Block 2

Front 1

Cyclosporine, Tacrolimus, and Sirolimus all belong to this category of immunosupressant drugs:

Back 1

Immunophillin-binding drugs.

Front 2

CsA binds to this immunophillin:

Back 2

Cyclophillin.

Front 3

CsA and tacromilus both act by:

Back 3

Inhibiting dephosphorylation of NFAT.

Front 4

Tacromilus binds to this immunophillin:

Back 4

FKBP.

Front 5

The effects of these two immunophillin-binding drugs is synergistic:

Back 5

CsA and Sirolimus.

Front 6

Sirolimus inhibits T cell activation by:

Back 6

Inhibiting proliferation in response to cytokines.

Front 7

This drug is associated with an elevated risk of lymphocoele:

Back 7

Sirolimus.

Front 8

Mycophenolate, methotrexate, and azathioprine all belong to this category of immunosupressant drugs:

Back 8

Antimetabolites.

Front 9

This is a noncompetitive inhibitor of IMPDH

Back 9

MPA.

Front 10

MTX is useful in cancer chemotherapy because it has the ability to:

Back 10

Inhibit pyrimidine synthesis.

Front 11

Elevated levels of homocysteine is a risk factor for:

Back 11

Atherosclerosis.

Front 12

This metabolite of azathioprine causes apoptosis of WBCs:

Back 12

6-TGNs.

Front 13

This metabolite of azathioprine inhibits synthesis of purines:

Back 13

MeTIMP.

Front 14

This drug is ONLY used for treating transplant rejection:

Back 14

Muromonab.

Front 15

Daclizumab and basiliximab are monoclonal antibodies that target:

Back 15

The IL-2 receptor.

Front 16

Freckles in the armpit or groin region with neurofibromatosis:

Back 16

Crowe's sign.

Front 17

The most common drug allergy is to this drug:

Back 17

Penicillin.

Front 18

A genetically determined, qualitatively abnormal
reaction to a drug related to a metabolic or enzyme deficiency:

Back 18

Drug idiosyncracy.

Front 19

Hemolytic anemia, agranulocytosis and thrombocytopenia are clinical manifestations of this type of hypersensitivity:

Back 19

Type II.

Front 20

Edema, erythema, and serum sickness are clinical manifestations of this type of hypersensitivity:

Back 20

Type III.

Front 21

The most common clinical characteristic of drug hypersensitivity:

Back 21

Cutaneous reactions.

Front 22

This enzyme released during mast cell degranulation can be used in immunological testing for hypersensitivity:

Back 22

Tryptase.

Front 23

One gene affecting multiple tissues:

Back 23

Pleiotropy.

Front 24

These influence the phenotype of single gene disorders:

Back 24

Modifier genes.

Front 25

These disorders usually affect structural or regulatory proteins:

Back 25

Autosomal dominant.

Front 26

These disorders usually affect enzymes:

Back 26

Autosomal recessive.

Front 27

This triplet repeat is found in fragile X syndrome:

Back 27

CGG.

Front 28

Increased severity or earlier age of onset with expansion of triplet repeats:

Back 28

Anticipation.

Front 29

Huntington's disease is characterized by this triplet repeat:

Back 29

CAG.

Front 30

Myotonic dystrophy is characterized by this triplet repeat:

Back 30

CTG.

Front 31

This is evidenced by the birth of 2 or more children with the same disorder and no family history:

Back 31

Gonadal mosaicism.

Front 32

This action of neurofibromin is lost in NF1:

Back 32

Inactivation of Ras.

Front 33

Connective tissue nevus associated with tuberous sclerosis:

Back 33

Shagreen patch.

Front 34

The fibrillin gene mutated in Marfan's syndrome is located on chromosome:

Back 34

15

Front 35

Blue tinting to the sclera is a common finding in:

Back 35

Osteogenesis imperfecta.

Front 36

Marfan's syndrome's pattern of inheritance is:

Back 36

Autosomal dominant.

Front 37

Achondroplasia's pattern of inheritance is:

Back 37

Autosomal dominant.

Front 38

Osteogenesis imperfecta's pattern of inheritance is:

Back 38

Autosomal dominant.

Front 39

Most mutations of collagen are the result of replacing a:

Back 39

Glycine.

Front 40

Autosomal dominant trait characterized by high myopia beginning in childhood with an increased chance of retinal detachment:

Back 40

Stickler syndrome.

Front 41

PKU's mode of inheritance is:

Back 41

Autosomal recessive.

Front 42

Sickle cell anemia's mode of inheritance is:

Back 42

Autosomal recessive

Front 43

CF's pattern of inheritance is:

Back 43

Autosomal recessive

Front 44

Tay Sachs Disease's mode of inheritance is:

Back 44

Autosomal recessive.

Front 45

This disease has a high incidence among Asian and Mediterranian people:

Back 45

Thalassemia.

Front 46

French Canadians have a high incidence of:

Back 46

Tyrosinase deficiency.

Front 47

Tyrosinase deficiency leads to:

Back 47

Albinism.

Front 48

This is caused by a defect in copper metabolism:

Back 48

Menkes Kinky Hair.

Front 49

DMD's mode of inheritance is:

Back 49

X linked recessive.

Front 50

Neural tube defects are an example of:

Back 50

Multifactorial defects.

Front 51

When should neural tube closure complete normally?

Back 51

3rd to 4th week of gestation.

Front 52

Addition of this reduces the incidence of neural tube defects:

Back 52

Folic acid.

Front 53

Down Syndrome increases the chances of contracting:

Back 53

Leukemia.

Front 54

This trisomy often has midline facial defects:

Back 54

Trisomy 13.

Front 55

The least common trisomy is:

Back 55

Trisomy 13.

Front 56

Miller-Dieker syndrome is a result of a deletion on chromosome:

Back 56

17.

Front 57

Smith-Magenis syndrome is a result of a deletion on chromosome:

Back 57

17.

Front 58

Williams syndrome is a result of a deletion on chromosome:

Back 58

7.

Front 59

DiGeorge syndrome is a resulte of a deletion on chromosome:

Back 59

22.

Front 60

Which X chromosome is XIST expressed on:

Back 60

The inactive X.

Front 61

The short stature associated with Turner's syndrome is due to having only one copy of the:

Back 61

SHOX gene.

Front 62

The most common cause of 46, XX DSD is:

Back 62

Congenital adrenal hyperplasia.

Front 63

This technique is utilized to assess large deletions or duplications:

Back 63

aCGH (array comparative genomic hybridization)

Front 64

What is the most common autosomal recessive disorder?

Back 64

Cystic Fibrosis.

Front 65

Gene transfer is used to treat _________ disorders while microRNAs are used to treat _________ disorders:

Back 65

Recessive; dominant.

Front 66

Diseases mediated by IgE:

Back 66

Atopic diseases.

Front 67

The early phase reaction of allergic rhinitis is mediated by:

Back 67

Mast cells.

Front 68

The late phase reaction of allergic rhinitis is mediated by:

Back 68

Eosinophils and Th2 cells.

Front 69

Places where hydroxychloroquine concentrates:

Back 69

The skin and retina.

Front 70

This drug can take up to 2 years to reach inactive blood levels:

Back 70

Leflunomide.

Front 71

Proliferation of endometrium during the menstrual cycle and nodular prostatic hyperplasia are examples of:

Back 71

B9 cell proliferation.

Front 72

Continuously dividing tissues:

Back 72

Labile.

Front 73

Tissues with Low level of replication, but capable of undergoing proliferation in response to injury:

Back 73

Stable tissue.

Front 74

Rapidly dividing cells generated from stem cells:

Back 74

Transit amplifying cells.

Front 75

These are generated from transit amplifying cells:

Back 75

Progenitor cells.

Front 76

Ability of a cell to transdifferentiate into diverse lineages:

Back 76

Developmental plasticity.

Front 77

Stem cells are found in the liver in:

Back 77

Canals of Hering.

Front 78

Neural stem cells are found in two places:

Back 78

Dentate gyrus of hippocampus, subventricular zone.

Front 79

Growth and regeneration of skeletal muscle occurs by replication of:

Back 79

Satellite cells.

Front 80

Short peptides that facilitate endocytosis:

Back 80

CPP.

Front 81

Complexes of these two molecules drive the cell cycle:

Back 81

CDKs and cyclins.

Front 82

TGF-alpha is homologous to:

Back 82

EGF.

Front 83

Part of the EGFR family; overexpressed in some forms of breast cancer:

Back 83

HER2/Neu.

Front 84

Receptor for HGF:

Back 84

cMET.

Front 85

Leads to phosphorylation of SMADs; growth inhibitor for epithelial cells, leukocytes:

Back 85

TGF-B.

Front 86

These cytokines participate in wound healing:

Back 86

TNF and IL-1.

Front 87

These cytokines participate in liver regeneration:

Back 87

TNF and IL-6.

Front 88

Zonula adherins and desmosomes are formed by:

Back 88

Cadherins.

Front 89

Link cadherins to actin:

Back 89

Cathenins.

Front 90

Syndrome characterized by excessive angiogenesis:

Back 90

von Hippel Lindau.

Front 91

Severe generalized edema with diffuse swelling of all tissues and organs:

Back 91

Anasarca.

Front 92

Platelets are produced by:

Back 92

Megakaryocytes in bone marrow.

Front 93

Gray platelet syndrome is characterized by a lack of:

Back 93

Alpha granules.

Front 94

This is the physiologic initiator of secondary hemostasis:

Back 94

Factor VII.

Front 95

Hemophilia A is deficiency of:

Back 95

Factor VIII.

Front 96

Hemophilia B is deficiency of:

Back 96

Factor IX.

Front 97

Hemophilia C is deficiency of:

Back 97

Factor XI.

Front 98

What is the cause of acute transplant rejection?

Back 98

Recipient’s Tc cells react against foreign MHC I.

Front 99

The two most common malignancies associated with immunosuppressive therapy:

Back 99

Skin and lymphatic.

Front 100

Statins are metabolized by:

Back 100

CYP-3A4.

Front 101

Adverse drug reactions most commonly occur to:

Back 101

Antibiotics and NSAIDs.

Front 102

6-mercaptopurine is inactivated by this enzyme:

Back 102

TIMP.

Front 103

5-Fluorouracil is inactivated by this enzyme:

Back 103

DPD.

Front 104

Painful sensation to non-noxious stimuli:

Back 104

Allodynia.

Front 105

Increased sensitivity to painful stimuli:

Back 105

Hyperalgesia.

Front 106

Reserved for external keratolytic uses due to its irritant action:

Back 106

Na Salicylate.

Front 107

This is associated with the use of aspirin in children with viral infection:

Back 107

Reyes syndrome.

Front 108

Antidote for acetaminophen overdose:

Back 108

Acetylcysteine.

Front 109

Lysosomal storage in the growth plates of long bones can lead to:

Back 109

Dwarfism.

Front 110

Tay-Sachs disease and Sandhoff disease are both:

Back 110

GM2 gangliosidoses.

Front 111

These organs are severely enlarged in Gaucher disease:

Back 111

Liver and spleen.

Front 112

Symptoms of this lysosomal storage disease occur earlier than in other disorders:

Back 112

I-cell disease.

Front 113

Migrate to injured tissues and are able to generate chondrocytes, osteoblasts, adipocytes, and other cells depending on the tissue to which they migrate:

Back 113

Mesenchymal stem cells, marrow stromal cells (MSC).

Front 114

An inherited cancer syndrome characterized by germline mutations in p53:

Back 114

Li-Fraumeni syndrome.

Front 115

Causes proliferation and migration of fibroblasts, smooth muscle cells, and monocytes to areas of inflammation and healing skin wounds:

Back 115

PDGF.

Front 116

This is a growth inhibitor for epithelial cells and leukocytes; loss of its receptors provides a proliferative advantage for tumor cells:

Back 116

TGF-B.

Front 117

There is high expression of this in hypertophic scars, systemic sclerosis, and Marfan syndrome:

Back 117

TGF-B.

Front 118

Portions of the ECM that provide resilience, lubrication:

Back 118

Glycosaminoglycans and proteoglycans.

Front 119

This stabilized the collagen helix:

Back 119

Hydroxyproline.

Front 120

Due to a lack of vitamin C, this does not occur in scurvy:

Back 120

Hydroxylation of procollagen.

Front 121

Nonfibrillar collagen:

Back 121

Type IV.

Front 122

Binds fibrin to form a provisional blood clot that serves as a substrate for ECM deposition:

Back 122

Plasma fibronectin.

Front 123

Heparan sulfate, chondroitin sulfate and keratan sulfate are all:

Back 123

Proteoglycans.

Front 124

Deleterious mutations in lysosomal enzymes that break down glycosaminoglycans:

Back 124

Mucopolysaccharidoses.

Front 125

Laminin is commonly found in the:

Back 125

Basement membrane.

Front 126

Elastin is commonly found in the:

Back 126

Interstitial matrix.

Front 127

Replacement of parenchymal cells by ECM in any tissue:

Back 127

Scar formation.

Front 128

Cause degradation of the basement membrane during angiogenesis:

Back 128

MMPs.

Front 129

Signalling through this pathway provides regulation of angiogenesis:

Back 129

NOTCH.

Front 130

The most important fibrogenic agent in wound healing:

Back 130

TGF-B.

Front 131

What RBC parameter might be elevated if there are too many reticulocytes:

Back 131

RDW and MCV.

Front 132

Sickle cells are also called:

Back 132

Drepanocytes.

Front 133

Schistocytes may be indicative of:

Back 133

Microangiopathic hemolytic anemia.

Front 134

Severe malnutrition can cause RBCs to change to:

Back 134

Acanthocytes (spur cells).

Front 135

Plasma cell dyscrasia can cause formation of:

Back 135

Rouleaux.

Front 136

Failure of which side of the heart will result in pulmonary edema?

Back 136

Left.

Front 137

Chronic congestions is common in these organs:

Back 137

Lungs, liver, spleen.

Front 138

Hemosiderin-laden macrophages can be a sign of:

Back 138

Congestion.

Front 139

These cells will be atrophied in chronic liver congestion:

Back 139

Central hepatocytes.

Front 140

Which is larger, petechiae or purpura?

Back 140

Purpura.

Front 141

Loss of a significant amount of blood outside the body can cause:

Back 141

Iron deficiency anemia.

Front 142

This binds thrombin and activates Protein C, then cleaves factors Va and VIIIa, inhibiting thrombosis:

Back 142

Thrombomodulin.

Front 143

What does plamsin do?

Back 143

Degrades fibrin.

Front 144

This is often prolonged in von Willebrand's disease:

Back 144

aPTT.

Front 145

Abnormal vWF receptor:

Back 145

Bernard-Soulier syndrome.

Front 146

Abnormal fibrinogen receptor:

Back 146

Glanzmann's Thrombasthenia.

Front 147

The extrinsic pathway is monitored with:

Back 147

PT time (prothrombin)

Front 148

If a patient has an abnormal PT and a normal aPTT, they have a problem with:

Back 148

Factor VII.

Front 149

The intrinsic pathway is monitored with:

Back 149

aPTT time.

Front 150

Warfarin, coumadin, inhibit this pathway:

Back 150

Extrinsic.

Front 151

Heparin inhibits the:

Back 151

Intrinsic pathway.

Front 152

This cleaves fibrinogen to active fibrin:

Back 152

Thrombin.

Front 153

When is t-PA most active (antithrombotic)?

Back 153

When attached to fibrin.

Front 154

An aPTT mixing study will not correct a clotting problem if there are:

Back 154

Inhibitors present.

Front 155

Point mutation causing abnormal receptor on factor V for protein C:

Back 155

Factor V Leiden.

Front 156

A septal defect of the heart can allow this to occur:

Back 156

Paradoxical embolus.

Front 157

Most systemic (arterial) emboli originate from the:

Back 157

Heart.

Front 158

Systemic emboli, even if silent, always result in:

Back 158

Infarction.

Front 159

The most common cause of air embolism is:

Back 159

Decompression sickness.

Front 160

The most common cause of fat embolism:

Back 160

Fracture of long bones.

Front 161

A ____________ is more susceptible to osmotic lysing than a normal RBC.

Back 161

Spherocyte.

Front 162

The first characterized gene mutation was the one that results in:

Back 162

Sicle cell anemia.

Front 163

Hydroxyurea used for sickle cell disease has this effect:

Back 163

Increases HbF.

Front 164

The reduction or absence of a-globlin chains in a thalassemia is usually due to:

Back 164

Deletions.

Front 165

Specific defect in PIG-A which is required to form a red cell anchor:

Back 165

Paroxysmal Nocturnal Hemoglobinuria.

Front 166

This is typically used today to diagnose paroxysmal nocturnal hemoglobinuria (PNH):

Back 166

Flow cytometry.

Front 167

RBCs of patients with PNH are deficient in these cell-surface proteins that protect from cell lysis:

Back 167

CD55, CD59.

Front 168

Paroxysmal cold hemoglobinuria is commonly associated with:

Back 168

Syphillis.

Front 169

A PT time 1.5 times the average is an indication for transfusion of:

Back 169

FFP.

Front 170

Cryoprecipitate is used to increase:

Back 170

Fibrinogen.

Front 171

The most common cause of acute intravascular hemolytic reactions:

Back 171

ABO incompatibility.

Front 172

Most common transfusion reactions are:

Back 172

Febrile and allergic.

Front 173

Severe anaphylactic reaction to transfusion could mean the patient has:

Back 173

An IgA deficiency.

Front 174

Most common cause of death from transfusion:

Back 174

Transfusion-related acute lung injury (TRALI)

Front 175

This is more common in platelets than RBCs:

Back 175

Bacterial contamination.

Front 176

Neutrophil granules develop during which stage of development?

Back 176

Myelocyte stage.

Front 177

Neutrophils develop through this stage in the bone marrow:

Back 177

Myelocyte stage.

Front 178

Steroids can cause neutrophilia through:

Back 178

Demargination.

Front 179

Marrow replaced by tumor:

Back 179

Myelophthisis.

Front 180

The number one cause of neturopenia is:

Back 180

Drugs.

Front 181

These phagocytic cells synthesize, secrete, and degrade compliment:

Back 181

Monocytes.

Front 182

The body's compensation for neutropenia:

Back 182

Monocytosis.

Front 183

These cells sequester immune complexes:

Back 183

Eosinophils.

Front 184

The first and second most common cause of eosinophilia:

Back 184

Parasite
Allergy

Front 185

This type of cell has very rapid transit in the blood:

Back 185

Basophils.

Front 186

These cells contain histamine and are involved in allergic reactions:

Back 186

Basophils.

Front 187

Major cause of basophilia is:

Back 187

Chronic myelogenous leukemia.

Front 188

Lymphocytosis due to pertussis infection can look like:

Back 188

Lymphoma.

Front 189

This MDS is associated with iron overload at diagnosis:

Back 189

Refractory anemia with ringed sideroblasts.

Front 190

This MDS is associated with a dimorphic blood picture:

Back 190

Refractory anemia with ringed sideroblasts.

Front 191

Charcot-Leyden crystals are remnants of:

Back 191

Eosinophils.

Front 192

Airway lumen casts of exudate:

Back 192

Cuschmann's spirals.

Front 193

Clumps of sloughed epithelial cells:

Back 193

Creola bodies.

Front 194

Hard nodules present on the dorsal surface of the PIP joints:

Back 194

Bouchard's nodes.

Front 195

Hard nodules present on the dorsal surface of the DIP joints:

Back 195

Heberden's nodes.

Front 196

Two pro-inflammatory cytokines involved in rheumatoid arthritis:

Back 196

TNF alpha, IL-1.

Front 197

Proliferative synovium in RA:

Back 197

Pannus.

Front 198

Gold standard of DMARDs; inhibits IL-1 and leukotriene-4:

Back 198

Methotrexate.

Front 199

This has been proven to be important in driving inflammation of synovium in RA:

Back 199

TNF alpha.

Front 200

Two of the most frequent manifestations of SLE:

Back 200

Glomerulonephritis and arthritis.

Front 201

Lupus that only affects the skin:

Back 201

Discoid.

Front 202

This SLE skin condition is associated with antiphospholipid antibody syndrome:

Back 202

Livedo reticularis.

Front 203

Besides ANA, another autoantibody common in SLE:

Back 203

dsDNA.

Front 204

Recurrent spontaneous abortions, thrombocytopenia, & arterial and venous thromboses are characteristics of this condition associated with SLE:

Back 204

Antophospholipid antibody syndrome (APAS).

Front 205

The first morphological observation in folate deficiency:

Back 205

Hypersegmented neutrophils.

Front 206

A functional folate deficiency is caused by:

Back 206

B12 deficiency.

Front 207

Most common cause of B12 deficiency:

Back 207

Pernicious anemia.

Front 208

Liver disease and alcoholism cause this type of macrocytosis:

Back 208

Non-megaloblastic.

Front 209

B12/folate deficiency will cause this type of macrocytic anemia:

Back 209

Megaloblastic.

Front 210

megaloblastic anemia due to absence of IF secondary to gastric atrophy:

Back 210

Pernicious anemia.

Front 211

Treatment for Heparin induced thrombocytopenia:

Back 211

Direct thrombin inhibitors.

Front 212

Classic pentad of thrombotic thrombocytopenia purpura:

Back 212

Thrombocytopenia
MAHA
Renal dysfunciton
Neurological disturbance
Fever

Front 213

There is a lack of this enzyme in TTP:

Back 213

ADAMTS13.

Front 214

Why is plasma exchange effective in treating TTP:

Back 214

Provides ADAMTS13
Removes the autoantibody against ADAMTS13.

Front 215

Low platelet count and elevated PT and aPTT could indicate:

Back 215

DIC.

Front 216

D-dimer number in DIC:

Back 216

Elevated.

Front 217

Cytometric classification of anemia of chronic disease:

Back 217

Normochromic, normocytic.

Front 218

Cytometric classification of iron deficiency anemia and thalassemias:

Back 218

Hypochromic, microcytic.

Front 219

Cytometric classificatio of anemia of B12/folate deficiency and liver disease:

Back 219

Normochromic, macrocytic.

Front 220

Why are sickle cell patients at risk for infection by encapsulated organisms:

Back 220

Eventual autosplenectomy damages spleen, the site of removal of encapsulated organisms.

Front 221

This is required for diagnosis of chronic myelogenous leukemia:

Back 221

Philadelphia chromosome, t(9,22).

Front 222

What is the result of the abnormal philadelphia chromosome in CML?

Back 222

Consititutive overactivity of tyrosine phosphokinase.

Front 223

High red cell count and low EPO levels is indicative of:

Back 223

Polycythemia vera.

Front 224

Basophils are almost always high in:

Back 224

CML.

Front 225

Massive splenomegaly is indicative of:

Back 225

Primary myelofibrosis.

Front 226

Most effective treatment for allergic rhinitis:

Back 226

Intranasal steroids.

Front 227

A major cause of morbidity and mortality in SLE:

Back 227

Atherosclerosis.

Front 228

Nonbacterial verrucous vegetations (seen with increased frequency in those with APAS):

Back 228

Libman Sacks vegetations.

Front 229

Hallmark is low platelets and low fibrinogen:

Back 229

DIC.

Front 230

Vitamin K dependent factors:

Back 230

2, 7, 9, 10

Front 231

This clotting assay increases first in vitamin K deficiency:

Back 231

PT time.

Front 232

Blast marker that regular cells should not have:

Back 232

CD34.