• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/111

Click to flip

111 Cards in this Set

  • Front
  • Back
Which fetal structure secretes B-hCG?
Syncitiotrophoblast.
What is the maternal component of the placenta?
Decidua basalis.
Order the following molecules by how much energy they contain that can be used to fuel endergonic reactions: pyruvate, glucose, adenosine, AMP, ATP.
Glucose > pyruvate > ATP > AMP > adenosine.
What are the stages of conception between an conception and an inner cell mass?
zygote --> morula --> blastocyst
List several important drugs that are contraindicated in pregnancy.
ACEi, warfarin, tetracycline, aminoglycosides, thalidomide, DES, carbamazapine, phenytoin, valproate, lithium, fluoroquinolones, sulfanamides, chloramphenicol, MTX, clarithromycin, VitA.
During what weeks of fetal development does organogenesis occur?
Weeks 3-8.
What is the embryological origin of the anterior pituitary?
Surface ectoderm.
What is the embryological origin of the cornea?
Neural crest.
What is the embryological origin of the lens of the eye?
Surface ectoderm.
What is the embryological origin of the retina?
Neural ectoderm.
What is the embryological origin of the olfactory epithelium?
Surface ectoderm.
What is the embryological origin of the mammary gland?
Surface ectoderm.
What is the embryological origin of the salivary glands?
Surface ectoderm.
What is the embryological origin of the sweat glands?
Surface ectoderm.
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?
Endoderm; Surface ectoderm.
What effect do ACEi have on fetal development?
Renal abnormalities.
What effect do aminoglycosides have on fetal development?
Deafness; compromised CNVIII.
What effect does DES (diethylstilbestrol) have on fetal development?
Vaginal clear cell adenocarcinoma.
What effect do tetracyclines have on fetal development?
Discoloration of the teeth.
What effect does valproic acid have on fetal development?
Neural tube defects.
During what week of fetal development do genitalia begin to exhibit differentiation into male and female specific organs?
Week 10.
During what week of fetal development does the heart begin to beat?
Week 4.
What is the significance of the Sonic hedgehog gene?
Involved in patterning along the A-P axis.
Where is the Sonic hedgehog gene produced?
Base of limbs in zone of polarizing activity.
What is the significance of the Wnt-7 gene?
Produced at the apical ectodermal ridge (distal end of developing limb) and is necessary for proper organization along D-V axis (front-back).
What is the significance of the FGF gene?
Produced at apical ectodermal ridge and is responsible for lengthening of limbs.
What is the significance of the HOX genes?
Involved in segmental organization of the embryo in a craniocaudal direction -- mutations in HOX genes lead to appendages located in the wrong places!
What are the neural crest derivatives?
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.
What are the neuroectoderm derivatives?
Brain and spinal cord (CNS), retina.
What are the surface ectoderm derivatives?
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.
What are the derivatives of the endoderm?
Gut tube epithelium and derivatives (e.g., lungs, liver, pancreas, thymus, parathyroid, thryoid follicular cells).
What is the leading cause of congenital malformations in the United States?
Fetal alcohol syndrome.
Which anti-coag is safe for use in pregnancy?
Heparin.
What must be present on a protein in order for that protein to gain entry into the nucleus?
Nuclear localization signal.
Which AA are contained in the nuclear localization signal?
Proline, lysine, arginine.
Which types of proteins are responsible for fostering the progression through the cell cycle?
Cylins and CDKs.
Which cyclin-CDK complexes assist in the progression from G1 phase to S phase?
Cyclin D + CDK4; Cyclin E + CDK2.
Which tumor supressor proteins prevent the progression of the cell into S phase?
Rb and p53.
Which cyclin-CDK complexes assist in the progression from G2 phase to M phase?
Cyclin A + CDK2; Cyclin B + CKD1.
What molecule targets proteins in the ER for lysosomes?
Mannose-6-phosphate (M6P).
What is deficient in I-cell disease?
M6P.
What are the different methods that a cell uses to break down proteins?
Proteasome; Lysosome; Calcium-dependent enzymatic degradation.
Which cell types are rich in SER?
Hepatocytes (detoxifying); Chromaffin cells of the adrenal cortex (steroid-synthesizing).
What targets defective proteins for proteasomal degredation?
Ubiquitin.
Name the cell types that are considered "labile" (never enter G0 and have a very short G1 phase).
Skin cells, hair follicles, gut epithelium, bone marrow.
What types of cells are considered "stable, quiescent" (only enter G1 from G0 when stimulated)?
Hepatocytes, lymphocytes.
What are Nissl bodies?
RER of neurons. They synthesize enzymes and peptide neurotransmitters.
Which AA residues are modifiable by the Golgi?
Serine, threonine, asparagine.
Describe the vesicular trafficking proteins COPI and COPII.
COPI: retrograde, Golgi --> ER.
COPII: anterograde, RER --> cis-Golgi.
What is the mechanism of I-cell disease?
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.
What are the characteristics of I-cell disease?
Coarse facial features, clouded corneas, restricted joint movement, high plasma levels of lysosomal enzymes. Often fatal in childhood.
What drugs act on microtubules?
Mebendazole/Thiabendazole (antihelminthic), Colchicine (anti-gout), Vincristine/Vinblastine (anti-cancer), Paclitaxel (anti-breast cancer), Griseofulvin (anti-fungal).
Which organelle is responsible for the breakdown of very long-chain fatty acids?
Peroxisome.
What are the intermediate filaments for connective tissue?
Vimentin.
What are the intermediate filaments for muscle tissue?
Desmin.
What are the intermediate filaments for epithelial tissue?
Cytokeratins.
What are the intermediate filaments for axons?
Neurofilaments.
What are the defects seen in Kartagener syndrome?
Male and female infertility, recurrent sinusitis, and bronchiectasis. Associated with situs inversus.
What is Kartagener syndrome?
Immotile cilia due to a dynein arm defect.
Describe the function of dynein.
Retrograde transportation (+ to -) of cellular cargo to microtubule.
Describe the function of kinesin.
Anterograde transportation (- to +) of cellular cargo to microtubule.
What are the intermediate filaments of the nuclear envelope and DNA within?
Nuclear lamins.
What protein is involved in transporting an endocytosed vesicle from the plasma membrane to the endosome?
Clathrin.
Which arachadonic acid product(s) causes increased bronchial tone?
LTD4, LTC4, Thromboxane (TXA2).
Which arachadonic acid product(s) causes decreased bronchial tone?
Prostacyclin (PGI2), Prostaglandin.
Which arachadonic acid product(s) causes increased platelet aggregation?
Thromboxane.
Which arachadonic acid product(s) causes decreased platelet aggregation?
Prostacyclin (PGI2).
Which arachadonic acid product(s) causes increased uterine tone?
PGs (PGE2, PGF).
Which arachadonic acid product(s) causes decreased uterine tone?
Prostacyclin (PGI2).
Which arachadonic acid product(s) causes increased vascular tone?
Thromboxane (TXA2)
Which arachadonic acid product(s) causes decreased vascular tone?
Prostacyclin (PGI2), PGs (PGE2, PGF).
What are the two most abundant substances in the plasma membrane?
Cholesterol and phospholipids.
What is LTB4 responsible for?
Neutrophil chemotaxis.
Which drugs act on the arachadonic acid pathway and what enzyme(s) to they affect?
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).
Which signaling molecules utilize a tyrosine kinase receptor?
Insulin and IGF-1.
What is the first step in the signaling cascade that is initiated by tyrosine kinase receptors?
Autophosphorylation.
Name a molecule that utilizes clathrin coated pits to enter the cell. What happens when its receptor is mutated?
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.
What drug inhibits the Na+/K+ ATPase?
Cardiac glycosides (i.e., digoxin and digitalis) and Ouabain.
What histologic features are seen in apoptotic cells?
Cell shrinkage, nuclear shrinkage and basophilia (pyknosis), membrane blebbing, nuclear fragmentation (karyorrhexis), nuclear fading (karyolysis), formation of apoptotic bodies. NO INFLAMMATION!
What substances do cytotoxic T cells and NK cells use to induce apoptosis in the cells infected with virus?
Perforin and granzymes.
Describe the two extrinsic pathways for apoptosis.
1. Ligand receptor interactions (Fas ligand binding to Fas [CD95]).
2. Immune cell (cytotoxic T-cell release of perforin and granzyme B).
Describe the intrinsic pathway for apoptosis.
Mitochondrial. Changes in proportions of anti- (Bcl-2) and pro-apoptotic (Bax) factors lead to increased mitochondria permeability and release of cytochrome C.
What are some of the substances that can trigger apoptosis?
Cytochrome C, Increase in Bax, decrease in Bcl-2, deprivation of growth factors, cell stress, DNA damage (p53).
What highly damaging events can cause irreversible cell injury?
Ischemia, radiation, calcium influx (activates caspases), plasma membrane disruption, ruptured lysosome, mitochondrial permeability, nuclear damage.
What are some ways free radical injury is initiated?
Radiation exposure, metabolism of drugs, redox reaction, nitric oxide, transition metals, leukocyte oxidative burst.
Which metals are known to facilitate the generation of oxygen free radicals?
Transition metals (e.g., iron, copper).
What cellular particles are responsible for handling oxygen free radicals?
Catalase, superoxide dismutase, glutathione reductase, peroxidase, antioxidants.
Describe the basis for the Erythrocyte Sedimentation Rate (ESR).
Products of inflammation (e.g., fibrinogen) coat RBCs and cause aggregation. When aggregated, RBCs fall at a faster rate within the test tube.
What would cause an elevated ESR?
Infection, inflammation (e.g., temporal arteritis), cancer, pregnancy, SLE.
What would cause a decline in ESR?
Polycythemia (too many), sickle cell disease (altered shape, RBCs can't stick together).
What is C-Reactive Protein (CRP)? Where is it synthesized? Under what circumstances might it be elevated?
Acute-phase reactant synthesized by the liver. Elevations are a strong predictor of MI, stroke, PAD, and sudden cardiac death.
What is the first step in leukocyte extravasation?
Rolling via E-selectin and P-selectin on the vasculature/stroma and Sialyl Lewis on the leukocyte.
What is the second step in leukocyte extravasation?
Tight binding between ICAM-1 on the vasculature/stroma and LFA-1 ("integrin") on the leukocyte.
What is the third step in leukocyte extravasation?
Diapedesis via PECAM-1s.
What is the fourth step in leukocyte extravasation?
Migration through interstitium guided by chemotactic signals generated by C5a, IL-8, LTB4, Kallikrein.
What are the three main cytokine inflammatory mediators?
IL-1, IL-6, TNF-alpha.
What cytokine is particularly important in the formation of TNF-alpha?
TNF-alpha.
What cell type plays a role in inflammation by generating fibrinogen and CRP?
Hepatocyte.
Describe the stages of epithelial wound healing.
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.
What should always be done prior to beginning a patient on anti-TNF-alpha therapy?
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.
What are the different types of collagen and where can they be found?
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.
Which AAs are abundant in collagen?
Proline,lysine, hydroxyproline, hydroxylysine.
What is the role of Vitamin C in collagen synthesis?
Hydroxylation of proline and lysine residues, of course!
What findings are associated with Ehlers-Danlos syndrome?
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").
Describe the pathogenesis and attributes of Osteogenesis Imperfecta.
Defect in Type I collagen. Autosomal dominant inheritance. Brittle bones leading to multiple BONE FRACTURES (can look like abuse) with minimal trauma. BLUE SCLERAE.
What is the genetic defect responsible for Alport Syndrome?
Abnormal Type IV collagen (BM collagen). Progressive hereditary deafness and nephritis. Possible ocular disturbances.
Describe elastin and where it can be found.
Stretchy protein within the lungs, large arteries, elastic ligaments, vocal cords.
Which AAs are abundant in elastin?
Proline and glycine.
What enzyme breaks down elastin and what regulates this enzyme?
Elastase. Inhibited by alpha1-antitrypsin.
A young adult non-smoker shows up in your office with signs and sx of emphysema and cirrhosis. What is the likely diagnosis?
Alpha1-antitrypsin deficiency. Elastase is running around uninhibited and destroying the elastin in the lungs and liver.
What is the defect responsible for Marfan's syndrome? What's the big thing you don't want to miss here?
Defect in elastin, specifically fibrillin. Don't miss aortic dissection in these patients.