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DIT > DIT Foundations 1-9 > Flashcards

DIT Foundations 1-9 Flashcards

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.

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2
Q

Derivatives of neuroectoderm

A

“think CNS” - Brain (neurohypophysis, CNS, neurons, oligodendrocytes, astrocytes, ependymal cells, pineal gland), retina, optic n, spinal cord

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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

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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

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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

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6
Q

Gibbs free energy forumla

A

Delta G = delta H - T x Delta S

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7
Q

What fetal placental structure secretes hCG?

A

Syncitiotrophoblast

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8
Q

Maternal component of placenta?

A

Decidua basalis

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9
Q

Stages of Fetal Development

A

Zygote -> Morula -> Blastocyst -> Inner cell mass (-> epiblast+hypoblast and bceomes fetus) + Trophoblast (becomes placenta and embryonic mem)

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10
Q

What embryonic structure (derived from hypoblast) serves as 2ry energy source?

A

Endodermal yolk sac

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11
Q

What embryonic structure serves as a resrovoir of nonspecialized (undifferentiated) stem cells?

A

Endodermal yolk sac

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12
Q

3 germ layers derived from epiblast?

A

Ectoderm, Mesoder, Endoderm

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13
Q

Neural Crest Derivatives of PNS

A

ANS, Vagus n., DRG, Sympathethic (celiac) ganglia, Schwann cells, sensory nn, CNs

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14
Q

Neural crest derivatives of Ear

A

Bones of inner ear

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15
Q

Neural crest derivatives of eye

A

Anterior chamber, cornea, sclera, iris pigment cells, ciliary mm.

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16
Q

Neural crest derivatives of adrenal gland

A

Chromaffin cells of adrenal medulla

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17
Q

Neural crest derivatives of mouth

A

odontoblast

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18
Q

neural crest derivatives of heart

A

aorticopulmonary septum

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19
Q

neural crest derivatives of digestive sys

A

Enterochromaffin cells, enteric nervous sys, celiac ganglion

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20
Q

Neural crest derivatives of thyroid

A

Parafollicular cells

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21
Q

Neural crest derivatives of skin

A

melanocytes

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22
Q

Embryo development of Forebrain structures

A

Prosencephalon -> (telencephalon -> cerebral hemispheres, basal gang, hippocampus, amydyla) + (diencephalon -> thalamus, hypothalamus, optnic n and tract)

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23
Q

Embryo development of midbrain structures

A

Mesencephalon -> Mesencephalon -> midbrain

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24
Q

Embryo development of hidbrain structures

A

Rhombencephalon -> (Metencephalon -> Pons and cerebellum) + (Myelencephalon -> medulla)

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25
Q

Teratogens

A

Antiseuzure: carbamazapine, valproate, penytoin. Abx: metronidazole, aminoglycosides, tetracyclines, fluorquinolines, sulfonamides, clarithromycin. Folate antag: MTX. Misc: vit A, ACE inhibitor, Warfarmin, Thalidomide, DES

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26
Q

Sonic Hedgehog Gene: produced where, invovled in, mutation causes?

A

Produced at base of limb. Involved in: patterning along anterior-posterior axis (crainal-caudal), CNS development. Mutation-> holoprosencaphaly.

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27
Q

Wnt-7 gene: produced where and needed for?

A

Produced at apical ectodermal ridge. Needed for proper organization along dorsal-ventral axis.

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28
Q

FGF gene: produced where and stimulates what?

A

Produced in apical ectoderm. Stimulates miosis of mesoderm -> lengthening of limbs

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29
Q

Homeobox (HOX) gene: involved in what and mutation?

A

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.

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30
Q

Leading cause of congenital malformation in US?

A

Fetal alcohol syndrome-MR, microcephaly, holoprosencephaly, facial abnorm, limb dislocation, heart and lung fistulas

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31
Q

Shotest cell cycle phase?

A

Mitosis

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32
Q

Functions of the Golgi Apparatus

A

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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33
Q

COPI

A

Golgi -> Golgi (retrograde); Golgi -> ER

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34
Q

COP II

A

Golgi -> Golgi (anterograde); ER -> golgi

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35
Q

3 methods of protein degradation?

A

1) Ubiquitin-proteosome. 2) Lysosome. 3) Ca2+ depending enzyme

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36
Q

Function of dehydrogenase?

A

Catalyzes oxidation-reduction reactions

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37
Q

Funciton of carboxylase?

A

Transfers CO2 group w/ help of biotin (B6)

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38
Q

Embry origin of tissue psoximal to pectinate line?

A

Endoderm

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39
Q

Embryo origin of tissue distal to pectinate line?

A

surface ectoderm

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40
Q

What are nuclear localization signals?

A

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.

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41
Q

Regulation of G1 -> S?

A

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.

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42
Q

Regulation of G2 -> M?

A

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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43
Q

Corneal clouding, coarse facies, HSM, skel abnorm, restricted joint movements, MR

A

I-cell disease due to defy in mannose-6-phosphorylation

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44
Q

Molecule needed for receptor mediated endocytosis?

A

Clathrin

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45
Q

What proteins regulate transition from one phase of cell cycle to another?

A

CDKs and cyclins

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46
Q

Dynein

A

retrograde to MT (+ -> -); toward nucleus

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47
Q

Kinesin

A

anterograde to MT (- -> +); away from nucleus

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48
Q

Chediak-Higashi Syndrome

A

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.

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49
Q

Kartagener’s Syndrome

A

immotile cilia due to dynein arm defect -> male infertility, dec F infertility, recurrent sinusisit, assoc w situs inversus

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50
Q

Vimentin

A

CT

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51
Q

Desmin

A

Muscel cells

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52
Q

Cytokeratin

A

Epithelial cells

53
Q

Glial fibrillary acid proteins (GFAP)

A

Astrocytes, Schwann cells, other neuroglia

54
Q

Peripherin

A

Neurons

55
Q

Neurofilaments

A

Axons w/in neurons

56
Q

Nuclear Lamins (A, B, C)

A

Nuclear envelope and DNA w/in

57
Q

Drugs that act on the MT

A

Vincristine/Vinblastine, Paclitaxel, Colchicine, Mebendazole/Thiobendazole, Griseofulvin

58
Q

2 fundametnal substances needed to make most things work inside cell?

A

Ca2+ and ATP

59
Q

What membrane lipid forms AA?

A

Phosphotidylinositol

60
Q

Lipoxygenase pwy

A

AA -> Hydroperoxides -> Leukotrienes

61
Q

What drug inhibits Lipoxygenase pwy? Where?

A

Zileuton inhibits lipoxygenase. Zafirlukast and Montelukast inhibit receptors on Leukotrienes

62
Q

Effects of leukotrienes?

A

Neutrophil chemotaxis (LTB4) and inc bronchial tone

63
Q

Cyclooxygenase pwy?

A

AA -> Endoperoxides -> Prostacyclin (PGI2) + Prostaglandins (PGE2 and PGF2) + Thromboxane (TXA2)

64
Q

Effects of prostacyclin

A

dec: platelet aggregation, vascular tone, bronchial tone, uterine tone

65
Q

Effects of Prostaglandins

A

increase uterine tone, dec vascular and bronchilar tone

66
Q

Effects of thromboxane

A

inc: platelet aggregation, vascular tone, bronchial tone

67
Q

Drug that inhibits COX?

A

NSAIDS, aspirin, acetominophen (inactivated peripherally, no blood thinning effect), COX-2 inhibitors

68
Q

Drug that inhibits phosphlipase A2?

A

corticosteroids

69
Q

Cellular characteristics of apoptosis

A

Cell shrinkage, nuclear shrinkage (pyknosis) and basophilia, membrane blebbing, nuclear fragmenting (karyohexis), apoptotic bodies, karyolysis

70
Q

Coagulative necrosis seen in which organs?

A

Heart, liver, kidney

71
Q

Liquefactive necrosis seen in which organs?

A

Brain, bacterial abscess, pleural effusion

72
Q

Caseous necrosis seen in which organs?

A

TB, systemic fungi

73
Q

Fatty necrosis seen in which organs?

A

Peripancreatic fat (saponification via lipase)

74
Q

Fibrinoid necrosis seen in what?

A

Blood vessels

75
Q

Gangrenous necrosis seen in what?

A

Dry (ischemic coagulative) or wet (w/ bacteria or liquefactive)- GI tract and limbs

76
Q

Characteristics of Reversible Cell Injury

A

Dec ATP -> no Na+/K+ ATPase -> CELL SWELLING-> ribosomes call off RER -> no protein synth. Dec. glycogen, fatty change, nuclear chromatin clumping.

77
Q

Characteristics/Causes of Irreversible Cell Injury

A

MEMBRANE DAMAGE. Plasma membrane damage and mito permeability -> Ca2+ influx -> caspase activation. Lysosomal rupture.

78
Q

Mechanisms of Cell Injury

A
  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
Q

What cellular byproducts would you see w/ cardiac myocyte damage?

A

Troponin, CKMB, CPK, Myoglobin

80
Q

What cellular byproducts would you see w/ skeletal myocyte damage?

A

Aldolase, CPK

81
Q

What cellular byproducts would you see w/ hepatocyte damage?

A

AST, ALT, GGT, Alk phos

82
Q

What cellular byproducts would you see w/ salivary gland cell damage?

A

Amylase

83
Q

What cellular byproducts would you see w/ pancreatic exocrine cell damage?

A

Amylase and Lipase

84
Q

What cellular byproducts would you see w/ RBC damage?

A

Heme and bilirubin

85
Q

Red Infarcts occur in what?

A

Loose tissues w/ collaterals such as: liver, lung, intestine, or following reperfusion (injury due to free radicals)

86
Q

Pale Infarcts occur in what?

A

Solid tissues w/ a single blood supple such as: heart, kidney, and spleen.

87
Q

Enzymes responsible for handling oxygen free rad damage?

A

Catalse, Superoxide dismutase, Glutathione peroxidase

88
Q

Substances that can trigger apoptosis?

A

Cytotoxic T cells, deprived of GF, cell stress, DNA damage/repair process fails -> p53 triggers apop, cytokines (TNF)

89
Q

Characteristics of infalmmation

A

Rubor, calor, tumor, dolor, functio lasea

90
Q

Vascular component of inflammation?

A

inc vascular perm, vasodilation, endothelial injury

91
Q

Cellular component of inflammation?

A

Neutrophils extravasate from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator rel.

92
Q

Main cells/mediators in acute inflammation?

A

Neutrophil, eosinophil, antibody mediated. IL-6, IL-1, TNF-a

93
Q

Time course of acute inflammation

A

Rapid onset (sec to min), lasts min to days.

94
Q

Outcomes of acute inflammation?

A

Complete resolution, abscess formation, and progression to chronic inflammation

95
Q

Describe the steps and receptors of Leukocyte extravasation

A

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
Q

Characteristics and causes of Transudate

A

“WATERY.” Hypocellular, protein poor, specific gravity < 1.012. Due to: inc hydrostatic pressure, dec oncotic pressure, Na+ retention

97
Q

Characteristics and causes of exudate

A

Cellular, protein rich, specific gravity > 1.010. Due to: lymphatic obstruction, inflammation

98
Q

Main cell type in chronic inflammation?

A

Mononuclear cells (macrophage)

99
Q

Characteristic of chronic inflmmation?

A

Persistent destruction and repair

100
Q

Chronic inflammation is associated w?

A

Blood vessel proliferaiton, fibrosis, granuloma

101
Q

What is a granuloma? How are they formed?

A

Nodular collection of epithelioid macrophages and giant cells. Th1 cells secrete IFN-gamma -> stim MO to secrete TNF-a -> form and maintain granuloma

102
Q

Outcome of chornic inflammation?

A

Scarring and amyloidosis

103
Q

Granulomatous Diseases (ddx of granuloma)

A

Mycobacterium tuberculosis, Fungal infexn, Trepnoema pallidum, M. leprae, Bartonella henselae, Sarcoidosis, Crohn’s, Granulomatosis w/ polyangitis (Wegner’s), Churg-Strauss syndrome, Berlliosis, silicosis

104
Q

Causes of increased ESR

A

Infections(osteomyelitis), malignancy, SLE and RA, pregnancy, inflammation (temporal arteritis)

105
Q

Causes of decreased ESR

A

Sickle cell (altered shape), polycythemia (too many), CHF

106
Q

What are C-Reactive proteins?

A

Acute-phase reactants synthesized by the liver. Also can be secreted from cells w/in atherosclerotic plaques to induce prothrombotic state.

107
Q

Function of C-reactive proteins?

A

Part of innate immune sys: opsonizes bacteria and activates complement.

108
Q

3* Steps in Collagene Synthesis

A

(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
Q

Osteogenesis imperfecta

A

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

110
Q

Ehlers Danlos Syndrome

A

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
Q

Alport Syndrome

A

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
Q

Elastin is rich in what aa?

A

Proline and glycine, nonhydroxylated forms

113
Q

What is elastin made of? Where is it “processed?”

A

Tropoelastin with fibrillin scaffolding. Cross-linking takes place extracellulary.

114
Q

What breaks elastin down? Disease association?

A

Elastase which is normally inhibited by a1-antitrypsin. Emphysema can be caused by a1-antitrypsin defy -> excess elastase activity.

115
Q

What is deficient in Marfan’s syndrome?

A

Fibrillin

116
Q

Why is Vit C important in collagen?

A

Hydroxyaltion of proline and lysine to form cross-links

117
Q

Where is Type I Collagen found?

A

STRONG: Bone, Skin, Tendons

118
Q

Where is Type II collagen found?

A

SLIPPERY: Cartilage, vitreous body, nucleus pulposus.

119
Q

Where is Type III Collagen found?

A

BLOODY: Reticulin-skin, blood vessels, uterus, fetal tissue, granulation tissue

120
Q

Where is Type IV Collagen found?

A

BM: kidney and lens

121
Q

Phases of wound healing?

A

Inflammatory (immediate), Proliferative (2-3 days after wound), Remodeling (1 week after wound)

122
Q

What happens during the first phase of wound healing? Mediators?

A

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
Q

What happens during the second phase of wound healing? Mediators?

A

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
Q

What happens during the third phase of wound healing? Mediators?

A

Fibroblasts. Type III collagen replaced by Type I to inc tensile strength. Months later

125
Q

What is atrophy?

A

Reduction in the size or # of cells.

126
Q

Causes of atrophy?

A

dec hormones, dec innervation, dec blood flow, dec nutrients, inc pressure, occlusion of secretory ducts (CF)

127
Q

Function of cholesterol in plasa mem?

A

dec fluidity, inc melting point

128
Q

What occurs at the cellular level during atrophy?

A

Dec metabolic activity -> dec protein synthe. Ubiquitin tags unused protein -> inc protein degradation. Autophagy -> free radical oxidaiton and lipocuscian. Dec # of organelles.

129
Q

What is a lipocuscian granule?

A

Residual body w/in cell. Contain brown pigment that results from free radical induced lipid peroxidation.

DIT (14 decks)

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