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P1 > Intro to Med - Phase 1 > Flashcards

Intro to Med - Phase 1 Flashcards

1
Q

What are the seven major organelles and their functions?

A

NUCLEUS – site of DNA transcription + translation

SMOOTH ER – lipid synthesis

ROUGH ER – protein synthesis

MITOCHONDRIA – sites of cellular metabolism, generation of ATP

GOLGI APPARATUS – vesicular packaging/transport

RIBOSOME – site of translation

LYSOSOME – enzymes for degradation of cellular products or pathogens

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2
Q

Layers of the EPIDERMIS- skin (structure and function)

A

STRATUM CORNEUM

  • thick outer layer of dead cells
  • physical/chemical barrier

STRATUM LUCIDUM

  • thin layer of cells only in thick skin
  • strengthening

STRATUM GRANULOSUM

  • flattened cells with keratohyalin and lamellar granules, – nuclei disintegrate
  • permeability barrier

STRATUM SPINOSUM

  • spiny cells with desmosomes, Langerhans cells
  • immune function, strength to resist abrasion

STRATUM BASALE

  • stem cells, melanocytes, Merkel cells
  • generate new keratinocytes, pigment, sense of fine touch
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3
Q

Structure and function of DERMIS and HYPODERMIS

A

DERMIS important for immune surveillance, thermoregulation

  • papillary layer: anchors epidermis, immune cells, fibroblasts
  • reticular layer: blood vessels, nerves, lymph

HYPODERMIS: adipocytes for thermoregulation/insulation, energy storage, cushioning

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4
Q

Types of burns (layers, signs/symptoms, management)

A

SUPERFICIAL:

  • epidermis only, hair follicle invaginations allow for regeneration
  • pain, heat, erythema, swelling, tenderness
  • cold water, pain management

PARTIAL:
Superficial Partial = papillary,
Deep partial = reticular
- some pain insensitivity, blistering
- infection control

FULL THICKNESS:

  • all three layers,
  • no ability to regenerate due to loss of basal stem cells
  • black charring or white from fat necrosis
  • skin graft required,
  • high risk of infection and dehydration
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5
Q

Define Homeostasis and describe the feedback mechanisms

A

Homeostasis = the maintenance of a constant internal environment by various physiological processes despite changing conditions

Negative feedback: stable, changes are counteracted with opposite changes to maintain homeostasis

Positive feedback: unstable, changes perpetuate further changes in the same direction

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6
Q

Process of action potential generation

A

Graded potentials occur due to release of neurotransmitter at the dendrites, summation of GPs at axon hillock leads to depolarisation

  1. Voltage change triggers opening of VGSCs, rapid Na+ influx depolarises membrane
  2. Opening of VGPCs due to depolarisation, K+ efflux repolarises → hyperpolarisation
  3. Na+/K+ ATPase returns membrane to resting potential (-70mV)
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7
Q

Types of hormones (synthesis, receptors, solubility, examples)

A

PROTEINS
Synthesis: amino acids
Solubility: hydrophilic
Receptor: membrane-bound
Examples: insulin, ACTH

STEROID
Synthesis: cholesterol
Solubility: lipophilic
Receptor: nuclear → forms TF
Examples: cortisol, oestrogen

AMINE
Synthesis: tryptophan/tyrosine
Solubility: varied
Receptor: varied
Examples: adrenaline, T3, T4

Lipid hormones will have longer half-life as protein bound and more prolonged but delayed effect as they require protein synthesis, compared to protein hormones

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8
Q

Composition of bodily fluids (intracellular and extracellular)

A

ICF – K+, proteins
ECF – Na +, Cl-, HCO3-, plasma proteins

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9
Q

Stages of dehydration

A

MILD: (4-6%)

  • increased thirst
  • oral fluids

MODERATE: (7-10%)

  • sunken eyes, dry membranes,
  • tachycardia, ↓ urination/sweating
  • oral or IV fluids

SEVERE: (>10%)

  • neurological dysfunction, hypotension, anuria
  • oral, IV or interosseous fluids
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10
Q

Causes of dehydration

A

There are three major categories for causes of dehydration:

  • Decreased intake – water scarcity, behavioural problems
  • Increased water loss – vomiting, diarrhoea, profuse sweating
  • Fluid shift – ascites, pleural effusion
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11
Q

Definitions of tonic vs. osmotic

A

Tonic = used when comparing a solution to a cell e.g. hypertonic, hypotonic, isotonic

Osmotic = used when comparing two solutions e.g. hyperosmotic, hypoosmotic, isosmotic

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12
Q

Four types of body tissues and their characteristics

A
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13
Q

Levels of structural organisation for proteins

A

Primary – polypeptide chain made of a sequence of amino acids

Secondary – α-helices and β-sheets

Tertiary – folding of chains into final protein shape

Quaternary – combination of multiple protein subunits together

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14
Q

Cell adhesion structures

A

Tight junctions: form barriers to block movement between cells

Desmosomes: anchor cells together with cadherin proteins

Gap junctions: allow flow of ions for intercellular communication

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15
Q
  • *Branches of the autonomic nervous system:
  • Origin
  • Fibre Length
  • Ganglia
  • Neurotransmitter
  • Receptors
  • Function**
A
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16
Q

Types of sweat glands

A

Merocrine/eccrine = most common, sweating for thermoregulation (SNS via ACh + muscarinic)

Apocrine = located in arm pits and groin, nervous sweating + pheromones

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17
Q

Types of cellular receptors

A
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18
Q

Mechanisms for membrane transport

A

FAVS

Facilitated diffusion: pores, channels, carriers (uniporters, symporters, antiporters)

Active transport: primary and secondary

Vesicular transport

Simple diffusion

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19
Q

Social determinants of health

A

ERASER

Education + Training

Resources availability of food, housing, medication

Access to healthcare, education and economic opportunity

Social support

Employment and socio-economic status

Rurality

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20
Q

Barriers to health care access for Indigenous Australians

A

RICE

  • Rurality - living in remote communities, geographical barrier
  • Intergenerational trauma - mistrust of health care system due to past experiences and intergenerational trauma
  • Culture- care may not be culturally safe including focus on SEWB, prejudice, representation
  • Economic barriers
21
Q

Types of muscarinic receptors

A

M1 – CNS and autonomic ganglia,

M2 – heart

M3 – most other peripheral functions

22
Q

Mitosis vs. Meiosis

  • Location
  • Outcome
  • Function
  • Summary
A
23
Q

Reversible precancerous changes

A
  • Hyperplasia: more cells
  • Hypertrophy: larger cells
  • Metaplasia: abnormal change in tissue type
  • Dysplasia: loss of normal cellular differentiation (abnormal cells)
24
Q

Phases of the cell cycle and regulation

A

G1: growth and function of the cell, preparation for DNA replication

  • G1 checkpoint: cell can be arrested into G0 phase to prevent further progression of the cycle if conditions are not favourable or cell is not ready, mediated by cyclins and CDKs which interact with retinoblastoma and p53

S: replication of DNA

G2: further growth of cell and preparation for mitosis

  • G2 checkpoint: ensures replication has occurred and cell has necessary requirements for mitosis, cyclins/CDKs involved with role of p53 also important

M: mitosis occurs

spindle checkpoint at the end of metaphase, ensures that all sister chromatids are correctly attached to spindle fibres to facilitate separation

25
Q

Enzymes involved in DNA replication

A
  • Helicase separates DNA strands to form replication fork
  • Gyrase/topoisomerase prevents supercoiling
  • DNA polymerase III adds new nucleotides at the 3’ end
  • Primase is as form of RNA polymerase that synthesises RNA primers
  • DNA polymerase I removes RNA primers from lagging strand and replaces with DNA
  • Ligase repairs phosphodiester bonds in lagging strand due to primers
26
Q

Major routes of metastasis

A

Haematogenous spread – through blood vessels

Lymphatic spread

Trans coelomic – through body walls and cavities

27
Q

Transcription and Translation overview

A

Transcription = DNA helix separates which allows RNA polymerase to recognise and binds to promoter sequences and synthesise a single strand of mRNA from the template strand

  • transcription factors regulate which genes are transcribed
  • epigenetic tags e.g. methyl groups alter DNA coiling which influences expression

Translation = at the ribosome, codons of mRNA are matched with complementary anticodons of tRNA which facilitates the addition of corresponding amino acids to a growing polypeptide

28
Q

Initial stages of embryological development

A
29
Q

Apoptosis vs. Necrosis (cause, histological features)

A

Apoptosis = programmed cell death induced by intrinsic enzymes (caspases) which degrade cellular contents but maintain membrane integrity therefore without causing inflammation

  • intact membrane
  • cellular blebbing
  • condensation of chromatin and shrinking of cell

minimal host response but macrophages will phagocytose apoptotic remnants

Necrosis = pathological cell death due to enzymatic digestion and denaturation of intracellular proteins, contents leak and cause inflammation

  • coagulative: cellular architecture preserved as pink anuclear ghost outlines (ischaemia)
  • liquefactive: highly inflammatory, no cellular structures remain (abscess, CNS hypoxia)
  • caseous: mix of other two, cheese-like appearance (mycobacterial infection)
30
Q

Three types of skin malignancy

  • Origin
  • Appearance
  • Metastasis
  • Local Invasion
  • Prognosis
  • Incidence
A
31
Q

Major types of malignant melanoma

A

LANS

Lentigo maligna – older people with sun damaged skin, especially on face

Acral lentiginous – thick skin (palms, soles, nail beds)

Nodular – typically on the trunk, very aggressive

Superficial spreading – common in young people

32
Q

Hallmarks of cancer

A

SALTIE

  • Self-sufficiency of growth
  • Angiogenesis
  • Limitless replication
  • Tissue invasion + metastasis
  • Insensitivity to inhibitory signals
  • Evasion of apoptosis
33
Q

Gene mutations that contribute to neoplastic growth

A

(gain of function)

proto-oncogenes – normally promote cellular growth, mutation causes uncontrolled growth signalling which stimulates cancer development

e.g. Ras, Myc, B-RAF

(loss of function)

tumour suppressor genes – normally inhibit excessive growth but can become dysfunctional due to mutation, allowing for proliferation

e.g. p53, Rb

DNA repair enzymes – proteins which normally function to correct errors/damage in DNA, mutation causes dysfunction allowing for further mutations to accumulate

e.g. BRCA1/2, MSH

34
Q

Principles of tumour grading and staging

A

Grading = measuring the degree of similarity/differentiation between tumour and origin tissue, tumour is assigned as either high grade or low grade

Staging = classification of cancer based on extent of spread, method depends on cancer type

TNM is a common method (tumour size, nodes, metastases)

35
Q

Six types of necrosis

A
  • Coagulative – ghost outlines with architecture preserved (ischaemia, infarcts)
  • Liquefactive – digestion of cells, pus, inflammatory infiltrate (CNS hypoxia, abscess)
  • Caseous – cheese-like and friable, mixture of liquefactive and coagulative (TB)
  • Fat necrosis – focal fat destruction e.g. pancreas and fatty tissues
  • Fibrinoid – Ag-Ab complexes in vessel walls (vasculitis)
  • Gangrenous – coagulative with bacterial infection
36
Q

7 major groups of human pathogens (features and examples)

A
37
Q

Normal skin microflora and common skin infections

A

S. epidermidis, S. aureus, Propionibacterium spp., Corynebacterium spp., Candida spp. (fungi)

major skin infections include:

  • impetigo: superficial infection of the face and limbs due to S. aureus and/or S. pyogenes
  • folliculitis: infection of hair follicles that forms furuncles and carbuncles
  • cellulitis: diffuse infection of all three layers of the skin due to skin damage
  • necrotising fasciitis: S. pyogenes infection of subcutaneous fat, medical emergency

fungal infections include tinea/ringworm, candidiasis, pityriasis

38
Q

Methods used to classify bacteria with examples

A

Shape + clustering: bacilli/cocci, staph/strep/diplo

Gram stain reaction:

  • +ve: thick layer of PG stains purple e.g. Neisseria spp., E. coli, H. influenzae
  • –ve: thin layer of PG with outer membrane stains pink e.g. Staphylococcus spp., GAS

Mycobacteria –very lipid rich (hydrophobic, waxy, mycolic) cell wall, stains with Acid Fast stain

39
Q

Stages of bacterial infection

A
  1. Encounter/contact
  2. Colonisation (adherence)
  3. Invasion of host cells/tissues
  4. Spread to other host sites
  5. Damage by bacterial enzymes (endotoxins, exotoxins)
  6. Resolution: recovery, death, chronic infection
40
Q

Examples of bacterial virulence factors

A
  • Adherence and colonisation factors
  • Invasion factors e.g. degradative enzymes
  • Nutrient acquisition
  • Toxins
  • Immune evasion and suppression
41
Q

Commonly used antibiotics and their targets

A

β-lactams e.g. penicillin → target peptidoglycan cross-linking

Macrolides e.g. clarithromycin → inhibit ribosomal subunit 50S

Tetracyclines e.g. doxycycline → inhibit ribosomal subunit 30S

42
Q

Mechanisms of antibiotic resistance

A

CRED

  • Change - modification of a drug target
  • Removal - active efflux of the drug
  • Entry - limiting uptake of the drug
  • Destroy - inactivation of a drug

Genetic mutations that results in the development of antibiotic resistance can be transferred to other bacteria both vertically (to progeny) and horizontally (via plasmids)

43
Q

Innate vs Acquired immunity

  • Timeline
  • Specificity
  • Memory
  • Cellular mediators
  • Humoral Mediators
A
44
Q

Major types of immune cells

A
  • Neutrophils: acute inflammation, phagocytosis
  • Monocytes: differentiate into macrophages, chronic inflammation, antigen presentation
  • Basophils/mast cells: allergic responses
  • Eosinophils: allergic responses and antiparasitic immunity
  • Lymphocytes: mediators of the adaptive immune response (B and T cells)
45
Q

Classes of immunoglobulin

  • Structure
  • Heavy chain
  • Serum
  • Binding Sites
  • Function
A
46
Q

Overview of complement cascade and acute phase proteins

A

Several mechanisms can activate the cascade:

  • constant C3 tick-over/breakdown stabilised by presence of bacterial cell wall
  • binding of C1 complex to antibody or mannose binding lectin and mannose recruits C2 + C4 to form the C3 convertase
  1. C3 is then converted to C3a (chemoattractant) and C3b (opsonin, forms C5 convertase)
  2. C5 is converted into C5a (chemoattractant) and C5b
  3. C5b recruits C6-9 which recruits and forms the membrane attack complex to lyse bacteria

acute phase proteins = proteins that rapidly increase in serum concentration in response to inflammatory cytokines e.g. C-reactive protein, mannose binding protein, complement factors

47
Q

Cardinal signs of inflammation

A
  • swelling
  • redness
  • heat
  • pain
  • loss of function
48
Q

Vascular and Cellular events that occur in an inflammatory response

A

Vascular

  1. hyperaemia (pre-capillary sphincters open)
  2. increased capillary permeability due to chemical mediators
  3. margination of neutrophils as blood thickens and slows

Cellular

  1. adhesion of WBCs
  2. diapedesis/extravasation
  3. immune cell functioning e.g. phagocytosis, antigen presentation
49
Q

Sequelae of inflammation

A

the potential outcomes of an acute inflammatory response include:

  • resolution
  • organisation (granulation tissue)
  • suppuration
  • chronic inflammation
  • long term healing with fibrosis

P1 (30 decks)

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