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Foundations 2 > 9/13 > Flashcards

9/13 Flashcards

1
Q

Different types of cell cycle cells

A
  1. Labile Cells: skin, lung, GIT, GUT
    Spend little time in Go cycle

Skin has stem cells at basal layer, lung stem cells are Type II pneumocytes

Cancer is common like skin, lung, prostate, leukemia, and colon

  1. Stable Cells: liver, renal tubules, mesenchymal tissue (except heart and skeletal muscle)

Stop dividing to sit in Go cycle, can re-enter cell cycle and proliferate to replenish damaged tissue

Cancers caused by external factors like hepatitis, know that renal tube injury can regenerate but would need dialysis in mean time

  1. Permanent cells: neurons, cardiac/skeletal muscle

Cancer is much less common

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2
Q

Granulation tissue

A

Part of proliferative phase of wound healing

Consists of tissue edema, inflammation, angiogenesis, and type III collagen

Tissue is weak and friable

Deposited by fibroblasts

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3
Q

Growth Factor

A

Naturally produced substance capable of stimulating cellular growth via migration, proliferation, healing, maturation, and differentiation

Act on GF receptors to initiate STP to alter gene expression, mutations in receptors are almost always oncogenic

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4
Q

Platelet Derived Growth Factor (PDGF)

A

Secreted by platelets and macrophages

Act on tyrosine kinase receptors

Activate fibroblasts to synthesize collagen, stimulate smooth muscle migration to allow angiogenic remodeling

Over stimulation involved in hypertophic scars and keloids

Atherosclerosis: macrophages activated by LDL release PDGF,stimulates smooth muscle migration and collagen deposition, smooth muscle cells go from media into intima, creates fibrous cholesterol plaque that is prone to problems

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5
Q

Transforming Growth Factor Beta

GF version

A

Stimulates angiogenesis and fibrosis

Cell cycle inhibitor (cancer therapeutic use) and inhibits inflammatory response

Acts on TGF-beta receptors with Smads that alter gene expression, use Ser/Thr kinase receptor

Released by playlets first then leukocyte, macrophages, fibroblasts, and keratinocytes

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6
Q

Fibroblast Growth Factor

A

Produced by macrophages, endothelial cells, fibroblasts, and others

Receptors have tyrosine kinase activity

Regulates embryonic development, tissue differentiation, chemotaxis, angiogenesis, cell proliferation, and tissue repair

FGF 1 and 2: stimulate angiogenesis and fibroblast activity

FGF 7: stimulates cell proliferation, for skin wounds and regeneration of hepatic stem cells

FGFR 3: achondroplasia, receptor is constitutively active, has negative regulatory effect on bone growth

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7
Q

Vascular Endothelial Growth Factor

A

Stimulates wound healing, angiogenic source for developing embryo

Forms collateral circulation, densely packed vessels that make up for chronically slowed blood flow to an area

Pathology: wet age-related macular degeneration, cancer

Bevacizumab: monoclonal antibody that inhibits VEGF, for cancers and age related macular degeneration

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8
Q

Epidermal Growth Factor

A

Stimulates cell proliferation

Erb-B1 receptor with tyrosine kinase activity, ErB receptors are proto-oncogenes

Common in lung cancer, adenocarcinoma

Erlotinib inhibits, cetuximab inhibits EGFR in cancers if no mutation in KRAS

HER2/c-neu mutation in Erb-B2 causes breast cancer

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9
Q

How wounds heal

A

Primary intention: sutured wounds, fibrin seals in 24-48 hours, short inflammatory phase, proliferative phase results in red raised scar

Secondary Intention: no effort made to approx. epithelium, prolonged inflammatory phase

Wounds close by contracture (caused by myofibroblasts), deposition of granulation tissue, progressive epithelialization from intact skin around the periphery of the wound

Tertiary Intention: infected wounds where bacterial count contradicts primary closure, wound edges approximated within 3-4 days and tensile strength develops as with primary closure

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10
Q

Signs of infection

A

Increased or new pain around wound

Discharge from wound

Unusual color of granulation tissue, unusual staining on wound dressing

Odor

General malaise

Inflammation

Not healing at expected rate

Cellulitis

Wound breakdown

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11
Q

Chronic wound infections

A

Rule out infections for wounds that are stalled for 2 weeks

50/50 shot of diagnosing wound infection based on observation

Biosy/swap: wound infection defined as x>10^5 CFU/gm tissue after debridemenet

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12
Q

Types of Chronic Wounds

A
  1. Venous Ulcers: stasis or varicose ulcers, improper functioning of venous valves like in the legs and esp. medial malleolus, full-thickness defect of skin
  2. Arterial Ulcers: occur on lower leg so similar to venous ulcers, caused by atherosclerosis, can be caused by both acute/chronic arterial insufficiency

Determining the ankle-brachial index will give an indication of patient’s ability to heal, divide the systolic BP at ankle by the systolic BP at arm

  1. Diabetic Ulcers: most common foot injuries leading to lower extremity amputation

Peripheral neuropathy, peripheral vascular disease, and infection combine and can lead to gangrene/amputation

Stage B is infected, Stage C is ischemic

  1. Pressure Ulcers: usually over a bony prominence due to unrelieved pressure, problem for physically limited or bedridden elderly
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13
Q

Wound assessment and primary care

A
  1. Patient history and physical exam: time and mechanism of injury, neurological and vascular examination distal to injured site, check tetanus status
  2. Details from history and physical examination-
    Thrombo-cytopenia: too few platelets
    Thrombocythemia: too many platelets
    Certain meds: methotrexate, anti-coagulants, transplant rejection, corticosteroids
    Nutrition
  3. Wound exploration and hemostasis: explore wound for foreign bodies and assess tissue injury, tissue lost, and degree of injury to deeper structures

Hemostasis by direct pressure, elevation, electrocautery, or suture ligation

  1. Debribement: remove all devitalized tissue and excise ragged edges to make a clean bleeding margin of viable tissue
  2. Wound closure
  3. Dressing
  4. Antibiotic Usage: can be used prophylactically, should consider location/age of wound and mechanism of injury/surgical incision to determine microbes likely for infection
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14
Q

3 Cornerstones of Wound Management

A
  1. Moist wound healing: dressings to maintain a moist environment, increase epithelialization, promote dermal matrix synthesis, improve patient comfort, provides optimum conditions for newly growing cells, prevents scanning and scarring
  2. Exudate: manage wound fluid, remove proteolytic environment and remove microorganisms, excessive exudate can inhibit wound healing, has increased levels of MMPs that inhibit wound healing, chronic wound fluid can inhibit the production of key wound healing cells

Compression, negative pressure devices and vacuum-assisted devices help wound healing, drains important in preventing exudate from accumulating in wound site

  1. Debridement: remove dead/dying tissues and foreign material, exposes healthy tissue and optimizes wound healing

Surgical, mechanical like hydrotherapy, autolytic through topically applied chemicals that stimulate breakdown of necrotic tissue, enzymatic like collagenase, biological like maggot therapy

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15
Q

Connective Tissue

A

Bone, tendons, ligaments, cartilage, fat, aponeuroses, blood

Architectural framework for organs, role in metabolism, immunity, ion transport, and storage

Important for wound healing, inflammation, and tumorigenesis

Key components-

  1. Cells
  2. Ground substance
  3. Fibers: (not for blood/lymph), collagen and elastic/reticular fibers
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16
Q

Loose Connective Tissue

Areolar CT

A

Loosely arranged fibers, many cells, and plenty of ground substance

Most abundant CT, holds organs in place, attaches epithelial tissues and glands to other tissues, found beneath epithelial linings

Lamina propria: lines tubes of GUT and GIT

Loose consistency and not very dense, appears light on microscopy

17
Q

Dense Connective Tissue

A
  1. Dense Irregular: irregularly arranged fibers, few cells

Submucosa of GIT, reticular layer of dermis

  1. Dense Regular: densely packed organized parallel fibers, few cells like fibroblasts to maintain ground substance and make ECM

Tendons, ligaments, aponeuroses

18
Q

Connective tissue cells

A

Permanent Cells-
1. Fibroblasts: most numerous CT cells
Secrete ground substance, MMPs, fibers, and GFs

Nuclei are present but smashed by ground substance, hard to make out borders

  1. Myofibroblasts: express alpha smooth muscle actin and can contract to close a wound, important in secondary intention

Secrete ground substance and MMPs

Large nucleus and nucleoli

  1. Macrophages (histiocytes): do innate/adaptive immunity, present antigens

Phagocytize foreign material, blood, and dead cells

Release cytokines, GFs, and enzymes that control inflammation and wound healing

  1. Mast cells: contain inflammatory mediators like histamine and heparin

Synthesize and release GFs, cytokines, and enzymes

Marked by tryptases

Key cell type in Type I hypersensitivity (allergy, asthma)

Infiltrating WBCs- neutrophils, T cells, B cells, eosinophils, and basophils

19
Q

Ground Substance Materials

A

Viscous substance that occupies space between cells/fibers in CT

  1. Proteoglycans
  2. Glycosaminoglycans
  3. Adhesive Glycoproteins
20
Q

Glycosaminoglycans

A

Unbranched polysaccharides, sulfate groups

Hyaluronic acid: large chain for ECM, shock absorber that regulates movement of molecules in the ECM and acts as a lubricant

Mucopolysacchsridoses- lysosomal storage disorders, heparan/dermatan sulfate buildup

  1. Hurler Syndrome: autosomal recessive defect in alpha -L-iduronase, developmental delay, gargoylism in hands, corneal clouding, hepatosplenomegaly
  2. Hunter Syndrome: X-linked recessive defect in iduronate sulfatase, aggressive behavior, normal eyes

Hunters see the X on their target and become aggressive

21
Q

Proteoglycans

A

Core proteins attached to many GAGs and hyaluronic acid

Negatively charged (due to GAGs) attracts water into ground substance and makes it viscous, permits nutrient diffusion while acting as a shock absorber

22
Q

Adhesive Glycoproteins

A
  1. Fibronectin: cell adhesion to ECM
    Binds to integrins, type IV collagen, heparin, and fibrin
  2. Laminin: attach cells to basement membrane
    Binds to integrins, type IV collagen, heparin, and fibrin
  3. Tenascin: modulates cell adhesion in ECM
    Binds to fibronectin, CAMs, heparin, and GFs
  4. Osteopontin: binds to osteocytes and integrin receptor on osteoclasts
    Binds calcium and hydroxyapatite
23
Q

3 Types of Fibers

A

Produced by fibroblasts

  1. Collagen fibers: type I is most abundant, provides tensile strength,
  2. Reticular fibers: heavily glycosylated collagen III, abundant in LCT, support system for organs
  3. Elastic Fibers: elastin and fibrillin

Are purple and wavy, collagen is a lighter pinkish and in between

24
Q

Main types of Collagen Fibers

A

I: bone, skin, tendons, late wound healing

II: cartilage

III: blood vessels, early wound healing/granulation tissue, fetus

IV: basement membrane (basal lamina)

After an ouchie you have type three, once it’s done you have type one

One: bone
Two: cartwolage
Three: bleed
Four: floor (basement membrane)

25
Q

Collagen Synthesis

A

INTRACELLULAR
Nucleus-
1. Transcription of preprocollagen mRNA

Rough ER-

  1. Translation of preprocollagen alpha chains
  2. Hydroxylation of Pro and Lys, Vitamin C
  3. Glycosylation of hydroxylysine
  4. Formation of procollagen triple helix of alpha chains

Golgi-
6. Packaging and exocytosis of procollagen into extracellular space

EXTRACELLULAR

  1. Cleavage of terminal regions to form insoluble tropocollagen
  2. Covalent lysine-hydroxylysine cross-linking of tropocollagen molecules via lysyl oxidase to form collagen fibrils, requires copper
  3. Aggregation of collagen fibrils to form a collagen fiber
26
Q

Collagen Pathology

A

Menkes Disease- defective ATP7A so less copper absorption and get less collagen cross-linking, slowed bone growth and developmental delay, “kinky hair disease”

Goodpasture’s disease: autoimmune attack on alpha-3 chain of Type IV collagen in basement membrane of lungs and kidneys

Alport Syndrome: mutation of Type IV collagen in basement membrane of inner ear, eyes, and kidneys

Get hearing loss, cataracts, and renal failure

27
Q

Osteogenesis Imperfecta

A

Autosomal dominant mutation in collagen I, poor triple helices, inadequate type I collagen from decreased type I collagen production or mutated chains

Brittle bone disease

Multiple fractures and loose joints, hearing loss from malformed ossicles, poor dentition, blue sclera due to underlying blue vessels show through thinner sclera

28
Q

Ehlers-Danlos Syndrome

A

Heterogenous family of disorders due to defective collagen synthesis of skin, joints, and blood vessels, mainly autosomal dominant

Classical type: Type V collagen, hyperextensible skin and joint instability

Vascular type: Type III collagen, more severe, easy bleeding and bruising, abnormal wound healing, vessel wall degeneration

Weak connective tissue in organs (from reticular fibers) makes organs fragile and prone to rupture

Prone to lethal vascular problems like valvular prolapse, rupturing aneurysms, dissections

Difference between Marfan: more prone to berry aneurysm in brain vs thoracic aneurysm, no lens subluxation or long limb/fingers, have easy bruising/bleeding and hyperlax skin

29
Q

Elastic Fibers

A

Elastin: Insoluble, precursor is tropoelastin

Rich in Pro, Gly, and Lys but hydrophobic, little/no hydroxylated AA residues

Desmosine and isodesmosine randomly cross-link and unlink between elastin molecules outside cell

Fibrillin-1: Scaffolding around which elastin is added to, coded for by FBN1, binds TGF-beta and sequesters it

Broken down by elastase, which can be inhibited by anti-elastase

30
Q

Emphysema

A

Loss of elasticity in lung along with destruction of connective tissue

Smoking increases elastase production

31
Q

Alpha-1 antitrypsin deficiency

A

Mutated A1AT, an anti-elastase

Can’t stop elastase from degrading lung

Can get emphysema without smoking, get at younger age if smoke

Misfolded A1AT builds up in liver and causes cirrhosis

When have young patient with unexplained cirrhosis and shortness of breath

32
Q

Marian Syndrome

A

Mutation in FBN1 gene for fibrillin-1, so less TGF-beta is sequestered and get less tissue elasticity

Dolichostenomelia (wingspan > height), arschnodactyly (long fingers), pectins excavatum (inverted sternum), scoliosis, hyperflexability at joints

Systemic Symptoms-
Eyes: Ectopia Lentis (lens subluxation from loss of elasticity of ciliary muscles)

Lungs: blebs of air can rupture and cause pneumothorax

Cardiovascular: aneurysm commonly in aorta, aortic dissection where vessel wall tears and blood escapes into new space created, floppy mistrial valve prolapse that leads to improper pumping

Foundations 2 (18 decks)

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