GP final exam preparation Flashcards

(51 cards)

1
Q

Name the 3 germ layers

A

Bilaminar embryonic disc becomes trilammar disc

  1. Ectoderm: (EVERYTHING EXTERNAL) Epidermis, CNS, PNS, eyes, internal ears neural crest cells and connective tissues of the head
  2. Mesoderm: (MUSCLE) Skeletal muscles, blood cells, serosal linings, CVS, cartilages, bones, tendons, dermis
  3. Endoderm: (EVERYTHING ENCLOSED) Epithelial linings of the resp and GI tract, glandular cells of the digestive organs- pancreas
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2
Q

Types of collagen (5)

A

Type I - bONEstructural collagen (bone, skin/dermis, tendons, ligaments)
Longitudinal fibrils
bundled into parallel collagen fibres

Type II - single fibres (hyaline cartilage)

Type III - Reticular fibres (branched / supporting meshwork)
Located around soft tissues, i.e. liver, spleen, bone marrow, lymphoid tissues

Type IV - Meshwork arrangement
located in basement membranes

Type VII - ‘anchoring collagen’
Links ECM to the basement membrane.

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3
Q

Name the CLASS types of enzymes and functions ‘OTHILL’

A

O: Oxidoreductases
Transfer electron/hydrogen/02 atom. From one substraight to another.
e.g. dehydrogenases, oxidase, oxygenase, catalase

T: Transferases
Transfer from functional group e.g Kinase transferases

H: Hydrolase
Transfer functional group to water, using H20 to break down water

I: Isomerase
Intramolecular changes in a substrate, group changes to a different location e.g

L: Lygase
Joining of 2 molecules by forming new bands e.g DNA ligase at end of DNA replication

L: Lyases
Removal or addition of a group to a substrate e.g dopamine or serotonin

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4
Q

Naked Vs Enveloped viruses

A

Naked:
-Capsid (protein coating) but no outer lipid membrane.
-More resilient, resist heat, dry conditions, UV radiation
-Protein coating is robust
-Causes lysis of host cell
- High survival rate
- Triggers strong immune response because doesn’t look like host

e.g Parvovirus, Adenovirus, polio virus

Enveloped:
- LIPID membrane
-Less resilient, destroyed by hot temp, acid environments, detergents
- Membrane more susceptible to environmental stressors
- Releases by budding
- Doesn’t cause lysis of host cells
- Low survival rate
- Not detected as easily because they mimic host cell

e.g HIV, influenza virus

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5
Q

Types of necrosis

A

-Coagulative
-Liquefactive (brain)
- Caseous (TB) cheese like appearance
-Fibrinoid autoimmune, vasculitis, necrotic foci surrounded by intact & fragmented neutrophils
- Fat necrosis (chalky white fatty deposits)

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6
Q

Hallmarks of cancer cells

A
  1. Sustained proliferative signalling
  2. evade growth suppressors
  3. resist cell death
  4. Replicate immortality
  5. Inducing angiogenesis
  6. Activating invasion and metastasis
  7. Invade immune system
  8. Abnormal metabolic pathways
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7
Q

Discuss Autosomal dominant

A
  • Single mutated allele (heterozygous for the disease)
  • Generally does not skip a generation
  • Males and females are usually affected equally

-Huntington’s disease
- Marfan syndrome
- Myotonic dystrophy

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8
Q

Discuss Autosomal recessive

A
  • Affected person has both mutated allele (homozygous) OR carriers have one affected allele (heterozygous)
  • Common to skip a generation
  • Males and females are usually affected equally
  • Most commonly, two heterozygous parents (carriers) can produce a homozygote offspring.
  • Cycstic fibrosis
  • Sickle cell anaemia
  • Phenylketonuria (PKU)
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9
Q

X- Linked dominant

A
  • Twice as prevalent in females
  • Affected males will always pass it on to females
  • Doesn’t skip generation
  • No male-to-male transmission
  • Rett syndrome
  • Fragile X syndrome
  • Rickets
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10
Q

X linked recessive

A
  • Prevalent in males (because males only have one X chromosome and therefore they will always be affected (never carriers)).
  • Females are generally the carriers
  • Affected females will always pass it to 100% of male offspring
  • It’s common to skip a generation
  • No male-to-male transmission

Examples
- Duchenne muscular dystrophy
- Hemophilia A & B
- Glucose-6- phosphate dehydrogenase deficiency

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11
Q

Discuss Trisomy disorders

A
  • Trisomy 13, Patau syndrome
    Cleft lip, extra fingers and toes, small eyes, mental retardation
    Poor prognosis
  • Trisomy 18, Edwards syndrome
    Similar to down syndrome, with clenched fist, overlapping fingers and rocker bottom feet
    Poor prognosis

Trisomy 21, Down Syndrome
- Short stature, decreased muscle tone, almond eyes, flat face, flat occupit

Testing:
Decreased signs of trisomy disorder
unless increase of hvG = trisomy 21

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12
Q

Discuss sex chromosome disorders

A

XXY (extra X chromosome)
Only occurs in males
Klinefelter syndrome, tall stature gynaecomastia, small testes, osteoporosis, decrease body hair

45X or 45 XO
Tunner syndrome, only monosomy consistent with life
- short stature, oedema of ankles/ wrists, webbed neck, amenorrhea, infertility

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13
Q

Types of blotting

A

Southern: DNA
Northern: RNA
Western: Protein

Dot RNA, DNA and protein

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14
Q

Discuss the process of blotting

A

Technique used to manipulate DNA and RNA. It involved cutting and rejoining DNA.

Separate molecules using gel mixture

Transfer molecules transfer onto a solid surface.

Identify molecules: techniques to identify specific nucleic acids or genes

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15
Q

What is the difference between Osteomalacia, Osteoporosis and Osteoarthritis

A

Osteomalacia: (Rickets) soft bones due to vitamin D deficiency,

Osteoporosis: Decreased bone density, due to low calcium intake and changes in estrogen

Osteoarthritis: degenerative joint disease where cartilage breaks down

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16
Q

What does ELISA test stand for and explain test

A

Enzyme Linked Immunesorbent Assay

Diagnostic test that detects antigen- antibody binding through colour change

Antigen is placed in well of plate, serum added to well (horseradish) antibody binds to targets making a colour change

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17
Q

Name WBC and actions

A

Neutrophills: kill bacteria, fungi, foreign debris

Leukocytes

Mast cells

Eosinophils: Cirulate in the blood, some are in mucosal lining e.g Resp, GI and GI. Defends against helminthic parasites

Basophils: Bind to IgE

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18
Q

Innate Vs Adaptive

A

Innate immune system:
-Immediate response (within first 12 hours): first line of defence to response to invading pathogens/microbes.
- Non-specific and no memory: recognises common pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). It has no memory.
-Key components: includes physical barriers (i.e. skin/mucous membranes), chemical barriers (i.e. stomach acid), and immune cells and proteins (i.e. complement, phagocytes (neutrophils/macrophages), dendritic cells, mast cells, NK cells and ILCs.

Adaptive immune system:
- Delayed response (days to weeks)
- Specific response and memory: more specific response to antigens on pathogens with a targeted response. Also forms memory of an antigen once it is exposed to it (this provides a stronger response to it upon re-exposure).
-K components: B and T lymphocytes, antibodies.

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19
Q

Active vs Passive

A

Active: Microbial antigen (via vaccine or infection) lasts days or weeks then recovery with immunity the cells have a memory

Passive: Serum (antibodies) from immune individual is then administered via a serum to uninfected individual causes infection. However, not stored in long term memory

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20
Q

Discuss the 5 Isotypes

A

IgM: 5 Subuits (pentamer), found on surface of B cells, very first stages of immune response

IgA: Prevents attachment of microorganisms to mucous. Found in saliva, tears, colostrum, breast milk, resp, GI and UT secretion

IgG: 4 subclasses (G1,G2,G3,G4), only one that goes over the placenta

IgE: Binds to allergens, involved in allergy, triggers histamine from mast cells, protects against parasitic worms

IgD: Functions on the B cells as part of the BCR

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21
Q

Cell cycle

A

G0: No replication but growth

Interphase

G1: Growth of cell

Check point

S: DNA synthesis/ replication
Histone synthesis nucleus

Check point: no genetic abnormalities

G2: DNA check and repair (irreparable - apoptosis)

22
Q

Communication pathways

A

Endocrine: Circulates through blood distant target cells, Hormones such as insulin/glucagon, oestrogen/ testosterone, adrenaline

Paracrine: Regulate nearby cells such as histamine, IL

Autocrine: Hormones that act on the same cell that secreted them. Growth factors in tumour growth

23
Q

Virus replication
R A PURple Apple May Redden

A

Attachment: To receptor on host cell

Penetration: Into the cell

Uncoating: Capsid shed

Replication: Synthesis of viral messenger RNA and nucleic acid synthesis of viral protein for new capsid

Assembly: Capsid forms around nucleic acid

Maturation: Final changes within a immature virus

Release: By budding forming envelope

24
Q

Sliding filament theory

A

Mechanism of muscle contraction.

Thick (Myosin) and thin filament (actin) muscle fibers, slide past during muscle contraction whilst remaining at constant length.

Myosin filament uses ATP to “walk” along the actin filaments with their cross bridge.

25
What a cell does
Provides structure and shape to the body, contains hereditary materials Cell membrane: Semi permeable membrane surrounds the cell Cytoplasm: Gel like fluid Nucleus: Contains DNA and reguates cell function Ribosomes: makes protein for cells Golgi apparatus: Receives protein and lipid milecules from the ER. packaged for transportation Endoplasmic reticulum (ER) Helps process molecules made by cell Smooth: Synthesis lipid substance in cell, no ribosomes on surfer RER: Synthesis new protein molecules in cell, has ribosomes on surface Lysosomes: "intracellular digestive system' Membrane bound organelles containing digestive enzymes. Mitochondria: Makes ATP
26
Life cycles of HIV
Infection of cells gp120 binds to CD4 and to chemokine receptors on human cell, virus enters cell cytoplasm. Production of DNA copy of viral RNA- synthesized by the viral reverse transcriptase Integration into the host genome: by action of viral integrase enzymes. The integrated DNA is called provirus Expression of viral genes: Activation of infected T cells by some extrinsic stimulus Production of viral particles: Migration to cell membrane, acquiring a lipid envelope from host and budding out as an infectious viral particle, ready to infect others
27
List the cells affected by HIV infection and briefly describe their functions and roles in HIV infection
Directly affects: - T helper cells – use these cells as their host to replicate and control immunity. - Macrophages – penetrates and replicates in macrophages - Dendritic cells – penetrates and replicates in dendritic cells This indirectly affects: - Macrophages – Th1 releases cytokines to activate macrophages in response to foreign microbes - Eosinophils – Th2 releases cytokines to activate eosinophils in response to foreign microbes - Neutrophils – Th17 releases cytokines to activate neutrophils to respond to foreign microbes. - B cells – Tfh release cytokines to activate B cells to release antibodies to fight infections. - CTL – Tregs release IL-2 and TFG-β to activate CTLs to fight infection.
28
Antibiotics (PCGTMASFRP)
Peptidoglycan Inhibit cell wall synthesis People: Penicillin Can: Cephalothin Generally: Glycopeptides (vancomycin) Inhibit protein synthesis (translation) Trust: Tetracycline My: Marcolides (erythromycin) Amazing: Aminoglycosides (streptomycin) Inhibit cell metabolism Smart: sulfonamides (sulfa drugs, trimethoprim) Inhibits nucleic acid synthesis Funny: fluoroquinolones Rude: Rifamycins Damage cell wall integrity Polly: Polypeptides- polymyxin B, bacitracin
29
Stem Cells
Unipotent: Becomes one cell type in epidermis Multipotent: Becomes multiple cell types e.g blood Pluripotent: Capable of self renewal in germ layer Totipotent: Can be any cell type e.g muscle, nerve cell etc
30
Different types of inflammation
Acute Chronic:
31
Discuss the Muscarinic receptors
M1: CNS, salivary glands, parietal cells M2: Heart M3: Smooth muscle, endocrine glands, endotherlium M4
32
MHC 1 vs MHC 2
MHC 1: presents antigen CD8+, Cytotoxic Tcells, expressed from inside the cell MHC II: CD4+ Via helper Tcells, external antigens. expressed on B cells
33
Robertsonian translocation
Genetic material is exchanged between nonhomologous chromosomal translocation two long arms fuse together. Short arms contain no gentic material
34
Different types of transplant
Xenogenic: From animals Autologous: same person Allogeneic: From another human Syngenic: Identical twins
35
Types of rejections
HVGR: Solid organ transplant Hyperacute- can occur with minutes to hours. Acute: days to weeks after transplant Chronic: takes months to years GVHR: stem cell, immune cell transplant, mediated by transplanted immune competent cells. GVHD: Disease caused by GVHR which can damage host
36
Carcinoma vs sarcoma
Carcinoma: Starts in epithelial tissue, its common, spread via lymph tissue, common in older pts Sarcoma: Starts in connective tissue, rare, spreads through blood system, common in younger people
37
Necrosis vs apoptosis
Apoptosis: Programmed cell death bodies way to get rid of abnormal cells e.g cancer Necrosis: Accidental cell death as a result of external factors, activation of inflammatory markers
38
Affinity vs efficacy and potency and role in half life
Potency (EC50) concentration of dose of a drug required to produce 50% of that a drugs maximal effect Efficacy (Emax) maximum effect which can be expected from this drug Binding affinity: is how well a drug binds to receptor determined by the percentage of receptors bound by a drug
39
Explain huntington's, type of disorder and gene it effects
Trinucleotide repeat disorders (CAG) progressive movement disorder and dementia Characterized by jerky, hyperkinetic, dystonic movements using all parts of the body. Located HTT, chromosome 4p16.3 encode 348-kD
40
Osteoclasts vs Osteoblasts
Osteoblasts: form new bone and add growth to exisiting bone tissue. -Regulates calcium in and out of bone -Produces osteoid which is a protein that helps form and maintain bone structure Osteoclasts: Cleve bone/ dissolve old bone so it can be replaced with new bone. - Express a protein called RANKL on their membrane which activates
41
What are the 4 receptors?
Type 1: Ligand- gated ion channels aka ionotropic receptors, fast synaptic transmission. works on Ion channel e.g Nicotinic acetylcholine, GABA a, gluatmate, NMDA Type 2: G protein coupled receptors aka metabotropic or 7 TDM, 7 membrane spanning a- helices. 3 subunits a,b,y possessing GTPase activity Target for G proteins- Adenylyl cyclase, phospholipsase C, ion channels, Muscarinic Type 3: Kinase- linked and related receptors. Insuline, growth factors, cytokine receptors Type 4: Nuclear receptors, sense lipid and hormone signals, modulate gene transcription. Via DNA hormones, thyroid hormones, lipids
42
2nd messenger GPCRs
Target for G proteins- Adenylyl cyclase, phospholipase C, ion channels Ga subunit Adenylyl cyclase- production of cAMP cAMP- Activate protein kinase A (PKA) modulate the activity of ion channels K+, Cl- and Ca2 - Translocate to the nucleus modulate transcription factors, expression of genes -Phosphodiesterase can terminate action of cAMP Phospholipase C PLC- Ga subunit. Catalyze Phosphatidylinositol 4,5- bisphosphate (PIP) generates two second messengers Insitol-1 4.5 triphospahate (IP3) and Diacylgycerol (DAG)
43
Discuss DAG
Activates protein Kinase C (PKC) targets a number of targets in signal transduction proteins (serine/threonine) residues Target proteins vary- tissue dependent e.g smooth muscle contraction GI tract, eye, uterus, urinary sphincter, vascular and bronchial
44
Meiosis I vs Meiosis II
Meiosis 1: separation of homologous chromosomes - 2 daughter cells that are haploid - Each homologous chromosomes still contains the sister chromatid Meiosis II -Separation of the sister chromatids Conclusion of meiosis 4 haploid daughter cells (contain one sister chromatid)
45
Meiosis I
PMAT Prophase: Pairing of sister chromatids, crossing over Metaphase: Meet at the metaphase plate Anaphase: Pairs separate, chromatids stay together Telophase: Cytokinesis two haploid daughter cells produced
46
Meiosis II (egg)
PII: Pause until puberty, P1 finishes when, puberty kicks in MII: Sister chromatids line at the metaphase plate, AII: Sister chromatids separate TII: Cytokinesis 4 haploid cells genetically different from the original diploid cells
47
Spermatogensis
48
Mitosis
P: Condensing thickening M: Meet at the metaphase plate A: chromosomes pulled away T: Cytokinesis 2 identical diploid cells, complete divide
49
Embryogenesis
Oocyte released, Oocyte penetrated by sperm Forms Zygote Cleavage: undergo mitosis continues to divide. Morula: formulation of multiple cell 12-32 blastomeres Blastulation: Cleavage itself Blastocysts Implantation:
50
Antibiotics and actions
5 modes of action: 1) Inhibit the synthesis of the bacterial cell well Examples – penicillin (β-lactams); amoxicillin (semisynthetic penicillin); vancomycin (a glycopeptide used against MRSA) 2) Bind to ribosomes and inhibit protein synthesis Examples – streptomycin (aminoglycosides), erythromycin (macrolides) and tetracycline. 3) Damages cytoplasmic membranes Examples – Bacitracin (polypeptide). 4) Inhibit nucleic acid (DNA and RNA) synthesis Examples – Ciprofloxacin (Quinolones) and rifampicin (rifamycin) 5) Inhibit cell metabolic pathways – folate synthesis Examples – sulpha drugs and trimethoprim (sulfonamides)
51
Discuss the stages of first pas metabolism
Phase 1: Pre- conjugation Breaks down using 'Cytochrome P450' called NADPH CYP reducatse. The drug becomes more hydrophilic and cane pass through the kidneys more easily P450 can be inhibited by grapefruit juice, brussle sprouts, smoking, St John' Wort Phase 2 (conjugation) Making the drug become more polar or water soluble with substance such as Acetate. This phase needs ATP