What are ANCA negative (immune complex) diseases

A

Henoch- Schönlein purpura, Cryoglobulinemic vasculitis, cutaenous leucocytoclastic vasculitis

160
Q

Name characteristics of Churg Strauss syndrome

A

young male adults, rhinitis, asthma, skin, systemic vasculitis, eosinophilic infiltration

161
Q

Name characteristics of Henoch-Schönlein purpura

A

mainly children, acute upper respiratory infection (type 3 hypersensitivity reaction & lgA deposition), skin rash (purpura on buttocks and thighs), abdominal colic, joint pain, mild glomerulonephritis

162
Q

Name characteristics of Wegener’s granulomatosis

A

upper respiratory tract, lungs, kidneys,rhinorrhoea, cough, hemoptysis, pulmonary nodular infiltrates, glomerulonephritis

163
Q

Behçet’s disease characteristics

A

silk road, recurrent oral and genital ulcers, uveitis, positive skin pathergy test, arthritis, thromboses

164
Q

Sjögren’s syndrome characteristics

A

dry mucosa, primary or with other autoimmune diseases, increased risk of hodgkin b-lymphoma, positive schirmers test, RF, ANA, Anti-Ro

165
Q

What is Serum Sickness

A

Is a immune reaction to proteins in antiserum

166
Q

Name characteristics of Serum sickness

A
  • rash, fever, malaise, polyarthralgias, polyarthritis (1-2 weeks after exposure to agent, resolve within weeks)
  • in patients who have already been exposed to agent, syndrome starts earlier (1-7 days after admin.), illness has more severe and explosive onset
  • rash is pruritic urticarial and morbilliform eruption
  • NO mucosal membranes involved
167
Q

Name characteristics of an Arthus reaction

A

reactions presents as painful local swelling and erythema beginning within a few hours, peaking by 24hours at sites of booster injections of vaccine

has been reported with tetanus, diphteria, hepatitis B vaccines

168
Q

Characteristics of Contact Hypersensitivity

A
  • max at 48h
  • predom epidermal reaction
  • langerhans cell as antigen presenting cell (dendritic antigen presenting cell, carry antigen to lymph node)
  • associated with hapten-induced eczema (nickel salts in jewellry, picryl chloride, acrylates, p-Phenylene diamine in hair dyes, chromates, chemicals in rubber, poison ivy (urushiol)
169
Q

What are clinical signs of poison icy contact dermatitis

A

blisters, bulla, pustules

170
Q

What are characteristics of Tuberculin Hypersensitivity

A
  • max at 48-72h
  • infiltration of lesion with mononuclear cells
  • first described as reaction to lipoprotein antigen of tubercle bacillus
  • responible for lesions associated with bacterial allergy - cavitations, caseating, general toxemia seen in TB
  • in unresolved reaction might -> granulomatous reaction

IGRA test

171
Q

Name characteristics of Granulomatous Hypersensitivity

A
  • most important DTH
  • causes many pathologic effects in diseases involving t cell mediated immunity
  • max at 14 days
  • cont. release of cytokines
  • leads to accumulation of large no. of macrophages
  • granulomas can also arise from persistence of indigestible antigens auch as talc
172
Q

Characteristics of Epitheloid cell granuloma formation

A
  • large flattened cells with incr. endoplasmic reticulum
  • multinucleate giant cells with little ER
  • (necrosis)
  • damage due to killer t cells recognizing antigen-coated macrophages, cytokine-activated macrophages
  • attempt by body to wall-off site of persistent infection
173
Q

Name examples of microbial induced DTH

A

Viruses (smallpox, measles, herpes)
Fungi (histoplasmosis, dematomycosis)
Parasites (leishmaniasis, schistosomiasis)

174
Q

What are characteristics of Type V Stimulatory Hypernsensitivity

A
  • interaction of autoantibodies with cellular receptors
  • antibody binding mimics receptor-ligand interaction
  • e.g thyroid stimulating antibody (mimics thyroid stim. hormone (TSH) of pit. binds to thyroid cell receptor)
175
Q

What are characteristics of Toxic shock syndrome (Innate Hypersensitivity Reactions)

A
  • S.aureus TSS toxin
  • hypotension, hypoxia, oliguria, microvascular abnormalities
  • excessive release of TNF, IL-1, IL-6
  • intravascular activation of complement
176
Q

What are characteristics of Septicemia - Septic Shock

A

primarily due to lipopolysaccharide

177
Q

What are characteristics of adult respiratory distress syndrome

A

high accumulation of neutrophils in lung

178
Q

What are characteristics of Superantigens

A

gram positive enterotoxins, react directly with T-cell receptors and induce massive cytokine release

179
Q

What are b12 deficiency symptoms?

A

memory loss, numbness, weakness, loss of dexterity, symmetric neuropathy, personality changes, subacute degeneration of dorsal (posterior) and lateral spinal columns, macrocytosis

180
Q

Is Anaemia of chronic disease normocytic and normochromic or microcytic and hypochromic

A

both, in the beginning or mild to moderate anemia its normocytic and normochromic, however it can progress into microcytic and hypochromic

181
Q

What are hereditary anemia?

A

G6PD deficiency, pyruvate kinase deficiency, thalassemia

182
Q

What are acquired anemias?

A

autoimmune: warm and cold AB type
alloimmune: hemolytic transfusion reactions, hemolytic disease of newborn, allograft

drug associated

red cell fragmentation syndrome

infections: malaria, clostridia

chemical and physical agents: drugs, industrial/domestic substances, burns

secondary: liver and renal disease

paroxysmal nocturnal hemoglubinuria

183
Q

Where does warm antibody AIHA (autoimmune hemolytic anemia) occur?

A

Lymphoproliferative disease (lymphoma), autoimmune disease (SLE, colitis ulcerosa)

CLL,HD, AUTOIMMUNE DISORDERS, VIRAL BACTERIAL INFECTIONS, VACCINATIONS, SOLID ORGAN TRANSPLANTS

184
Q

Where does cold antibody AIHA (autoimmune hemolytic anemia) occur?

A

Lymphoproliferative disease auch as lymphoma and M. Waldenstrom, as well as infections (mycoplasma, EBV)

MYCOPLASMA PNEUMONIA; INFECTIOUS MONONUCLEOSIS, WALDENSTROM MACROGLOBULINEMIA

185
Q

What are characteristics of Warm autoimmune hemolytic anemia?

A

most common AIHA (70%), usually IgG1 or igG3, with or without complement, max reactivity at 37 degrees, 60% idiopathic, children up to 4 years or adults under 40 years

186
Q

What are characteristics of cold autoimmune hemolytic anemia?

A

lgM antibody that fixes complement, under 37 degrees, auto-anti-I, intravascular and extravascular hemolysis, usually chronic

187
Q

What are the three phases of Raynaud phenomenon?

A

Phase 1: Ischemia due to vasospasm of artery leading to occlusion and impeded blood flow

Phase 2: Cyanosis due to persistent vasospasm and dilation of capillaries as well as venules filled with deoxygenated blood (blueish)

Phase 3: Rubor due to relaxation of vasospasm, greatly increased blood flow and widened cappillaries with now oxygenated blood (purple ish)

188
Q

What are hemolytic anemias?

A

congenital (thalassemia, hereditary spherocytosis)

acquired (autoimmune hemolytic anemia)

189
Q

What are haematology malignancies?

A

Myelofibrosis, Chronic myeloid leukemia, lymphomas

190
Q

Non- Hematological Disorders

A

Liver disease (cirrhosis), infections (malaria, leishmaniasis), autoimmune disorders (SLE)

Semiology (2 decks)

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