GP final exam preparation Flashcards
Name the 3 germ layers
Bilaminar embryonic disc becomes trilammar disc
- Ectoderm: (EVERYTHING EXTERNAL) Epidermis, CNS, PNS, eyes, internal ears neural crest cells and connective tissues of the head
- Mesoderm: (MUSCLE) Skeletal muscles, blood cells, serosal linings, CVS, cartilages, bones, tendons, dermis
- Endoderm: (EVERYTHING ENCLOSED) Epithelial linings of the resp and GI tract, glandular cells of the digestive organs- pancreas
Types of collagen (5)
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.
Name the CLASS types of enzymes and functions ‘OTHILL’
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
Naked Vs Enveloped viruses
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
Types of necrosis
-Coagulative
-Liquefactive (brain)
- Caseous (TB) cheese like appearance
-Fibrinoid autoimmune, vasculitis, necrotic foci surrounded by intact & fragmented neutrophils
- Fat necrosis (chalky white fatty deposits)
Hallmarks of cancer cells
- Sustained proliferative signalling
- evade growth suppressors
- resist cell death
- Replicate immortality
- Inducing angiogenesis
- Activating invasion and metastasis
- Invade immune system
- Abnormal metabolic pathways
Discuss Autosomal dominant
- 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
Discuss Autosomal recessive
- 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)
X- Linked dominant
- 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
X linked recessive
- 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
Discuss Trisomy disorders
- 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
Discuss sex chromosome disorders
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
Types of blotting
Southern: DNA
Northern: RNA
Western: Protein
Dot RNA, DNA and protein
Discuss the process of blotting
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
What is the difference between Osteomalacia, Osteoporosis and Osteoarthritis
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
What does ELISA test stand for and explain test
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
Name WBC and actions
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
Innate Vs Adaptive
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.
Active vs Passive
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
Discuss the 5 Isotypes
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
Cell cycle
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)
Communication pathways
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
Virus replication
R A PURple Apple May Redden
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
Sliding filament theory
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.
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
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
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.
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
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
Different types of inflammation
Acute
Chronic:
Discuss the Muscarinic receptors
M1: CNS, salivary glands, parietal cells
M2: Heart
M3: Smooth muscle, endocrine glands, endotherlium
M4
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
Robertsonian translocation
Genetic material is exchanged between nonhomologous chromosomal translocation two long arms fuse together. Short arms contain no gentic material
Different types of transplant
Xenogenic: From animals
Autologous: same person
Allogeneic: From another human
Syngenic: Identical twins
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
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
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
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
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
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
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
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)
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
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)
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
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
Spermatogensis
Mitosis
P: Condensing thickening
M: Meet at the metaphase plate
A: chromosomes pulled away
T: Cytokinesis 2 identical diploid cells, complete divide
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:
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)
