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MSK/Hematology Flashcards

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1
Q

This antibiotic can cause tendon rupture

A

floroquinolones (ciprofloxacin)

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2
Q

CML (chronic myeloid leukemia)

A

9:22 translocation. BCR-ABL translocation that constituitly activates tyrosine kinase. Tx with gleevec.

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3
Q

Bacteria causing Lyme Disease

A

Borrelia Burgdorferi, a corkscrew-shaped spirochete that causes lyme disease. The natural reservoir is the mouse and is transmitted by the Ixodes deer tick.

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4
Q

Cause for albinism

A

recessive mutation the gene for tyrosinase (converts DOPA –> Melanin)

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5
Q

Staph Toxic Shock Syndrome

A

Can happen when leave a tampon in for too long. The S.aureus exotoxin is a superantigen. Binds to MHC II and T-cell receptor causing polyclonal T-cell activation.

Dx: it is often not identified until desquamation of the palms occurs

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6
Q

Ankylosing Spondylitis

A

90% positive for HLA B27. Symmetric involvement of spine or sacroiliac joints. Often see “bamboo spine” tx: Adalimumab (TNF-alpha), infliximab (TNF-alpha)

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7
Q

Osteoporosis lab findings for Ca, Phos, Alkaline Phosphatase

A

ALL NORMAL

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8
Q

Paget disease lab findings (Ca, P, Alk Phos)

A

Normal Ca, Normal Phos, Elevated Alk Phos

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9
Q

CML translocation and associated problem and tx

A

9:22 BCR-ABL (philadelphia). constitutively active Tyrosine Kinase. Treat with Imatinib=Gleevec (a tyrosine Kinase inhibitor)

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10
Q

CREST syndrome. What is it and what does it stand for

A

Limited Scleroderma: anticentromere autoantibody C: calcinosis R: Reynaud E: esophageal dysmotility S: sclerodactyl (thickening of skin of fingers/toes) T: telangectasia (small red skin marks from abnormally dilated blood vessels)

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11
Q

Reactive arthritis triad and when is it seen

A
  1. Conjunctivitis 2. Urethritis 3. Arthritis “Can’t see, can’t pee, can’t bend my knee” Seen post GI/Chlamydia Positive for HLA-B27
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12
Q

Hereditary spherocytosis smear

A

defect in RBC membrane that shows small RBC with lack of central pallor and abundant reticulocytes Howell-Jolly bodies (fragments of nuclear material in RBC are present)

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13
Q

Polymyositis

A

subacute inflammatory myopathy with CD8+ T cells and macrophages progressive symmetrical proximal muscle weakness -like dermatomyositis but without SLE rash

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14
Q

Follicular Lymphoma

A

neoplastic proliferation of SMALL B Cells that are CD20+ Driven by 14;18 translocation 14: Ig heavy chain 18: BCL2 (get inhibition of apoptosis) Can progress to DLBCL (diffuse large cell) Tx: rituximab

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15
Q

14:18 translocation

A

Follicular lymphoma (get inhibition of apoptosis due to overexpression of BCL2)

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16
Q

Mantle Cell Lymphoma

A

neoplastic proliferation of SMALL B cells (CD20) that expands the mantle zone. Driven by t(11;14) 11: Cyclin D1 gene (overexpression of D1 promotes G –> S transition in cell cycle 14: Ig heavy chain

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17
Q

Marginal Zone Lymphoma

A

neoplastic proliferation of SMALL B cells (CD20) that expands the marginal zone. Associated with chronic inflammatory states such as Hashimoto thyroiditis, Sjogren syndrome (parotid), H. Pylori gastritis (MALToma) If treat the gastric MALToma H. Pylori, can cure lymphoma (only lymphoma that can cure with abx)

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18
Q

Burkitt Lymphoma

A

INTERMEDIATE sized B cells (CD20). Associated with EBV (a herpesvirus) Two types: 1. African- extranodal mass in jaw 2. Sporatic- shows up in abdomen t(8;14) translocation 8: c-myc (oncogene that is overexpressed that causes cell growth) 14: Ig heavy chain Starry sky appearance on microscope (due to high mitotic rate)

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19
Q

Diffuse large B-cell lymphoma

A

Neoplastic proliferation of LARGE B-Cells (CD20) Most common form of NHL Clinically aggressive (makes sense since the cells are not well differentiated) -Arises sporadically or can develop from Follicular lymphoma

  • One risk factor for developing Hodgkin Lymphoma is immunosuppression (can occur in HIV or immunosuppressant drugs such as those for IBD)
  • Increasing age is also a risk factor
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20
Q

Hodgkin Lymphoma

A

Neoplastic proliferation of Reed-Sternberg cells (owl eye nuclei). CD15+, CD30+ RS cells secrete cytokines! Results in B-sx (f/c, wt loss, night sweats) Bulk of tumor is reactive cells that attracted by cytokines.

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21
Q

4 types of Hodgkin Lymphoma

A
  1. Nodular Sclerosis (most common). Presents with cervical or mediastinal lymph node in young female.
  2. Lymphocyte-rich (best prognosis) *This is the type that is associated with B-symptoms (fever, chills, night sweats)
  3. Mixed Cellularity (abundant eosinophils via IL-5). Has the highest number of Reed Sternberg cells
  4. Lymphocyte depleted (worst prognosis)
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22
Q

Multiple Myeloma (overview)

A

Malignant proliferation of plasma cells in bone marrow. Most common primary malignancy of bone. High serum IL-6 present that stimulates plasma cell growth.

-Plasma cells have abundant Rough Endoplasmic Reticulum (the site of synthesis of secretory proteins)

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23
Q

Multiple Myeloma (clinical features) 6 of them

A
  1. Bone pain with hypercalcemia due to activation of RANK on osteoclasts (causes lytic lesions)
  2. Elevated serum protein (M-spike, due to IgG or IgA) 3. Increased risk infection (due to lack of antigenic diversity)
  3. Rouleaux formation of RBC (decreased charge btw RBC)
  4. Free light chains –> amyloidosis
  5. Proteinuria –> kidney failure (myeloma kidney)
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24
Q

Monoclonal Gammopathy of Undetermined Significance (MGUS)

A

Increased serum protein with M-spike but NO other findings of typical multiple myeloma. Common in elderly (5% of 70 year olds). Can be thought of as pre-myeloma (although only 1% develop each year to full fledged multiple myeloma)

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25
Sjogren Syndrome (and what is triad)
Destruction exocrine glands. Characterized by xerostomia, xeropthalmia, arthritis Usually found in women 35-45 years old Associated with Anti-SSA and Anti-SSB **Woman who comes in and feels like she has sand in her eye and has a dry mouth**
26
Treatments of Hodgkins Lymphoma
ABVD A: adriamycin (doxirubicin) B: bleomycin V: Vinblastine D: Dacarbazine
27
Treatment for Hereditary Spherocytosis
Splenectomy (due to defective RBC skeleton causing them to be round and defective) . Disorder leads to increased reticulocyte count
28
Most common cause of mononucleosis (and what is associated with it...4 things)
EBV. Infection with EBV is associated with nasopharyngeal carcinoma, CNS lymphoma, Hodgkin lymphoma, and splenic rupture
29
Osteomyelitis most common cause
Staph Aureus (accounts for \>50% cases) Gram + cocci Coagulase + Catalase +
30
Inheritance of Von-Willebrand Disease ## Footnote **Think Von Miller**
Autosomal Dominant (most common bleeding disorder) ## Footnote **VON IS DOMINANT**
31
G6PD results in reduced levels of what?
NADPH, thus unable to keep glutathione reduced and thus produce free radicals. Lead to hemolytic anemia due to decreased NADPH in RBC --\> Heinz Bodies
32
Vitamin C essential for
Hydroxylation of lysine and proline in ER. This allows for collagen cross-linking to occur. If it doesn't, one can get scurvy
33
Essential Thrombocytosis
Overproduction of platelets by megakaryocytes that causes obstruction of capillaries and arterioles Sx: bleeding and thrombosis
34
Anti-Smith Antibodies
Associated with SLE, as well as Antinuclear Antibodies (ANA), Anti-dsDNA, Antihistone Antibodies
35
Hepcidin
sequesters iron in storage sites by: 1. limiting iron transfer from macrophages to erythroid precursors 2. suppressing EPO production See an increase in anemia of chronic disease (anemia associated with chronic inflammation)
36
Sideroblastic Anemia
Anemia due to **defective protoporphyrin synthesis** Synthesized via a number of rxns Succinly CoA --\> ALA (via ALAS, Rate Limiting) --\> porphobilinogen (via ALAD)--\> --\> Protoporphyrin + Fe --\> Heme (ferrochelase) \*occurs in mitochondria. If deficiency in pathway, **iron build up in mitochondria and create RINGED SIDEROBLAST (iron stains blue)**
37
Types and causes of Sideroblastic Anemia
1. Congenital: most commonly from ALAS defect 2. Acquired a. Alcoholism (mitochondrial poisoning) b. Lead Poisoning (inhibit ALAD, Ferrochelase) c. Vitamin B6 deficiency (cofactor for ALAS)
38
Two enzymes that are affected by lead poisoning
Ferrocheletase ALA dehydratase
39
Treatment and presentation of Rocky Mountain Spotted Fever
Tx: Doxycycline promptly! (even before lab tests come back, can be fatal) -Can use other tetracyclines if need be Presentation is unique: rash appears on palms and soles of feet and hands and migrates inward toward trunk and face.
40
Erythema Nodosum is seen with what associated condition
**IBD (Crohn and UC)** -it is a painful inflammatory lesion of subcutaneous fat usually on anterior shins Also can be seen in **sarcoidosis, coccidioidomycosis, histoplasmosis, TB, streptococcal**
41
Churg-Strauss presentation
tingling, numbness, pain, and purpura at the extremities associated with eosinophilia pANCA +
42
The most common form of arthritis in children
juvenile idiopathic arthritis
43
Fanconi Anemia (not syndrome) ## Footnote **FANCONI**
AR disorder in which cells have increased susceptibility to chromosomal breakage when exposed to DNA cross-linking agents. -See progressive bone marrow failure Tx: bone marrow transplant **FANCONI Anemia (not syndrome)** * *F**acial microcephaly * *A**bnormal testis and kidneys * *N**eutropenia * *C**afe au lait * *O**cular abnormality * *N**o thumbs and radius * *I**ncreased risk of AML * *S**kin abnormality
44
Muscle of the tongue that is innervated by vagus nerve?
palatoglossus
45
Achondroplasia
Autosomal DOMINANT mutation in fibroblast growth factor receptor 3 gene (FGFR3) Failure of endochondral ossification --\> short limbs Associated with older paternal age
46
ligaments associated with ankle sprains
1. anterior talofibular ligament (most common) ATF =always tears first 2. posterior talofibular ligament 3. calcaneofibular ligament
47
Which interleukin is associated with acute-phase reactants
IL-6
48
Yersinia Pestis
organism responsible for the plague (black death). transmitted by fleas from a rodent host causes painful lymphadenopathy, sepsis, DIC
49
Plummer-Vinson Syndrome ## Footnote **Plummer Vincent's wife has a sore red tongue from trying to swallow his big iron pipe**
**Iron** deficiency anemia, dysphagia, esophageal webs may also present with glossitis, angular chelitis, koilonychia
50
Ehlers-Danlos syndrome (3 types)
1. Hypermobility type (most common) 2. Classical type: Type 5 collagen (joint and skin) 3. Vascular type: Type 3 collagen deficiency (vascular and organ rupture) -Vascular aneurysms are most feared complication
51
HLA-DR4
Rheumatoid Arthritis, Type 1 DM, Addison's Disease
52
HLA-B27
Psoriasis, Ankylosing Spondylitis, IBD, Reactive Arthritis (PAIR)
53
Thalassemia
Anemia due to decreased SYNTHESIS of the globin chains of hemoglobin
54
alpha thalassemia cis and trans deletions
cis: Asian, worse (possibly responsible for more spontaneous abortions, esp if pass the affected gene to offspring) Trans: African, including African Americans This happens in two gene deleted and results in mild anemia with increased RBC count
55
3 gene deletion and 4 gene deletion in alpha thalassemia (what are they called, what actually happens to RBC, what is the presentation)
when have 3 gene deletion, these deletions drastically reduce α -globin synthesis and cause β-globin chains to form tetramers known as hemoglobin HbH. HbH damages red blood cells causing hemolytic anemia and splenomegaly. This results in increased erythropoiesis which results in skeletal abnormalities such as the frontal bossing - HbH Disease, which is more prevalent in South East Asian populations - When have 4 gene deletion: hydrops fetalis (not compatible with life) =Hb Barts
56
alpha thalassemia vs beta thalassemia
alpha --\> gene DELETIONS (can be 1,2,3,4) beta --\> gene mutations (can be B0, absent or B+ diminished
57
Beta Thalassemia minor
B/B+ is mildest form, usually asymptomatic Microcytic, hypochromic, RBC and target cells See increased HbA on electrophoresis
58
Beta Thalassemia major (Cooley's Anemia)
B0/B0 the most severe form of disease. Severe anemia several months after birth (once HbF is gone) Get Alpha4 resulting in ineffective erythropoiesis and extravascular hemolysis. - Erythroid hyperplasia results in expansion of hematopoiesis to skull (crewcut sign) - Tx: transfusions --\> leads to secondary hemochromatosis. Smear shows microcytic, hypochromic, RBC with target cells and nucleated RBC (due to being made in abnormal location) - Little or NO HbA on electrophoresis
59
Muscles of rotator cuff
SItS Supraspinatous: abducts arm initially (empty/full can test) Infraspinatous: laterally rotates arm, pitching injury Teres Minor: adducts, laterally rotates Subscapularis: medially rotates and adducts
60
OsteoPETrosis (marble bone disease)
due to failure of bone reabsorption and remodeling secondary to **malfunctioning osteoclasts** Bone fills marrow space --\> pancytopenia Carbonic anhydrase II mutations impair ability of osteoclast to generate acidic environment necessary for bone resorption
61
B12 (cobalamin) deficiency presentation
neurological disturbances, increased serum homocysteine and increased methylmalonic acid\*\* \*\*most diagnostic
62
inheritance of Duchenne Muscular Dystrophy
X-Linked Recessive (due to a frameshift mutation)
63
inheritance of G6PD
X-linked Recessive
64
Anthrax toxin mechanism
increase cAMP, causes inflammation of mediastinum and potential fatal occlusion of the airway
65
Severe Combined Immunodeficiency (SCID)
adenosine deaminase deficiency. Failure to thrive, chronic diarrhea, thrush Absence of thymic shadow, germinal centers, T-cells
66
Hereditary Spherocytosis
Defect of RBC cytoskeleton membrane tethering proteins -Ankryin, Spectrin, Band 3 Less able to maneuver through splenic sinusoids, consumed by macrophages, cause anemia and splenomegaly Dx: osmotic fragility test
67
Sickle Cell pathophys
AR mutation in Beta chain of hemoglobin Glutamic Acid (hydrophilic) --\> Valine (hydrophobic) Disease present when two abnormal B genes. Results in \>90% HbS. HbS polymerizes when deoxygenated (increased risk of sickling with hypoxemia, dehydration, acidosis) HbF protective against sickling (why don't see till 6mo age)
68
Sickle Cell presentation (5)
1. Dactylitis (swollen hands/feet) due to vaso-occlusion infarct in bones \*\*CLASSIC PRESENTATION 2. Autosplenectomy (shrunken, fibrotic spleen). Increased risk osteomyelitis (from salmonella, NOT S. Aureus like normal) 3. Acute chest syndrome: vaso-occlusion in pulm microcirculation. ppt by pneumonia \*\*\*MOST COMMON CAUSE OF DEATH IN SICKLE PTS \*\* 4. Pain Crisis 5. Renal papillary necrosis (hematuria, proteinuria)
69
osteomalacia/rickets
Due to **defective mineralization**/calcification of osteoid soft bones that bow out. decreased vitamin D--\> decreased serum Ca2+ --\> increased PTH secretion --\> increased serum PO43−. Hyperactivity of **osteoblasts, Alk Phos** Most **common cause is Vitamin D deficiency** (in children this is called rickets)
70
unhappy triad of knee injury
1. ACL (anterior drawer test) 2. MCL (joint laxity under valgus stress) 3. Medial meniscus (McMurry test: click with external rotation and extension of knee)
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73
Radial nerve innervation
BEST 1. Brachioradialis 2. Extensors of the wrist 3. Supinator 4. Triceps See damage to radial nerve in humerus fracture (no problems with abduction of arm becasue that would be axillary nerve farther up)
74
Thoracic duct
Drains lymph from LEFT side of body and BOTH lower limbs
75
layers of skin
Stratum **Corneum** (keratin) Stratum **Lucidum** (found only in areas like palms of feet) Stratum **Granulosum** Stratum **Spinosum** (desmosomes) Stratum **Basale** (stem cell site) **Californian's Love Girls String Bikinis**
76
**_Chromosomal Translocations_** ## Footnote t(8;14) t(9;22) t(11;14) t(14;18) t(15;17)
t(8;14) Burkitt Lymphoma (c-myc activation) t(9;22): AML (BCR-ABL) t(11;14): Mantle Cell Lymphoma (cyclin-D1) t(14;18): Follicular Cell Lymphoma (BCL-2) t(15;17): M3 Type of AML (tx: ATRA)
77
Factor V Leiden Mutation
Production of mutant factor V that is resistant to degradation by activated protein C. Most common cause of inherited hypercoagulability in whites. -predisposes pts to thromboses, esp in unusual locations (such as mesenteric vein)
78
Treatment of anemia of chronic disease with positive dsDNA antibodies and a low C3
- Need to know what chronic disease is causing the problem in the first place - Here the problem is SLE presenting as Lupus Nephritis - Best treatment is EPO because SLE and CKD are causing a decrease in EPO production from the kidney
79
Three branches of the celiac trunk
1. L Gastric Artery 2. Splenic Artery 3. Common Hepatic Artery
80
Chronic Lymphocytic Leukemia (CLL)/Small Lymphocytic Leukemia
**-Most common adult leukemia.** CD20+, **CD5+** B-cell neoplasm. Often **asymptomatic**, progresses slowly; **smudge cells** in peripheral blood smear; autoimmune hemolytic anemia. SLL same as CLL except CLL has peripheral blood lymphocytosis or bone marrow involvement
81
Symptoms of **LEAD** poisoning
**L: L**ead **L**ines on gingivae (burton lines) and on metaphyses of long bones **E: e**ncephalopathy and **e**rythrocyte basophilic stippling **A: a**bdominal colic and sideroblastic **a**nemia **D**: **d**rops. Wrist and foot drops. Also treat with **D**imercaprol and E**D**TA (succimer used for chelation for kids...sucks to be a kid who eats lead)
82
Pt is in heart failure with fluid overload, what is going to happen to their: BNP Sympathetic System RAAS
**BNP INCREASED**: released in response to stretch (fluid overload). It is often used to help diagnose congestive heart failure exacerbation **Sympathetic System is INCREASED** due to a perceived initial drop in blood pressure, which triggers compensatory neurohurmoral stimulation directed at maintaining blood pressure and tissue perfusion **RAAS system is also INCREASED** for the same reason as above to improve cardiac output by increasing chronotropy and inotropy, expanding the ECF comparment and promoting atrial and venous vasoconstriction
83
What does von Willebrand factor actually do?
After endothelial damage, vWF binds GP1b receptors on the platelet membrane and mediates platelet aggregation and adhesion to subendothelial collagen Deficiency presents as gingival bleeding often
84
Indications for clozapine
**Treatment resistent schizophrenia or schizophrenia associated with suicidal ideation** Remember side effect of agranulocytosis need to **monitor clozely with clozapine**
85
Halothane induced hepatotoxicity, what is it and what are some of the lab findings
Predominantly cause a hepatocelluar pattern of liver injury. Can range from mild to fulminent hepatitis with 50% mortality rate. Liver looks very atrophied on exam at autopsy Lab: **elevated serum aminotransferases, prolonged PT (due to failure of production of factor VII),** leukocytosis, eosinophilia
86
HbA2 level grealty increased 7.5% (normal 1-3), is indicative of what?
Beta-thalassemia trait. HbA2 is increased in minor and greatly increased in major
87
What nerves travel through the jugular foramen?
9,10,11, jugular vein Lesion here can cause Jugular foramen syndrome. Sx related to nerves involved (loss taste, loss gag reflex, dysphagia, hoarsness, deviation uvula, SCM and trapezius weakness)
88

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