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Foundations 2 > 10/2 > Flashcards

10/2 Flashcards

1
Q

Anatomical Position

A

Body is erect (upright), facing forward, feet together and parallel, feet flat in floor, head level with eyes facing forward, palms facing forward and thumbs point away from body

Body lying down-
Prone: face down
Supine: face up

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2
Q

Anatomical Directional Terminology

A

Anterior (Ventral): toward the front of the body (belly)
Posterior (Dorsal): toward the back of the body (butt)

Superior (Cranial): toward the head or upper part of a body/structure
Inferior (Caudal): away from the head or upper part of a body/structure

Proximal: closer to the origin of a body part, leg attached to trunk, arm attached to shoulder
Distal: further from the origin of a body part

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3
Q

Human Body Planes and Sections

A

Sagittal: creates right/left halves, midsagittal/median divides into equal halves, parasagittal divides into unequal parts

Frontal (Coronal): divides into anterior/posterior parts

Transverse (Horizontal): divides into superior/inferior parts

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4
Q

Anatomical Terminology for Movements

A

Gliding (Translation): simplest, flat surfaces glide or slip over one another, intercarpal and intertarsal joints

Flexion: decreases angle in a joint
Extension: increases the angle in a joint, hyperextension if move head past 180°

Abduction: moving a limb away from the median plane of the body, raise arm
Adduction: moving a limb towards the median plane

Circumduction: moving a limb so that it creates a cone in space, distal end of limb moves in a circle while proximal connection is basically stationary
Includes flexion, extension, adduction, abduction

Rotation: turning a bone around its own axis, can be medial or lateral

Plantar flexion: depress the foot, pointing of the toes
Dorsiflexion: brings the superior surface of the foot towards the shin

Inversion: sole of the foot turns medially
Eversion: soles faces laterally

Pronation: rotating the forearm medically, palm is posterior, radius is across the ulna
Supination: radius and ulna are parallel, palm is anterior, anatomical position

Protraction: nonangular anterior movement in transverse plane
Retraction: posterior movement in transverse plane

Opposition: saddle joint between metacarpal 1 (at thumb), touch thumb and another fingertip

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5
Q

Superficial Veins of the Upper Limb

A

Cephalic Vein: runs along lateral upper limb, drains into axillary vein

Basilic vein: runs along medial forearm, dives through brachial fascia and becomes axillary vein

Median Cubital Vein: communicating branch between cephalic Vein and basilic vein in cubital fossa, used for venipuncture

Dorsal Venous Network: veins of the hand

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6
Q

Major Arteries of the Upper Limb

A

Brachial artery

Radial artery

Ulnar artery

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7
Q

Superficial Veins of the Lower Limb

A

Great saphenous vein: courses anterior to medial malleolus, ascends up medial leg and thigh, drains into femoral vein

Small saphenous vein: courses posterior to lateral malleolus, as ends up the posterior leg, dives deep in popliteal fossa, drains into popliteal vein

Dorsal venous arch

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8
Q

Cutaneous Nerves of the Upper Limb

A

Intercostobrachial nerve

Medical cutaneous nerve of forearm

Lateral cutaneous nerve of forearm: cutaneous branch of musculocutaneous nerve

Radial nerve

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9
Q

Arteries of the Lower Limb

A

Femoral Artery

Popliteal Artery

Posterior Tibial Artery

Anterior Tibial Artery

Dorsalis Pedis Artery

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10
Q

Femoral Triangle

A

NAVL

Femoral Nerve
Femoral Artery
Femoral Vein
Lymph Nodes

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11
Q

Cutaneous Nerves of the Lower Limb

A

Anterior Cutaneous Branches of Femoral Nerve

Saphenous Nerve (from femoral nerve)

Superficial fibular nerve becoming dorsal digital nerves

Posterior cutaneous nerve of thigh

Medical sural cutaneous nerve (from tibial nerve)

Sural nerve

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12
Q

Pulse Points of the Upper Extremity

A

Axillary

Radial

Ulnar

Brachial

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13
Q

Pulse Points of the Lower Extremity

A

Femoral

Posterior tibial

Dorsal pedis

Popliteal

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14
Q

Nuclear Changes in Neoplastic Cells

A

High nucleus:cytoplasm ratio

Multiple nuclei, piling up of nuclei

Multiple and large nucleoli

Coarse chromatin, makes nucleus stain darker than normal cells

Pleomorphism

Irregular chromatin

Irregular nuclear membranes

Increased presence of mitotic figures

Abnormal mitotic figures: sign of aneulploidy and anaplasia, loss of cell polarity leads to alteration in the mitotic spindle or excess centrosomes

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15
Q

Cytoplasmic Features of Neoplastic Cells

A

Hypercellularity

Pleomorphism, Abnormal cell contours

Anaplasia: poor cellular differentiation, lose characteristics of mature cells, and orientation with respect to each other

Loss of cell polarity

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16
Q

Clinical Aspects of Hyperplasia

A
  1. Physiologic Hormone Stimulation-

Normal response to hormone: estrogen stimulates proliferation of endometrial epithelial cells that converts proliferative endometrium into secretory endometrium

Response to tissue loss: hyperplasia of liver tissue after surgery due to HGF and IL-6

  1. Pathologic Hormone Stimulation-

GF or cytokine stimulation

Excessive response to a hormone or excessive hormone production: excess estrogen causes hyperplasia of the TDLUs in the breast, increased dihydrotestosterone causes prostate nodular hyperplasia

Inflammation, abnormal wound healing: psoriasis causes epidermis hyperplasia

17
Q

Progressive Endometrial Changes to Carcinoma

A
  1. Proliferative Endometrium: normal
  2. Simple Hyperplasia: increased number of glands that are more densely packed
  3. Complex Hyperplasia with atypia: increased number of glands with reduced intraglandular stroma, glands lined by Cells with Neoplastic changes changes like loss of polarity and nuclear piling up
  4. Adenocarcinoma: like previous but has invasion of myometrium
18
Q

Metaplasia

A

Distal esophagus: stratified squamous becomes columnar intestinal goblet cells that secrete mucin to deal with gastric reflux

Airways: pseudostratified ciliated columnar becomes stratified squamous due to smoking

Cervix: glandular becomes stratified squamous due to low pH or HPV

Urinary bladder: urothelium becomes stratified squamous to deal with stones or parasites

19
Q

Dysplasia

A

Disorderly cell growth and maturation that leads to architectural disorganization of the epithelium, doesn’t always lead to cancer

Mild to severe based on how much of the epithelium is replaced by abnormal cells

Carcinoma in situ has the cellular/nuclear features of neoplasia but no basement membrane penetration

20
Q

Proto-oncogene vs. Oncogene

A
  1. Proto-oncogene: normal gene that can become an oncogene with a single GOF of a single allele

Regulate cell growth/differentiation, signal transduction, mitosis signals

  1. Oncogene: proto-oncogene with a GOF change

Activation method: GOF mutation, loss of regulation, increased mRNA stability and life expectancy in cell, increase in copy number

21
Q

Proto-oncogene conversion

A
  1. Mutation in coding sequence: hyperactive protein made in normal amounts
  2. Gene amplification: normal protein greatly overproduced, usually a late change rather than driver, requires higher doses of treatment

Caused by unequal crossing over, replication slippage, aneuploidy

Childhood neuroblastoma: originate from any SNS tissue but mainly adrenal gland, amplification of MYCN that is a TF for neural crest cell proliferation/differentiation

Breast cancer: HER2/ERBB2, epidermal GF receptor, detected by tissue immunochemistry (3+) or FISH (>6 copies/nucleus), Trastuzumab (Herceptin) is a monoclonal antibody for the HER2 receptor

  1. Chromosome Rearrangement-
    A: Nearby regulatory DNA sequence causes normal protein to be overproduced

B: Fusion to actively transcribed gene greatly over produces fusion protein, or fusion protein is hyperactive

22
Q

Oncogene Activation by Chromosomal Translocstion

A

Somatic change, not inherited

Typical cause of lymphoma and leukemia
Chronic leukemia: normal differentiation but increased proliferation

Acute Leukemia: abnormalities in both differentiation and proliferation

23
Q

Chronic Myeloid Leukemia

A

GOF activations of tyrosine kinases

BCR/ABL gene fusion
Translocation between chromosomes 9 and 22, Philly chromosome, 3 lengths so 3 leukemias

Treatment: Imatinib is a tyrosine kinase inhibitor, also use a small molecule called phenylaminopyrimidine

Blocks ATP access at kinase pocket, develop resistance so need second line of inhibitors

24
Q

RET

A

Receptor tyrosine kinase for ligand of the glial cell line derived neurotrophic factor

Types of changes: germline GOF mutations, somatic fusion gene, LOF mutations

Constitutive autophosphorylation or change of substrate specificity in tyrosine kinase region, covalent intermolecular disulfide bonds in cysteine rich region

25
Q

Multiple Endocrine Neoplasia Type 2

A

All caused by GOF mutations of RET

Cysteine-rich region: extracellular region, MEN2A/FMTC, hyperparathyroidism, tumor in adrenal gland, most common MEN2

First Tyrosine Kinase region: FMTC, tumor of calcitonin-producing C cells of thyroid, thyroidectomy at early age

Second Tyrosine Kinase Region: MEN2B/FMTC, earlier age of onset, developmental abnormalities like neuromas of the mouth and increased intestinal innervation

26
Q

Carcinogenesis: The Basics

A

Mutations that allow tumor growth involve tumor suppressor genes, proto-oncogenes, and apoptosis regulators

Proto-oncogenes: GFs, GF receptors, and signal transducers like RAS

Knudsen Two-Hit Hypothesis: both alleles must be knocked out of tumor suppressor genes to have tumor formation

Bcl2: blocks release of cytochrome C from mitochondria and the ensuing apoptosis, tumors overexpress Bcl2 to prevent apoptosis, translocation makes Cell make Bcl2 instead of Ig heavy chain

27
Q

Multi step Carcinogenesis

A
  1. Tumor Initiation: due to irreversible genetic damage or epigenetics, causes a genetic error in stem cells by modifying its DNA structure like with a chemical adduct
  2. Tumor Promotion: selective clinal expansion of initiated cells,nude to defects in cell growth or programmed cell death

Foster the proliferation or expansion of a pop. of initiated cells

  1. Malignant Conversion: transformation of a pre-Neoplastic cell into one that expresses the malignant phenotype and usually requires further genetic changes

Summation of effects of initiators and promoters and the downstream effects they induce

  1. Tumor progression: expression of malignant phenotype and tendency of malignant cells to acquire more aggressive characteristics over time to become capable of spreading

Requires genetic change

28
Q

Cancer Initiators

A

Direct-acting compounds: don’t require chemical transformation, directly capable of reacting with DNA

Indirect-acting compounds: require metabolic conversion (often made electrophilic) to generate ultimate carcinogen, initiators are often tissue specific

Form DNA adducts that are covalently bound to nucleoside, not repaired and must be replicated

Effect is irreversible, permanent genetic changes that daughter cells carry

Linear relationship between initiator dose and quantity of tumors

29
Q

Cancer Promoters

A

Don’t covalently bind to DNA/macromolecules, can bind to receptors on cell surface that leads to increased cell proliferation

Tumor growth has threshold and maximum effects

Mechanisms-
1. Epigenetic

  1. Promoters induce cell proliferation, not mutagenic, like activate PKC
  2. Cells responding to promoters may have reduced GF Requirements or be less responsive to Inhibitors
  3. Oxidative stress: ROS, redox active metals like As/Cr/Ni, and polycyclic aromatic compounds like Dioxin
30
Q

Chemical Carcinogens

A
  1. Direct-alkylating agents: chemotherapeutic drugs, can cause secondary malignancy
  2. Polycyclic Hydrocarbons: cigarette smoke, broiled animal fat, smoked meat/fish

Need metabolism, why 15% smokers get lung cancer

Vinyl chloride exposure leads to hepatic angiosarcoma with dark red masses

  1. N-Nitrosamines: occur in smoke, water, alcohol, meats

Mainly cause gastric carcinomas in Japan

  1. Aromatic Amines and Azo Dyes: from rubber industry, need metabolism

Urothelial carcinoma

  1. Aflatoxin B1: from fungus Aspegeilus flavus, needs Metabolism, binds guanine residues in the TP53 gene and causes mutations

Hepatocellular carcinoma

31
Q

Inflammation as a Carcinogen

A

Chronic inflammation like IBS can cause colorectal cancer

Initiation: ROS can damage DNA

Promotion: ROS, GFs, and cytokines released from inflammatory cells can foster proliferation of initiated cells

Progression: angiogenic factors, ECM synthesis and degradation

32
Q

Radiation as a Carcinogen

A
  1. UV Radiation-

UVA: oxidation reactions that indirectly cause DNA damage, darkens and ages skin, penetrates deeper into epidermis so tans us

UVB: DNA photoadducts, sunburns, direct DNA damage from producing pyrimidine dimers

Initiator since cause DNA damage and mutations

Promoter by upregulating Inflammation that makes ROS and increased COX-2 activity

UVB Induced inflammation: dysregulation of apoptosis, mutations in p53, upregulation of COX-2 plays a role in squamous cell carcinoma

  1. Ionizing Radiation-
    Creates free radicals, use radiation therapy

Breast, colon, thyroid, and lung cancer

33
Q

Viral Carcinogens

A
  1. HPV: HPV Types 16 and 18 are found in most squamous carcinomas of the cervix

HPV viral oncoprotein E6 causes tags P53 for proteasome degradation, HPV viral oncoprotein E7 tags Rb for proteasome degradation

Squamous of vulva, vagina, anus, cervix, adenocarcinoma of cervix

  1. Epstein Barr Virus: Burkitt Lymphoma, infected B cells rearrange immunoglobulin genes to acquire t(8;14) that promotes cell proliferation by regulating c-Myc

Make c-Myc instead of immunoglobulin

Nasopharyngeal

  1. Hepatitis B Virus: Africa and Asia, liver injury and regenerative hyperplasia, Hbx protein binds to and inactivates p53 to interfere with growth suppression
  2. Human Herpes Virus 8 (HHV8): Kaposi’s sarcoma and certain lymphomas in HIV patients

Kaposi’s sarcoma: Neoplastic endothelial cells

  1. Human T-Lymphotropic Virus 1 (HTLV1): RNA virus, endemic in Japan and Caribbean, tropic for CD4 T Cells

Activates IL2 and IL2R resulting in polyclonal proliferation in which leukemia develops

Foundations 2 (18 decks)

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