Usmle Step 1 -- Dit: Foundations

Front 1

Which fetal structure secretes B-hCG?

Back 1

Syncitiotrophoblast.

Front 2

What is the maternal component of the placenta?

Back 2

Decidua basalis.

Front 3

Order the following molecules by how much energy they contain that can be used to fuel endergonic reactions: pyruvate, glucose, adenosine, AMP, ATP.

Back 3

Glucose > pyruvate > ATP > AMP > adenosine.

Front 4

What are the stages of conception between an conception and an inner cell mass?

Back 4

zygote --> morula --> blastocyst

Front 5

List several important drugs that are contraindicated in pregnancy.

Back 5

ACEi, warfarin, tetracycline, aminoglycosides, thalidomide, DES, carbamazapine, phenytoin, valproate, lithium, fluoroquinolones, sulfanamides, chloramphenicol, MTX, clarithromycin, VitA.

Front 6

During what weeks of fetal development does organogenesis occur?

Back 6

Weeks 3-8.

Front 7

What is the embryological origin of the anterior pituitary?

Back 7

Surface ectoderm.

Front 8

What is the embryological origin of the cornea?

Back 8

Neural crest.

Front 9

What is the embryological origin of the lens of the eye?

Back 9

Surface ectoderm.

Front 10

What is the embryological origin of the retina?

Back 10

Neural ectoderm.

Front 11

What is the embryological origin of the olfactory epithelium?

Back 11

Surface ectoderm.

Front 12

What is the embryological origin of the mammary gland?

Back 12

Surface ectoderm.

Front 13

What is the embryological origin of the salivary glands?

Back 13

Surface ectoderm.

Front 14

What is the embryological origin of the sweat glands?

Back 14

Surface ectoderm.

Front 15

What is the embryological origin of the tissue just above the pectinate line? What is the origin of the tissue just below the anal canal?

Back 15

Endoderm; Surface ectoderm.

Front 16

What effect do ACEi have on fetal development?

Back 16

Renal abnormalities.

Front 17

What effect do aminoglycosides have on fetal development?

Back 17

Deafness; compromised CNVIII.

Front 18

What effect does DES (diethylstilbestrol) have on fetal development?

Back 18

Vaginal clear cell adenocarcinoma.

Front 19

What effect do tetracyclines have on fetal development?

Back 19

Discoloration of the teeth.

Front 20

What effect does valproic acid have on fetal development?

Back 20

Neural tube defects.

Front 21

During what week of fetal development do genitalia begin to exhibit differentiation into male and female specific organs?

Back 21

Week 10.

Front 22

During what week of fetal development does the heart begin to beat?

Back 22

Week 4.

Front 23

What is the significance of the Sonic hedgehog gene?

Back 23

Involved in patterning along the A-P axis.

Front 24

Where is the Sonic hedgehog gene produced?

Back 24

Base of limbs in zone of polarizing activity.

Front 25

What is the significance of the Wnt-7 gene?

Back 25

Produced at the apical ectodermal ridge (distal end of developing limb) and is necessary for proper organization along D-V axis (front-back).

Front 26

What is the significance of the FGF gene?

Back 26

Produced at apical ectodermal ridge and is responsible for lengthening of limbs.

Front 27

What is the significance of the HOX genes?

Back 27

Involved in segmental organization of the embryo in a craniocaudal direction -- mutations in HOX genes lead to appendages located in the wrong places!

Front 28

What are the neural crest derivatives?

Back 28

ANS, PNS, dorsal root ganglia, cranial nerves, celiac ganglion, melanocytes, chromaffin cells of the adrenal medulla, parafollicular cells of the thyroid, Schwann cells, pia and archnoid, bones of the skull (bones of the inner ear!), odontoblasts, aorticopulmonary septum.

Front 29

What are the neuroectoderm derivatives?

Back 29

Brain and spinal cord (CNS), retina.

Front 30

What are the surface ectoderm derivatives?

Back 30

Anterior pituitary, lens of the eye, epithelial linings of the oral cavity, sensory organs of the ear, olfactory epithelium, epidermis, anal canal below the pectinate line, salivary, sweat, and mammary glands.

Front 31

What are the derivatives of the endoderm?

Back 31

Gut tube epithelium and derivatives (e.g., lungs, liver, pancreas, thymus, parathyroid, thryoid follicular cells).

Front 32

What is the leading cause of congenital malformations in the United States?

Back 32

Fetal alcohol syndrome.

Front 33

Which anti-coag is safe for use in pregnancy?

Back 33

Heparin.

Front 34

What must be present on a protein in order for that protein to gain entry into the nucleus?

Back 34

Nuclear localization signal.

Front 35

Which AA are contained in the nuclear localization signal?

Back 35

Proline, lysine, arginine.

Front 36

Which types of proteins are responsible for fostering the progression through the cell cycle?

Back 36

Cylins and CDKs.

Front 37

Which cyclin-CDK complexes assist in the progression from G1 phase to S phase?

Back 37

Cyclin D + CDK4; Cyclin E + CDK2.

Front 38

Which tumor supressor proteins prevent the progression of the cell into S phase?

Back 38

Rb and p53.

Front 39

Which cyclin-CDK complexes assist in the progression from G2 phase to M phase?

Back 39

Cyclin A + CDK2; Cyclin B + CKD1.

Front 40

What molecule targets proteins in the ER for lysosomes?

Back 40

Mannose-6-phosphate (M6P).

Front 41

What is deficient in I-cell disease?

Back 41

M6P.

Front 42

What are the different methods that a cell uses to break down proteins?

Back 42

Proteasome; Lysosome; Calcium-dependent enzymatic degradation.

Front 43

Which cell types are rich in SER?

Back 43

Hepatocytes (detoxifying); Chromaffin cells of the adrenal cortex (steroid-synthesizing).

Front 44

What targets defective proteins for proteasomal degredation?

Back 44

Ubiquitin.

Front 45

Name the cell types that are considered "labile" (never enter G0 and have a very short G1 phase).

Back 45

Skin cells, hair follicles, gut epithelium, bone marrow.

Front 46

What types of cells are considered "stable, quiescent" (only enter G1 from G0 when stimulated)?

Back 46

Hepatocytes, lymphocytes.

Front 47

What are Nissl bodies?

Back 47

RER of neurons. They synthesize enzymes and peptide neurotransmitters.

Front 48

Which AA residues are modifiable by the Golgi?

Back 48

Serine, threonine, asparagine.

Front 49

Describe the vesicular trafficking proteins COPI and COPII.

Back 49

COPI: retrograde, Golgi --> ER.
COPII: anterograde, RER --> cis-Golgi.

Front 50

What is the mechanism of I-cell disease?

Back 50

Inherited lysosomal storage disease. Failure of addition of M6P to lysosome proteins. Enzymes are secreted outside the cell instead of being targeted to the lysosome.

Front 51

What are the characteristics of I-cell disease?

Back 51

Coarse facial features, clouded corneas, restricted joint movement, high plasma levels of lysosomal enzymes. Often fatal in childhood.

Front 52

What drugs act on microtubules?

Back 52

Mebendazole/Thiabendazole (antihelminthic), Colchicine (anti-gout), Vincristine/Vinblastine (anti-cancer), Paclitaxel (anti-breast cancer), Griseofulvin (anti-fungal).

Front 53

Which organelle is responsible for the breakdown of very long-chain fatty acids?

Back 53

Peroxisome.

Front 54

What are the intermediate filaments for connective tissue?

Back 54

Vimentin.

Front 55

What are the intermediate filaments for muscle tissue?

Back 55

Desmin.

Front 56

What are the intermediate filaments for epithelial tissue?

Back 56

Cytokeratins.

Front 57

What are the intermediate filaments for axons?

Back 57

Neurofilaments.

Front 58

What are the defects seen in Kartagener syndrome?

Back 58

Male and female infertility, recurrent sinusitis, and bronchiectasis. Associated with situs inversus.

Front 59

What is Kartagener syndrome?

Back 59

Immotile cilia due to a dynein arm defect.

Front 60

Describe the function of dynein.

Back 60

Retrograde transportation (+ to -) of cellular cargo to microtubule.

Front 61

Describe the function of kinesin.

Back 61

Anterograde transportation (- to +) of cellular cargo to microtubule.

Front 62

What are the intermediate filaments of the nuclear envelope and DNA within?

Back 62

Nuclear lamins.

Front 63

What protein is involved in transporting an endocytosed vesicle from the plasma membrane to the endosome?

Back 63

Clathrin.

Front 64

Which arachadonic acid product(s) causes increased bronchial tone?

Back 64

LTD4, LTC4, Thromboxane (TXA2).

Front 65

Which arachadonic acid product(s) causes decreased bronchial tone?

Back 65

Prostacyclin (PGI2), Prostaglandin.

Front 66

Which arachadonic acid product(s) causes increased platelet aggregation?

Back 66

Thromboxane.

Front 67

Which arachadonic acid product(s) causes decreased platelet aggregation?

Back 67

Prostacyclin (PGI2).

Front 68

Which arachadonic acid product(s) causes increased uterine tone?

Back 68

PGs (PGE2, PGF).

Front 69

Which arachadonic acid product(s) causes decreased uterine tone?

Back 69

Prostacyclin (PGI2).

Front 70

Which arachadonic acid product(s) causes increased vascular tone?

Back 70

Thromboxane (TXA2)

Front 71

Which arachadonic acid product(s) causes decreased vascular tone?

Back 71

Prostacyclin (PGI2), PGs (PGE2, PGF).

Front 72

What are the two most abundant substances in the plasma membrane?

Back 72

Cholesterol and phospholipids.

Front 73

What is LTB4 responsible for?

Back 73

Neutrophil chemotaxis.

Front 74

Which drugs act on the arachadonic acid pathway and what enzyme(s) to they affect?

Back 74

Corticosteroids (blocks phospholipase A2 and both the Lipoxygenase and Cyclooxygenase pathways); NSAIDs, ASA, acetaminophen, selective COX-2i (blocks COX enzymes); Zileuton (blocks Lipoxygenase pathway); Montelukast and Zafirlukast (leukotriene antagonists).

Front 75

Which signaling molecules utilize a tyrosine kinase receptor?

Back 75

Insulin and IGF-1.

Front 76

What is the first step in the signaling cascade that is initiated by tyrosine kinase receptors?

Back 76

Autophosphorylation.

Front 77

Name a molecule that utilizes clathrin coated pits to enter the cell. What happens when its receptor is mutated?

Back 77

LDL. Mutant LDL receptor lacks the clathrin-coated pit binding site but retains a functioning LDL-binding site. Normal LDL binding but no ingestion of LDL. Increased risk for premature MI.

Front 78

What drug inhibits the Na+/K+ ATPase?

Back 78

Cardiac glycosides (i.e., digoxin and digitalis) and Ouabain.

Front 79

What histologic features are seen in apoptotic cells?

Back 79

Cell shrinkage, nuclear shrinkage and basophilia (pyknosis), membrane blebbing, nuclear fragmentation (karyorrhexis), nuclear fading (karyolysis), formation of apoptotic bodies. NO INFLAMMATION!

Front 80

What substances do cytotoxic T cells and NK cells use to induce apoptosis in the cells infected with virus?

Back 80

Perforin and granzymes.

Front 81

Describe the two extrinsic pathways for apoptosis.

Back 81

1. Ligand receptor interactions (Fas ligand binding to Fas [CD95]).
2. Immune cell (cytotoxic T-cell release of perforin and granzyme B).

Front 82

Describe the intrinsic pathway for apoptosis.

Back 82

Mitochondrial. Changes in proportions of anti- (Bcl-2) and pro-apoptotic (Bax) factors lead to increased mitochondria permeability and release of cytochrome C.

Front 83

What are some of the substances that can trigger apoptosis?

Back 83

Cytochrome C, Increase in Bax, decrease in Bcl-2, deprivation of growth factors, cell stress, DNA damage (p53).

Front 84

What highly damaging events can cause irreversible cell injury?

Back 84

Ischemia, radiation, calcium influx (activates caspases), plasma membrane disruption, ruptured lysosome, mitochondrial permeability, nuclear damage.

Front 85

What are some ways free radical injury is initiated?

Back 85

Radiation exposure, metabolism of drugs, redox reaction, nitric oxide, transition metals, leukocyte oxidative burst.

Front 86

Which metals are known to facilitate the generation of oxygen free radicals?

Back 86

Transition metals (e.g., iron, copper).

Front 87

What cellular particles are responsible for handling oxygen free radicals?

Back 87

Catalase, superoxide dismutase, glutathione reductase, peroxidase, antioxidants.

Front 88

Describe the basis for the Erythrocyte Sedimentation Rate (ESR).

Back 88

Products of inflammation (e.g., fibrinogen) coat RBCs and cause aggregation. When aggregated, RBCs fall at a faster rate within the test tube.

Front 89

What would cause an elevated ESR?

Back 89

Infection, inflammation (e.g., temporal arteritis), cancer, pregnancy, SLE.

Front 90

What would cause a decline in ESR?

Back 90

Polycythemia (too many), sickle cell disease (altered shape, RBCs can't stick together).

Front 91

What is C-Reactive Protein (CRP)? Where is it synthesized? Under what circumstances might it be elevated?

Back 91

Acute-phase reactant synthesized by the liver. Elevations are a strong predictor of MI, stroke, PAD, and sudden cardiac death.

Front 92

What is the first step in leukocyte extravasation?

Back 92

Rolling via E-selectin and P-selectin on the vasculature/stroma and Sialyl Lewis on the leukocyte.

Front 93

What is the second step in leukocyte extravasation?

Back 93

Tight binding between ICAM-1 on the vasculature/stroma and LFA-1 ("integrin") on the leukocyte.

Front 94

What is the third step in leukocyte extravasation?

Back 94

Diapedesis via PECAM-1s.

Front 95

What is the fourth step in leukocyte extravasation?

Back 95

Migration through interstitium guided by chemotactic signals generated by C5a, IL-8, LTB4, Kallikrein.

Front 96

What are the three main cytokine inflammatory mediators?

Back 96

IL-1, IL-6, TNF-alpha.

Front 97

What cytokine is particularly important in the formation of TNF-alpha?

Back 97

TNF-alpha.

Front 98

What cell type plays a role in inflammation by generating fibrinogen and CRP?

Back 98

Hepatocyte.

Front 99

Describe the stages of epithelial wound healing.

Back 99

1. Inflammatory: immediate. mediated by platelets, PMNs, and macrophages.
2. Proliferative: 2-3d after wound. mediated by fibroblasts, myofibroblasts, endothelial cells, keratinocytes.
3. Remodeling: 1w after wound. mediated by fibroblasts. type III collagen replaced by type I collagen.

Front 100

What should always be done prior to beginning a patient on anti-TNF-alpha therapy?

Back 100

PPD test. Anti-TNF-alpha therapy will break down any pre-existing granulomas and can lead to disseminated disease if a patient has a latent Tb infection.

Front 101

What are the different types of collagen and where can they be found?

Back 101

Type I: "Strong" collagen. Found in bone, skin, tendon, cornea.
Type II: "Slippery" collagen. Found in cartilage, vitreous body.
Type III: "Bloody" collagen. Found in skin blood vessels. AKA reticulin.
Type IV: "BM" collagen. Found in basement membranes of kidney, ears, and eyes.

Front 102

Which AAs are abundant in collagen?

Back 102

Proline,lysine, hydroxyproline, hydroxylysine.

Front 103

What is the role of Vitamin C in collagen synthesis?

Back 103

Hydroxylation of proline and lysine residues, of course!

Front 104

What findings are associated with Ehlers-Danlos syndrome?

Back 104

Type III collagen defect. Hypermobile joints. Stretchy skin. Easy bruising. May be associated with joint dislocation, organ rupture and BERRY ANEURYSMS ("worst HA of my life").

Front 105

Describe the pathogenesis and attributes of Osteogenesis Imperfecta.

Back 105

Defect in Type I collagen. Autosomal dominant inheritance. Brittle bones leading to multiple BONE FRACTURES (can look like abuse) with minimal trauma. BLUE SCLERAE.

Front 106

What is the genetic defect responsible for Alport Syndrome?

Back 106

Abnormal Type IV collagen (BM collagen). Progressive hereditary deafness and nephritis. Possible ocular disturbances.

Front 107

Describe elastin and where it can be found.

Back 107

Stretchy protein within the lungs, large arteries, elastic ligaments, vocal cords.

Front 108

Which AAs are abundant in elastin?

Back 108

Proline and glycine.

Front 109

What enzyme breaks down elastin and what regulates this enzyme?

Back 109

Elastase. Inhibited by alpha1-antitrypsin.

Front 110

A young adult non-smoker shows up in your office with signs and sx of emphysema and cirrhosis. What is the likely diagnosis?

Back 110

Alpha1-antitrypsin deficiency. Elastase is running around uninhibited and destroying the elastin in the lungs and liver.

Front 111

What is the defect responsible for Marfan's syndrome? What's the big thing you don't want to miss here?

Back 111

Defect in elastin, specifically fibrillin. Don't miss aortic dissection in these patients.