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Cell/Tissue Biology > Exam III > Flashcards

Exam III Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Type of Gland - Parotid

A

Compound Acinar

Purely Serous

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2
Q

Type of Gland - Submandibular

A

Compound Tubuloacinar

Mixed Gland - Primarily Serous

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3
Q

Type of Gland - Sublingual

A

Compound Tubuloacinar
Mixed Gland - Primarily Mucus
Intralobular Ducts not well developed

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4
Q

Type of Gland - Pancreas

A

Compound Acinar
Similar to Parotid but has islets of Langerhans, centroacinar cells, and NO striated ducts
Duct cells secrete bicarbonate

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5
Q

Sjogren Syndrome

A

Autoimmune disease
Salivary and Lingual Glans infiltrated by CD4+ T cells
Antibodies against ribonucleoproteins SS-A (Ro) and SS-B (La)
Usually F b/w 50-60
Parotid enlargement
Lymph nodes enlarged with B cells
Extraglandular manifestations: Synovitis, pulmonary fibrosis, peripheral neuropathy

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6
Q

Exocrine classifications and examples

A

Unicellular-Goblet Cell
Multicellular Sheet- Lumen of Stomach
Simple Acinar - Paraurethral glands
Simple Branched Acinar - Sebaceous Glands
Simple Tubular - Intestinal Glands
Simple Coiled Tubular - Sweat glands
Simple Branched Tubular - Glands of Stomach/duodenum
Compound Acinar - Pancreas
Compoud Tubular - Bulbourethral Glands
Compound Tubuloacinar - Submandibular/Sublingual

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7
Q

Langerhans Cells

A

Dendritic Cells of Epidermis
Mainly in S. Spinosum
Antigen Presenting Cells
Birbeck Granules

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8
Q

Merckel Cells

A

Mechanoreceptors in S. Basale
Fine, detailed touch
Numerous in fingertips
Unmyelinated nerve terminals approach Merckel Cells to form Merckel cell-neurite complexes

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9
Q

Special Inclusions of S. Granulosum cells

A

Keratohyalin Granules - soft keratin
Membrane-Coating Granules - aka lamellar bodies, contain lipids that exocytose to apex to waterproof the integument, chokes more superficial cells of nutrients leading to death

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10
Q

Special Inclusions of S. Spinosum cells

A 
Membrane coating granules - aka lamellar granules (same as granulosum)
Intermediate filaments (tonofilaments) = cytokeratin, in upper layers form bundles called tonofibrils
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11
Q

Epidermis derived from =

Dermis derived from =

A 
E= Ectoderm (melanocytes from neural crest)
D= Mesoderm
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12
Q

Receptors in Papillary Dermal layer

A 
Meissner Corpuscles (mechanoreceptors)
Krause End Bulbs
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13
Q

Receptors in Reticular Dermal Layer

A 
Pacinian Corpuscles (Pressure, vibrations)
Ruffini Corpuscles (tensile fores, numerous in soles)
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14
Q

Apocrine Sweat Gland mode of secretion

A

MEROCRINE

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15
Q

Sebaceous Gland mode of secretion

A

HOLOCRINE

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16
Q

Nail Bed

A

S. Basale and S. Spinosum

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17
Q

Where nail growth occurs

A

Nail Matrix (near EPOnychium -> proximal nail fold. Hyponychium is distal fold)

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18
Q

Normal Hematocrit

A

(% RBC in blood sample)
Male: 45
Female: 40
Neonate: 55 (drops to 35 by 2mo and slowly rises to adult level until about puberty

19
Q

Serum=?

A

Plasma - Fibrinogen

20
Q

Transmembrane Proteins of Erythrocytes

A

Glycophorin (A,B,C) - fxn unknown

Band 3 - HCO3-/Cl- antiporter

21
Q

Skeleton of Erythrocyte

A

Band 4.1 anchor cytoskeletal components by complexing spectrin, actin, and glyophorin

Band 3, band 4.2, akyrin and spectrin form another complex

Adducin (calmodulin binding protein) promotes actin-spectrin association

22
Q

Hereditary Spherocytosis

A

Mutations in ankyrin, band 3, spectrin, band 4.2

Spherical shaped RBCs destroyed in spleed -> anemia, jaundice, splenomegaly

23
Q

Elliptocytosis

A

Mutations in Spectrin, band 4.1, or glycophorin C

24
Q

Howell-Jolly Bodies

A

Basophilic Nuclear Fragments in cytoplams of RBCs
Pitted out by splenic macrophages
Present in pts with severe hemolytic anemia, spleen dsfxns, post-splenectomy

25
Q

Heinz Bodies

A

Inclusions of damaged Hb.
Result of oxidative damage (G6PD deficiency)
Splenic Macrophages remove and damage the membrane forming bite cells

26
Q

Dohle Body

A

Found in neutrophils in response to infection and certain other circumstances
Dilated ER.

27
Q

Four Zones of Platelets

A

Peripheral - Membrane and glycocalyx
Structural - Microtubules and actin/mysoin
Membrane - open canalicular/dense tubular system
Organelle - Mito, Glycogen granules, Peroxisomes, granules (alpha, delta, lambda… all lysosomes)

28
Q

Myoendothelial Junction

A

Shear stress on endothelial layer causes hyperpolarization of endothelial cell which synapses with smooth muscle cells via gap junctions. Hyperpolarization of SMCs leads to vasoDILATION

29
Q

Weibel-Palade Bodies

A 
Found in endothelial cells
Contain:
-Von Willebrand Factor (coag factor VIII)
-Tissue Plasminogen Activator
-IL8
-P Selectin
30
Q

Neovascularization from Epithelial Precursor Cells

A

EPCs mobilize from niche (usually red bone marrow), complete mechanism not well understood
This mechanism used to:
Replace lost endothelial cells
Re-endothelialize vascular implants
Neovascularization of ischemic organs, wounds, tumors

31
Q

Neovascularization from pre-existing vessels

A
  1. Vasodilation due to NO. Increases vascular permeability due to VEGF from parent vessel
  2. Degredation of basal lamina by metalloproteinases. Cell to cell contacts shed, mediated by plasminogen activator
  3. Endothelial cells migrate and proliferate, due to proangiogenic factors (VEGF, angiopoietin). Fibroblast growth factor-2 can induce this too
  4. Endothelial cells mature into endothelial capillary tue
  5. Elaboration of basal lamina due to TransformingGF-B.
    Periendothelial cells recruited by Ang 1 with Tie2 receptors on endo cells. Smooth muscle cells recruited by PDGF.

Ang 2 is involved in remodeling process by blocking stabilizing action of Ang 1

32
Q

Vascular Remodeling - Altered Flow

A

High Flow = Increase in luminal and outer diameter

Low Flow = Decrease in luminal and outer diameter

33
Q

Vascular Remodeling - Increased Pressure

A

Large Artery = Outward hypertrophy (thicker wall, lumen unchanged)
Small Artery = Inward hypertrophy (Thicker wall, lumen gets smaller
Arterioles:
-Inward hypertrophy
-Inward (eutrophic) remodeling - wall thickness AND diameter decrease
-Rarefaction - vessel degenerates

34
Q

3 AV valve layers

A

Atrialis (elastin, aids in contracting valve)
Spongiosa (proteoglycan, shock absorber)
Fibrosa (collagen, mechanical integrity)

35
Q

Semilunar valve layers

A

Fibrosa (Mechanical integrity, subjacent to vessel endothelium (aortic or pulmonic))
Spongiosa (Shock absorber)
Ventricularis (elastin, subjacent to ventricular surface endothelium)

36
Q

Myxomatous Degeneration of AV valve

A

Floppy Valve

Possibly due to overexpression of decorin (regulates fibril assembly), may lead to distensiblilty of myxomatous tissue

37
Q

Lipid/Cholesterol Guidelines

A

45mg/dL HDL

<150mg/dL triglycerides

38
Q

Frequencies of Coronary Artery Stenosis

A

Right Coronary: 30-40%
LAD: 40-50%
Circumflex:15-20%

39
Q

Progression of Cerebral Infarctions

A
  1. Eosinophilia of neurons
  2. Neutrophil invasion
  3. Macrophage and reactive gliosis
40
Q

Primary Lymph Tissues

A

Thymus, Bone Marrow

Sites of maturation

41
Q

Secondary Lymph Tissue

A

Nodes, MALT (galt, balt, tonsils), spleen

Places of antigen presentation and/or immunological defense

42
Q

Cells/Secretions of Islets in Pancreas

A

Alpha - Glucagon
Beta- Insulin
Delta - Somatostatin (reduce smooth muscle contraction of GI and bladder)
G cells - Gastrin (stimuates HCl synthesis by parietal cells in stomach mucosa)
PP (F cells) - Pancreatic Polypeptide (inhibits pancreated exocrine secretion)

43
Q

Cortical Adrenal Regions (and products)

A 
From superficial to deep:
Zona glomerulosa (mineralocorticoids eg aldosterone)
Zona Fasciculata (glucocorticoids eg cortisol) - is largest layer
Zone Reticularis (androgens)

Cell/Tissue Biology (4 decks)

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