DIT Foundations 1-9 Flashcards
(129 cards)
1
Q
Derivatives of Surface Ectoderm
A
“think special senses and things in head not influ by notochord”- Adenohypophysis (ant pit) from Rathke’s pouch, lens, epithelial linings of oral cavity, sensory organs of ear, olfactor epithelium, epidermis, anal canal BELOW pectinate line, parotid g, sweat g., mammary g.
2
Q
Derivatives of neuroectoderm
A
“think CNS” - Brain (neurohypophysis, CNS, neurons, oligodendrocytes, astrocytes, ependymal cells, pineal gland), retina, optic n, spinal cord
3
Q
Derivatives of neural crest cells
A
PNS (DRG, CNs, celiac gang, Schwann cells, ANS), melanocytes, odontoblasts, chromaffin cells of adrenal medulla, parafollicular cells of thyroid, pia and arachnoid, bones of skull, aorticopulmonary septum
4
Q
Derivatives of mesoderm
A
Muscle, bone, CT, serous lining of body cavities (peritoneum), spleen, CV structures, lymphatics, blood, wall of gut tube, wall of bladder, urethra, upper 1/3 vagina, kidneys, adrenal cortex, dermis, testes, ovaries
5
Q
Derivatievs of endoderm
A
Gut tube epithelium (including anal canal ABOVE pectinate line) and luminal epithlial derivatives (lungs, liver, GB, pancreas, eustachian tube, trachea, thymus, parathyroid, thyroid follicular cells), lower 2/3 vagina
6
Q
Gibbs free energy forumla
A
Delta G = delta H - T x Delta S
7
Q
What fetal placental structure secretes hCG?
A
Syncitiotrophoblast
8
Q
Maternal component of placenta?
A
Decidua basalis
9
Q
Stages of Fetal Development
A
Zygote -> Morula -> Blastocyst -> Inner cell mass (-> epiblast+hypoblast and bceomes fetus) + Trophoblast (becomes placenta and embryonic mem)
10
Q
What embryonic structure (derived from hypoblast) serves as 2ry energy source?
A
Endodermal yolk sac
11
Q
What embryonic structure serves as a resrovoir of nonspecialized (undifferentiated) stem cells?
A
Endodermal yolk sac
12
Q
3 germ layers derived from epiblast?
A
Ectoderm, Mesoder, Endoderm
13
Q
Neural Crest Derivatives of PNS
A
ANS, Vagus n., DRG, Sympathethic (celiac) ganglia, Schwann cells, sensory nn, CNs
14
Q
Neural crest derivatives of Ear
A
Bones of inner ear
15
Q
Neural crest derivatives of eye
A
Anterior chamber, cornea, sclera, iris pigment cells, ciliary mm.
16
Q
Neural crest derivatives of adrenal gland
A
Chromaffin cells of adrenal medulla
17
Q
Neural crest derivatives of mouth
A
odontoblast
18
Q
neural crest derivatives of heart
A
aorticopulmonary septum
19
Q
neural crest derivatives of digestive sys
A
Enterochromaffin cells, enteric nervous sys, celiac ganglion
20
Q
Neural crest derivatives of thyroid
A
Parafollicular cells
21
Q
Neural crest derivatives of skin
A
melanocytes
22
Q
Embryo development of Forebrain structures
A
Prosencephalon -> (telencephalon -> cerebral hemispheres, basal gang, hippocampus, amydyla) + (diencephalon -> thalamus, hypothalamus, optnic n and tract)
23
Q
Embryo development of midbrain structures
A
Mesencephalon -> Mesencephalon -> midbrain
24
Q
Embryo development of hidbrain structures
A
Rhombencephalon -> (Metencephalon -> Pons and cerebellum) + (Myelencephalon -> medulla)
25
Teratogens
Antiseuzure: carbamazapine, valproate, penytoin. Abx: metronidazole, aminoglycosides, tetracyclines, fluorquinolines, sulfonamides, clarithromycin. Folate antag: MTX. Misc: vit A, ACE inhibitor, Warfarmin, Thalidomide, DES
26
Sonic Hedgehog Gene: produced where, invovled in, mutation causes?
Produced at base of limb. Involved in: patterning along anterior-posterior axis (crainal-caudal), CNS development. Mutation-> holoprosencaphaly.
27
Wnt-7 gene: produced where and needed for?
Produced at apical ectodermal ridge. Needed for proper organization along dorsal-ventral axis.
28
FGF gene: produced where and stimulates what?
Produced in apical ectoderm. Stimulates miosis of mesoderm -> lengthening of limbs
29
Homeobox (HOX) gene: involved in what and mutation?
Blueprint in skeletal morphology (organization of embryo), code for transcription regulators. Mutation in HOXD-13 -> synpolydactyly. Mutaiton can also lead to appendages in wrong place (fruit fly). Retinoic acid alters HOX gene.
30
Leading cause of congenital malformation in US?
Fetal alcohol syndrome-MR, microcephaly, holoprosencephaly, facial abnorm, limb dislocation, heart and lung fistulas
31
Shotest cell cycle phase?
Mitosis
32
Functions of the Golgi Apparatus
1) Distribution center for proteins and lipids from ER to vesicles in PM. 2) Modifes N-oligosaccharides on asparagine. 3) Adds O-oligosaccharides on seirne and threonine. 4) Adds mannose-6-phosphate to proteins for trafficking to lysosome. 5) Formation of proteoglycan by glycosylation of chondroitin sulfate and heparin sulfate. 6) Sulfation of sugars in proteoglycans and tyrosination on protein.
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COPI
Golgi -> Golgi (retrograde); Golgi -> ER
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COP II
Golgi -> Golgi (anterograde); ER -> golgi
35
3 methods of protein degradation?
1) Ubiquitin-proteosome. 2) Lysosome. 3) Ca2+ depending enzyme
36
Function of dehydrogenase?
Catalyzes oxidation-reduction reactions
37
Funciton of carboxylase?
Transfers CO2 group w/ help of biotin (B6)
38
Embry origin of tissue psoximal to pectinate line?
Endoderm
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Embryo origin of tissue distal to pectinate line?
surface ectoderm
40
What are nuclear localization signals?
Amino acid sequence of 4-8 aa rich in lysine, proline, arginine. Component of proteins bound for nucleus that nuclear pore recognizes and then transports into nucleus via ATPase. Mutaiton->prevent nuclear transport.
41
Regulation of G1 -> S?
1) Cyclin D binds/activates CDK4 -> phosphorylation of Rb -> Rb relesaed from E2F -> unbound E2F is free to transcribe/synthesize the components needed to progress through S phase. 2) Cyclin E binds/activates CKD2 -> cell allowed to progress through S.
42
Regulation of G2 -> M?
1) Cyclin A--CDK2 complex -> mitotic prophase. 2) Cyclin B--CDK1 complex activated by cdc25 -> breakdown of nuc envelope and initiation of mitosis.
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Corneal clouding, coarse facies, HSM, skel abnorm, restricted joint movements, MR
I-cell disease due to defy in mannose-6-phosphorylation
44
Molecule needed for receptor mediated endocytosis?
Clathrin
45
What proteins regulate transition from one phase of cell cycle to another?
CDKs and cyclins
46
Dynein
retrograde to MT (+ -> -); toward nucleus
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Kinesin
anterograde to MT (- -> +); away from nucleus
48
Chediak-Higashi Syndrome
Recurrent pyogenic infections, partial albminsim, periph neuropathy. Due to mutaiton in lysosomal trafficking regulator gene (LYST) whose product is req for MT-dependent sorting of endosomal protesin into multivesicular endosomes.
49
Kartagener's Syndrome
immotile cilia due to dynein arm defect -> male infertility, dec F infertility, recurrent sinusisit, assoc w situs inversus
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Vimentin
CT
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Desmin
Muscel cells
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Cytokeratin
Epithelial cells
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Glial fibrillary acid proteins (GFAP)
Astrocytes, Schwann cells, other neuroglia
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Peripherin
Neurons
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Neurofilaments
Axons w/in neurons
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Nuclear Lamins (A, B, C)
Nuclear envelope and DNA w/in
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Drugs that act on the MT
Vincristine/Vinblastine, Paclitaxel, Colchicine, Mebendazole/Thiobendazole, Griseofulvin
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2 fundametnal substances needed to make most things work inside cell?
Ca2+ and ATP
59
What membrane lipid forms AA?
Phosphotidylinositol
60
Lipoxygenase pwy
AA -> Hydroperoxides -> Leukotrienes
61
What drug inhibits Lipoxygenase pwy? Where?
Zileuton inhibits lipoxygenase. Zafirlukast and Montelukast inhibit receptors on Leukotrienes
62
Effects of leukotrienes?
Neutrophil chemotaxis (LTB4) and inc bronchial tone
63
Cyclooxygenase pwy?
AA -> Endoperoxides -> Prostacyclin (PGI2) + Prostaglandins (PGE2 and PGF2) + Thromboxane (TXA2)
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Effects of prostacyclin
dec: platelet aggregation, vascular tone, bronchial tone, uterine tone
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Effects of Prostaglandins
increase uterine tone, dec vascular and bronchilar tone
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Effects of thromboxane
inc: platelet aggregation, vascular tone, bronchial tone
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Drug that inhibits COX?
NSAIDS, aspirin, acetominophen (inactivated peripherally, no blood thinning effect), COX-2 inhibitors
68
Drug that inhibits phosphlipase A2?
corticosteroids
69
Cellular characteristics of apoptosis
Cell shrinkage, nuclear shrinkage (pyknosis) and basophilia, membrane blebbing, nuclear fragmenting (karyohexis), apoptotic bodies, karyolysis
70
Coagulative necrosis seen in which organs?
Heart, liver, kidney
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Liquefactive necrosis seen in which organs?
Brain, bacterial abscess, pleural effusion
72
Caseous necrosis seen in which organs?
TB, systemic fungi
73
Fatty necrosis seen in which organs?
Peripancreatic fat (saponification via lipase)
74
Fibrinoid necrosis seen in what?
Blood vessels
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Gangrenous necrosis seen in what?
Dry (ischemic coagulative) or wet (w/ bacteria or liquefactive)- GI tract and limbs
76
Characteristics of Reversible Cell Injury
Dec ATP -> no Na+/K+ ATPase -> CELL SWELLING-> ribosomes call off RER -> no protein synth. Dec. glycogen, fatty change, nuclear chromatin clumping.
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Characteristics/Causes of Irreversible Cell Injury
MEMBRANE DAMAGE. Plasma membrane damage and mito permeability -> Ca2+ influx -> caspase activation. Lysosomal rupture.
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Mechanisms of Cell Injury
1. Dec ATP (dec O2 and nutrients; toxins). 2. Mito damage -> impaired ATP production and induction of apoptosis. 3. Influx of Ca2+ -> inc mito perm and activate phosphlipases, proteases, endonucleaes, and ATPases. 4. Accumulation of oxygen-derived free radicals-> mem damage via lipid peroxidation, protein mod, DNA break.
79
What cellular byproducts would you see w/ cardiac myocyte damage?
Troponin, CKMB, CPK, Myoglobin
80
What cellular byproducts would you see w/ skeletal myocyte damage?
Aldolase, CPK
81
What cellular byproducts would you see w/ hepatocyte damage?
AST, ALT, GGT, Alk phos
82
What cellular byproducts would you see w/ salivary gland cell damage?
Amylase
83
What cellular byproducts would you see w/ pancreatic exocrine cell damage?
Amylase and Lipase
84
What cellular byproducts would you see w/ RBC damage?
Heme and bilirubin
85
Red Infarcts occur in what?
Loose tissues w/ collaterals such as: liver, lung, intestine, or following reperfusion (injury due to free radicals)
86
Pale Infarcts occur in what?
Solid tissues w/ a single blood supple such as: heart, kidney, and spleen.
87
Enzymes responsible for handling oxygen free rad damage?
Catalse, Superoxide dismutase, Glutathione peroxidase
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Substances that can trigger apoptosis?
Cytotoxic T cells, deprived of GF, cell stress, DNA damage/repair process fails -> p53 triggers apop, cytokines (TNF)
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Characteristics of infalmmation
Rubor, calor, tumor, dolor, functio lasea
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Vascular component of inflammation?
inc vascular perm, vasodilation, endothelial injury
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Cellular component of inflammation?
Neutrophils extravasate from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator rel.
92
Main cells/mediators in acute inflammation?
Neutrophil, eosinophil, antibody mediated. IL-6, IL-1, TNF-a
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Time course of acute inflammation
Rapid onset (sec to min), lasts min to days.
94
Outcomes of acute inflammation?
Complete resolution, abscess formation, and progression to chronic inflammation
95
Describe the steps and receptors of Leukocyte extravasation
Rolling: P & E-selectins on vasculature and Sialyl-Lewis X on leukocytes. Tight-binding: ICAM-1 on vasculature and LFA-1 (integrin) on leukocytes. Diapedesis: PECAM-1 on vasculature and PECAM-1 on leukocytes. Migration: C5a, IL-8, LTB4, Kallikrein
96
Characteristics and causes of Transudate
"WATERY." Hypocellular, protein poor, specific gravity < 1.012. Due to: inc hydrostatic pressure, dec oncotic pressure, Na+ retention
97
Characteristics and causes of exudate
Cellular, protein rich, specific gravity > 1.010. Due to: lymphatic obstruction, inflammation
98
Main cell type in chronic inflammation?
Mononuclear cells (macrophage)
99
Characteristic of chronic inflmmation?
Persistent destruction and repair
100
Chronic inflammation is associated w?
Blood vessel proliferaiton, fibrosis, granuloma
101
What is a granuloma? How are they formed?
Nodular collection of epithelioid macrophages and giant cells. Th1 cells secrete IFN-gamma -> stim MO to secrete TNF-a -> form and maintain granuloma
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Outcome of chornic inflammation?
Scarring and amyloidosis
103
Granulomatous Diseases (ddx of granuloma)
Mycobacterium tuberculosis, Fungal infexn, Trepnoema pallidum, M. leprae, Bartonella henselae, Sarcoidosis, Crohn's, Granulomatosis w/ polyangitis (Wegner's), Churg-Strauss syndrome, Berlliosis, silicosis
104
Causes of increased ESR
Infections(osteomyelitis), malignancy, SLE and RA, pregnancy, inflammation (temporal arteritis)
105
Causes of decreased ESR
Sickle cell (altered shape), polycythemia (too many), CHF
106
What are C-Reactive proteins?
Acute-phase reactants synthesized by the liver. Also can be secreted from cells w/in atherosclerotic plaques to induce prothrombotic state.
107
Function of C-reactive proteins?
Part of innate immune sys: opsonizes bacteria and activates complement.
108
3* Steps in Collagene Synthesis
(steps 1-4 inside fibroblast) (steps 5, 6 outside) 1. Synthesis (RER): Translation of collagen a chains (preprocollagen)-usually Gly-X-Y (X and Y are proline and lysine). 2. Hydroxylation (ER): hydroxylation of specific proline and lysine (req vit C). 3. Glycolsylation (ER): glycosylation of pro-a-chain hydroxylysine residues and formation of procollagen via hydrogen and disulfide bonds (triple helix of 3 collagen a chains). 4. Exocytosis of procollagen into extracellular space. 5. Proteolytic processing: cleavage of disulfide-rich terminal regions of procollagen -> insoluble tropocollagen. 6. Cross-linking: reinforcement of many staggered tropocollagen molecules by covalent lysine-hydroxylysine cross-linkage (by Cu2+-containing lysyl oxidase) to make collagen fibrils.
109
Osteogenesis imperfecta
Brittle bone disease. AD. Abnormal Type I collagen causing: mult fx w/ minimal trauma, BLUE SCLERAE, hearing loss, dental imperfections. Do NOT confuse w/ child abuse. Problem with step 3
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Ehlers Danlos Syndrome
Hyperextensible skin, tendency to bleed, hypermobile joints. Can be assoc w/ joint disolaction, Berry aneurysm, organ rupture. Problems in Type I, III, V collagen. Problems in step 6.
111
Alport Syndrome
Abnormal Type IV collagen. Most common forms are X-linked recessive. Characterized by progressive hereditary nephritis (Type IV collagen important in BM of kidney, ears, eyes) and deafness. May be assoc w/ ocular disturbances. "Can't pee, can't see, can't hear me"
112
Elastin is rich in what aa?
Proline and glycine, nonhydroxylated forms
113
What is elastin made of? Where is it "processed?"
Tropoelastin with fibrillin scaffolding. Cross-linking takes place extracellulary.
114
What breaks elastin down? Disease association?
Elastase which is normally inhibited by a1-antitrypsin. Emphysema can be caused by a1-antitrypsin defy -> excess elastase activity.
115
What is deficient in Marfan's syndrome?
Fibrillin
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Why is Vit C important in collagen?
Hydroxyaltion of proline and lysine to form cross-links
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Where is Type I Collagen found?
STRONG: Bone, Skin, Tendons
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Where is Type II collagen found?
SLIPPERY: Cartilage, vitreous body, nucleus pulposus.
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Where is Type III Collagen found?
BLOODY: Reticulin-skin, blood vessels, uterus, fetal tissue, granulation tissue
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Where is Type IV Collagen found?
BM: kidney and lens
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Phases of wound healing?
Inflammatory (immediate), Proliferative (2-3 days after wound), Remodeling (1 week after wound)
122
What happens during the first phase of wound healing? Mediators?
Platelets, neutrophils, macrophages. Clot formaiton, inc vessel perm and neut migration into tissue; MO clear debris 2 days later. 0-3 hrs=hemorrhage and clotting; 12-24 hrs=PMNs
123
What happens during the second phase of wound healing? Mediators?
MO, fibroblasts, keratinocytes, endothelial cells, myofibroblasts. Deposition of granulation tissue and collagen, angiogensis, epithelial cell proliferatoin, dissolution of clot, and wound contraction. 2-4 days MO infiltraiton; 3-5 days granulation tissue
124
What happens during the third phase of wound healing? Mediators?
Fibroblasts. Type III collagen replaced by Type I to inc tensile strength. Months later
125
What is atrophy?
Reduction in the size or # of cells.
126
Causes of atrophy?
dec hormones, dec innervation, dec blood flow, dec nutrients, inc pressure, occlusion of secretory ducts (CF)
127
Function of cholesterol in plasa mem?
dec fluidity, inc melting point
128
What occurs at the cellular level during atrophy?
Dec metabolic activity -> dec protein synthe. Ubiquitin tags unused protein -> inc protein degradation. Autophagy -> free radical oxidaiton and lipocuscian. Dec # of organelles.
129
What is a lipocuscian granule?
Residual body w/in cell. Contain brown pigment that results from free radical induced lipid peroxidation.
