Week 6 Year 1 Med

What are the five types of chemical communication between cells?

Neurotransmitters (released at synapses, act locally), Endocrine hormones (travel in bloodstream to distant organs), Neuroendocrine hormones (secreted by neurons into bloodstream), Paracrine signalling (affect nearby neighbouring cells), Autocrine signalling (act on the same cell that secreted them).

How do water-soluble vs lipid-soluble hormones differ in their mechanism of action?

Water-soluble: circulate freely in blood → bind cell surface receptors → use second messenger systems (e.g. cAMP). Lipid-soluble: transported bound to carrier proteins → diffuse into cells → bind intracellular receptors → regulate gene transcription. Effect rate: hours to days.

What are the three ways hormone release is regulated?

Humoral stimuli (changes in blood ions/nutrients), Neural stimuli (nerve fibres stimulate hormone release), Hormonal stimuli (hormone cascades — one hormone triggers another).

How does hormonal communication differ from nervous system communication?

Hormones: travel via bloodstream, slower onset, longer-lasting effects, act on distant target organs. Nervous system: fast chemical signalling at synapses (milliseconds), localised, short-lived effects. Both regulate body functions but operate on different timescales.

What is a myotome?

A group of muscles innervated by a single spinal nerve root. Each muscle receives input from a specific spinal cord level and is controlled via motor (efferent) neurons.

What is the pathway of a motor signal from brain to muscle?

Motor cortex → corticospinal tract (most fibres decussate/cross in the medulla) → descend in spinal cord → synapse with interneurons or anterior (ventral) motor neurons → exit via anterior root → peripheral nerve → muscle.

How are myotomes used to determine spinal cord injury level?

Assess which movements are normal, weak or absent → match deficits to myotomes → the lowest functioning myotome indicates the level of intact spinal cord; injury is at or above the first level of deficit.

What is the difference between sensory (afferent) and motor (efferent) impulses?

Sensory: transmit information from receptors (skin, muscle) to brain/spinal cord via dorsal root and ascending pathways; cell bodies in dorsal root ganglion. Motor: transmit commands from CNS to muscles via corticospinal tract → anterior horn → ventral root → muscle contraction.

What is a dermatome?

An area of skin supplied by sensory fibres from a single spinal nerve. Sensory neuron cell bodies are located in the dorsal root ganglion; sensory input from each skin region travels to its matching spinal segment.

What sensory modalities can a single dermatome transmit?

Touch/pressure (mechanoreceptors), vibration, proprioception, pain (nociception) and temperature. All originate from the same dermatome but travel in different pathways and use different receptor types.

What are the two major sensory pathways and what do they carry?

Dorsal Column Medial Lemniscus (DCML): fine touch, vibration, proprioception — fast and precise. Spinothalamic tract: pain, temperature and crude touch.

What are the four qualities sensory systems encode?

Modality (type of stimulus), Location (where on body — dermatome), Intensity (strength of stimulus), Duration (how long it lasts).

What is the ANS and what does it regulate?

A division of the peripheral nervous system controlling involuntary physiological processes — smooth muscle, cardiac muscle, glands and internal organs. Uses a two-neuron pathway: preganglionic neuron (from CNS) and postganglionic neuron (innervates effector organ).

What are the sympathetic effects on the cardiovascular system?

Increased heart rate, increased cardiac contractility, vasoconstriction → increased blood pressure and cardiac output during stress or exercise.

What are the parasympathetic effects on the cardiovascular system?

Decreased heart rate, decreased cardiac conduction velocity, slightly decreased contractility → promotes resting cardiovascular function.

What are the consequences of ANS dysfunction?

Orthostatic hypotension (cardiovascular), reduced GI motility/constipation/gastroparesis (digestive), abnormal pupil size/impaired accommodation (eye), reduced sweating/poor temperature regulation (skin), impaired stress response (sympathetic failure).

What is the anatomical origin of the sympathetic nervous system?

Thoracolumbar division — originates from T1-L2 spinal cord. Preganglionic neurons in the intermediolateral horn. Short preganglionic neurons, long postganglionic neurons; ganglia near the spinal cord in the sympathetic chain.

What is the anatomical origin of the parasympathetic nervous system?

Craniosacral division — originates from brainstem nuclei and sacral spinal cord (S2-S4). Long preganglionic neurons, short postganglionic neurons; ganglia close to or within target organs.

Which cranial nerves carry parasympathetic fibres and what do they supply?

CN III (oculomotor — pupil constriction/accommodation), CN VII (facial — lacrimal and salivary glands), CN IX (glossopharyngeal — parotid gland), CN X (vagus — visceral organs), Sacral nerves S2-S4 (bladder, rectum, genitals).

What neurotransmitter do all preganglionic autonomic neurons release and what receptor does it act on?

Both sympathetic and parasympathetic preganglionic neurons release acetylcholine (ACh), which acts on nicotinic receptors on postganglionic neurons in autonomic ganglia.

What neurotransmitter do postganglionic sympathetic neurons release and what are the exceptions?

Most release norepinephrine (adrenergic neurons) acting on alpha receptors (vasoconstriction) and beta receptors (cardiac/metabolic effects). Exceptions: sweat glands, piloerector muscles and certain blood vessels use ACh instead.

What neurotransmitter do postganglionic parasympathetic neurons release and where does it act?

All release acetylcholine (ACh — cholinergic neurons), which acts on muscarinic receptors on smooth muscle, cardiac muscle and gland cells.

What does the adrenal medulla release and why is it considered a special sympathetic structure?

Acts as a modified sympathetic ganglion; releases epinephrine (80%) and norepinephrine (20%) directly into the bloodstream, prolonging sympathetic effects on cardiovascular activity, metabolic rate and stress response.

What are baroreceptors and where are they located?

Stretch-sensitive mechanoreceptors in the carotid sinus (at carotid bifurcation) and aortic arch. They detect changes in arterial pressure by sensing stretch in the arterial wall.

How do baroreceptor signals reach the brainstem?

Carotid sinus → Hering's nerve → glossopharyngeal nerve (CN IX). Aortic arch → vagus nerve (CN X). Both terminate in the nucleus tractus solitarius (NTS) in the medulla.

What is the role of the NTS in the arterial baroreflex?

First integration centre for baroreceptor signals. High BP: increased baroreceptor firing → NTS activated → inhibitory pathways reduce sympathetic activity. Low BP: reduced NTS activation → increased sympathetic activity.

What is the role of the CVLM in the baroreflex?

Caudal Ventrolateral Medulla acts as an inhibitory relay. High BP: NTS activates CVLM → CVLM inhibits RVLM → reduced sympathetic outflow. Low BP: less CVLM activation → RVLM disinhibited → increased sympathetic activity.

What is the role of the RVLM in the baroreflex?

Rostral Ventrolateral Medulla is the main sympathetic output centre controlling vascular resistance, cardiac output and sympathetic tone. RVLM activity increases → vasoconstriction → BP rises. RVLM activity decreases → vasodilation → BP falls.

What is MSNA and what is its role in the baroreflex?

Muscle Sympathetic Nerve Activity — sympathetic nerve signals to blood vessels in skeletal muscle. Low BP: increased MSNA → vasoconstriction → increased total peripheral resistance → BP rises. High BP: decreased MSNA → vasodilation → BP falls. MSNA is the final effector of the arterial baroreflex.

Describe the full arterial baroreflex pathway for a rise in blood pressure.

1. BP Rises (Increased stretches of the walls of the carotid sinus and aortic arch.)

2. Baroreceptors increase frequency of AP, signals through Glossopharnygeal nerve from Carotid, Vagus nerve from Aortic arch.

3. NTS (Nucleus Tractus Solitarius) Activated

4. The NTS excites neurons in Caudal Ventrolateral Medulla

5. CVLM release GABA onto Rostral Venterolateral Medulla

6. RVLM decreases → Sympathetic nervous system activity decreased

7. Reduced sympathetic outflow including reduced Muscle Sympathetic Nerve Activity

8. Less Vasoconstriction of arterioles and veins, reduced cardiac stimulation.

9. Vasodilation, resulting in decreased Total peripheral resistance and decreased venous return and stroke volume.

10. BP will fall back towards normal as CO and TPR decrease. (Homeostasis)

What is the cardiac baroreflex and how does it differ from the arterial baroreflex?

The cardiac baroreflex regulates heart rate in response to BP changes, primarily via the parasympathetic nervous system through the vagus nerve. The arterial baroreflex regulates vascular resistance via the sympathetic system (RVLM/MSNA).

What are the nucleus ambiguus (NA) and dorsal motor nucleus of the vagus (DMX)?

Both located in the medulla; contain preganglionic parasympathetic neurons projecting to the heart via the vagus nerve. NA: major controller of cardiac parasympathetic activity and heart rate. DMX: additional parasympathetic output to heart and visceral organs.

Describe the cardiac baroreflex response to a rise in blood pressure.

BP rises → baroreceptors fire more → NTS activated → NTS stimulates NA and DMX → parasympathetic vagal output increases → ACh released → heart rate decreases → BP falls toward normal.

What are the parasympathetic effects on the heart?

Decreased heart rate (negative chronotropy), reduced conduction through the AV node, slight reduction in atrial contractility. Mediated by ACh acting on muscarinic receptors.

What is commensalism?

A relationship where one organism benefits and the other is unaffected. Example: Staphylococcus epidermidis on human skin. Normal microbiota occupying ecological niches helps prevent pathogen colonisation (colonisation resistance).

What is mutualism?

A relationship where both organisms benefit. Example: E. coli in the colon synthesises vitamin K for the host. Gut bacteria also digest complex carbohydrates, produce B vitamins, stimulate the immune system and prevent pathogen colonisation.

What is parasitism?

A relationship where one organism (the parasite) benefits and the host is harmed. The parasite obtains nutrients/resources from the host, which may experience disease, tissue damage or immune responses. Example: H1N1 virus infecting a human.

What is opportunism in microbiology?

Normally harmless microorganisms causing disease under certain conditions — typically when host immunity is compromised (HIV/AIDS, chemotherapy) or microorganisms enter normally sterile sites (e.g. skin bacteria entering the bloodstream during procedures).

What are the key differences between gram-positive and gram-negative bacteria?

Gram-positive: thick peptidoglycan layer, no outer membrane, retain crystal violet stain → appear purple; generally more susceptible to antibiotics targeting cell walls. Gram-negative: thin peptidoglycan, outer membrane with lipopolysaccharide (LPS), do not retain crystal violet → appear pink/red.

What are the key features of viruses?

Acellular; consist of genetic material (DNA or RNA) + protein coat (capsid); some have a lipid envelope. Cannot reproduce independently — replicate by infecting host cells and using host machinery. Examples: influenza, SARS-CoV-2, HIV.

What are the key features of fungi as pathogens?

Eukaryotic; larger than bacteria; cell walls contain chitin; reproduce through spores. Yeasts: unicellular, reproduce by budding (e.g. Candida). Moulds: multicellular, filamentous hyphae (e.g. Aspergillus). Often cause opportunistic infections in immunocompromised individuals.

What are the two types of parasites and their characteristics?

Protozoa: single-celled eukaryotes, transmitted via contaminated food/water or vectors (e.g. Plasmodium — malaria). Helminths: multicellular parasitic worms (roundworms, tapeworms, flukes). Complex life cycles, often involving multiple hosts.

What are prions?

Infectious misfolded proteins with no DNA or RNA. Cause disease by inducing normal proteins to misfold. Extremely resistant to sterilisation. Diseases: Creutzfeldt-Jakob disease, mad cow disease → spongiform degeneration of brain tissue.

What is normal flora and what are its key functions?

Microorganisms normally living on/in the human body without causing disease. Functions: colonisation resistance (competing with pathogens), metabolic functions (vitamin production, carbohydrate digestion) and immune system development/maintenance of immune tolerance. Can cause opportunistic infections if immunity is compromised or they enter sterile sites.

What is cleavage in embryogenesis?

A series of rapid mitotic divisions after fertilisation producing progressively smaller cells (blastomeres) without increasing overall embryo size. Occurs as the zygote travels through the uterine tube; zona pellucida remains surrounding the embryo throughout.

What is the morula and what happens during compaction?

The morula is a solid ball of 16–32 cells (Day 3–4). During compaction, blastomeres pack tightly together, cell junctions form, and two populations develop: inner cell mass (embryoblast — forms the embryo) and outer cell mass (trophoblast — contributes to placenta).

What is the blastocyst and what are its components?

By Day 5, fluid enters the morula forming the blastocoel cavity → now called a blastocyst. Components: Embryoblast/inner cell mass (forms the embryo proper), Trophoblast/outer layer (forms placenta and supporting structures), Blastocoel (fluid-filled cavity).

What is hatching and why is it important?

Before implantation (~Day 5–6), the blastocyst breaks out of the zona pellucida. This allows the trophoblast to interact directly with the endometrium to initiate implantation.

What is implantation and when does it occur?

The process by which the blastocyst attaches to and embeds within the uterine endometrium. Begins ~Day 6–7; blastocyst attaches via the trophoblast layer, usually to the posterior or anterior wall of the uterus.

What are the two layers the trophoblast differentiates into during implantation?

Cytotrophoblast: inner cellular layer with mitotically active cells. Syncytiotrophoblast: outer multinucleated layer that invades the endometrium, releases enzymes allowing implantation, erodes maternal tissue and establishes early maternal-embryonic exchange.

What is the decidual reaction?

The endometrial response during implantation — endometrium thickens, becomes highly vascular and stromal cells enlarge to support the embryo. Blastocyst is fully embedded by Day 9–10.

What is gastrulation and what does it produce?

The process converting the bilaminar embryonic disc into a trilaminar disc with three primary germ layers: Ectoderm, Mesoderm and Endoderm. Establishes the basic body plan and embryonic axes. Begins ~Day 15.

What is the primitive streak and what does it establish?

A structure appearing on the dorsal surface of the epiblast ~Day 15. Defines the cranial-caudal axis, establishes left-right symmetry and provides a pathway for cell migration (ingression) during gastrulation.

What does each germ layer give rise to?

Endoderm (first migrating cells): lining of GIT and respiratory systems. Mesoderm (second wave): muscles, bones, blood vessels, kidneys, connective tissue, reproductive organs. Ectoderm (remaining epiblast): nervous system, skin, sensory organs.

What is the notochord and what is its role?

Forms from cells migrating through the primitive node; defines the primitive embryonic axis; foundation of the vertebral column; acts as an important signalling centre for neural development (induces neurulation).

What is neurulation and what does the neural tube develop into?

The process by which the ectoderm forms the neural tube → develops into the CNS (brain and spinal cord). Neural plate forms → folds to form neural folds and neural groove → folds fuse to form the neural tube. Closure: cranial neuropore closes Day 25, caudal neuropore Day 27.

What are neural crest cells and what do they form?

Cells that detach from the crest of the neural folds during neural tube closure. Form: peripheral nervous system, autonomic ganglia, Schwann cells, melanocytes, facial cartilage and bones.

What are the consequences of failure of neural tube closure?

Cranial neuropore fails to close → anencephaly. Caudal neuropore fails to close → spina bifida.

What causes embryonic folding and what are the two types?

Caused by rapid growth of the neural tube, expansion of somites and mesoderm, and growth of the amniotic cavity. Types: cephalocaudal folding (head-tail) and lateral folding — both occur simultaneously during Week 4.

What organs develop from the head fold during cephalocaudal folding?

The cardiogenic region moves to lie ventral to the foregut → heart enters the future thoracic region. Part of the yolk sac is incorporated into the foregut → forms pharynx, oesophagus, stomach and upper duodenum.

What does lateral folding contribute to organ development?

Forms the primitive gut tube (foregut, midgut, hindgut → digestive organs), the ventral body wall (encloses developing organs) and body cavities (intraembryonic coelom divides into pericardial, pleural and peritoneal cavities).

What are the normal microscopic layers of the appendix?

Mucosa (columnar epithelium + goblet cells + crypts), Lamina propria (connective tissue + lymphoid tissue — normally abundant), Submucosa (loose connective tissue, blood vessels, nerves), Muscularis propria (inner circular + outer longitudinal muscle), Serosa.

What are the key microscopic features of acute appendicitis?

Neutrophil infiltration of the muscularis propria (hallmark), dilated/oedematous wall, vascular congestion and dilation, mucosal ulceration and haemorrhage, transmural inflammation, serosal inflammatory exudate.

What are the normal microscopic layers of the gallbladder?

Mucosa (simple columnar epithelium forming folds for bile concentration), Lamina propria (loose connective tissue + blood vessels), Muscular layer (smooth muscle for contraction during bile release), Serosa/adventitia.

What are the key microscopic features of chronic cholecystitis?

Thickened wall (chronic inflammatory infiltrate + fibrosis), chronic inflammatory cells (lymphocytes, plasma cells, macrophages in lamina propria), fibrosis, mucosal changes (epithelial damage, flattening, irregular folds), and Rokitansky-Aschoff sinuses.

What are Rokitansky-Aschoff sinuses?

Diverticulum-like outpouchings of gallbladder mucosa extending deep into the muscular wall; caused by mucosal glands becoming trapped within fibrotic tissue due to increased pressure and chronic inflammation. Classic histological feature of chronic cholecystitis.

What are the general microscopic features of a neoplasm?

Increased cell proliferation (dense clusters/nests), abnormal tissue architecture, cellular atypia (pleomorphism, enlarged nuclei, increased nuclear-to-cytoplasmic ratio, hyperchromatic nuclei), increased mitotic activity (including abnormal mitoses), and invasion of surrounding tissue (malignant tumours).

What are the specific microscopic features of basal cell carcinoma?

Nests of basaloid cells extending from epidermis into dermis, peripheral palisading (cells at edges of nests align in parallel — fence-like pattern), basophilic (dark-staining) cells with large nuclei, peritumoral clefts (spaces between tumour nests and stroma), local tissue invasion with rare metastasis.

What is peripheral palisading in BCC?

A key diagnostic feature where cells at the edges of tumour nests align in a parallel, fence-like arrangement. It is characteristic of basal cell carcinoma.

What are the microscopic features of a healing skin scar?

Dense, disorganised collagen deposition (hallmark — thicker and more irregular than normal dermis), loss/distortion of normal adnexal structures (hair follicles, sweat glands), chronic inflammatory cells (lymphocytes, macrophages, plasma cells), granulation tissue (new capillaries, proliferating fibroblasts), and foreign body reaction (multinucleated giant cells around suture material).

What are the three fates of preganglionic fibres entering the sympathetic chain?

Synapse at the same spinal level → postganglionic fibre exits via gray ramus to spinal nerve. Ascend or descend before synapsing at another ganglion. Pass through without synapsing → travel as thoracic splanchnic nerves to prevertebral ganglia.

What are the three thoracic splanchnic nerves and what do they supply?

Greater splanchnic nerve (T5–T9): celiac ganglion → foregut organs (stomach, liver, spleen, proximal duodenum). Lesser splanchnic nerve (T10–T11): superior mesenteric ganglion → midgut (small intestine, proximal colon). Least splanchnic nerve (T12): aorticorenal ganglion → kidneys and adrenal glands.

How does cardiac sympathetic innervation reach the heart?

Originates from T1–T4 spinal cord → preganglionic fibres ascend in sympathetic chain → synapse in cervical and upper thoracic sympathetic ganglia → postganglionic fibres form cardiac nerves → cardiac plexus (near tracheal carina, formed with vagus nerve fibres).

What is the mechanism of referred pain from cardiac ischaemia to the chest wall and arm?

Cardiac ischaemia activates visceral pain receptors → afferents travel via sympathetic cardiac nerves → enter spinal cord at dorsal root ganglia T1–T4/T5 → converge with somatic sensory neurons from intercostal nerves and chest wall dermatomes in the dorsal horn → pain signals ascend via spinothalamic tract → brain interprets pain as coming from somatic structures (chest wall, left arm, left forearm).

What is the typical distribution of referred cardiac pain?

Because cardiac afferents enter at T1–T4/T5: retrosternal chest, left chest wall, left inner arm and left forearm.

What are the rotator cuff muscles and their function?

Supraspinatus, infraspinatus, teres minor and subscapularis. Stabilise the humeral head in the glenoid fossa and assist shoulder rotation.

What is a motor unit?

A single motor neuron plus all the muscle fibres it innervates. All fibres within a motor unit contract simultaneously when the neuron fires.

What are the three main parts of the neuromuscular junction?

Presynaptic terminal (motor nerve terminal): synaptic vesicles with ACh, voltage-gated Ca2+ channels, mitochondria. Synaptic cleft: contains acetylcholinesterase. Postsynaptic membrane (motor end plate): nicotinic ACh receptors, junctional folds increasing surface area.

What is the sequence of events at the neuromuscular junction during muscle activation?

Action potential reaches motor neuron terminal → voltage-gated Ca2+ channels open → Ca2+ enters terminal → triggers exocytosis of ACh → ACh diffuses across cleft → binds nicotinic receptors on end plate → Na+ influx → end plate potential → if threshold reached → muscle action potential generated.

What is excitation-contraction coupling?

The process converting electrical depolarisation of the muscle membrane into mechanical contraction: action potential spreads along sarcolemma → travels down T-tubules → activates SR → Ca2+ released → Ca2+ binds troponin → tropomyosin shifts → myosin-binding sites exposed → cross-bridge cycling → sarcomere shortens → muscle contracts.

What causes demyelination and what are its effects on neuromuscular transmission?

Loss of myelin (e.g. multiple sclerosis) → loss of saltatory conduction → slower nerve conduction → failure of impulse propagation → muscle weakness, poor coordination, sensory disturbances.

What is myasthenia gravis and how does it affect the NMJ?

Autoimmune condition — autoantibodies destroy nicotinic ACh receptors on the motor end plate → reduced end plate potentials → muscle weakness that worsens with activity. Treatment: acetylcholinesterase inhibitors (neostigmine, pyridostigmine).

What is Lambert-Eaton Myasthenic Syndrome and how does it affect the NMJ?

Autoimmune condition targeting presynaptic voltage-gated Ca2+ channels → reduced ACh release from nerve terminals → muscle weakness. Distinguishing feature: incremental response on repetitive nerve stimulation (repeated stimulation increases Ca2+ buildup → increased muscle response).

What is botulism and how does it affect the NMJ?

Bacterial toxin prevents ACh vesicle fusion with the presynaptic membrane → blocks ACh release → flaccid paralysis and muscle weakness. Botulinum toxin also used therapeutically for muscle spasms and cosmetic procedures.

What is Duchenne Muscular Dystrophy?

Progressive muscle degeneration caused by absence of dystrophin (a protein stabilising muscle cell membranes) → muscle fibre damage → weakness and wasting.

What is nerve conduction studies (NCS) and what does it measure?

Stimulating electrode applies impulse to nerve; recording electrode over muscle detects compound muscle action potential (CMAP). Measures conduction velocity (speed), latency (time taken) and amplitude (number of functioning fibres). In NMJ disorders: conduction velocity usually normal but muscle response may be reduced.

What is repetitive nerve stimulation and what patterns indicate NMJ disorders?

A motor nerve is stimulated repeatedly; CMAP amplitude recorded after each stimulus. Normal: stable amplitude. Decremental response (progressive amplitude decrease): indicates myasthenia gravis (reduced ACh receptors). Incremental response (amplitude increases): indicates Lambert-Eaton Myasthenic Syndrome (reduced ACh release, Ca2+ accumulates with repeated stimulation).

What is needle EMG and what does it assess?

A fine needle electrode inserted into muscle records electrical activity at rest, during slight contraction and during strong contraction. NMJ disorders: variable activation, reduced motor unit recruitment, fatiguability. Nerve disorders: fibrillation potentials, denervation. Muscle disorders: small motor unit potentials, early recruitment.

What are the connective tissue layers surrounding skeletal muscle?

Epimysium (surrounds entire muscle), Perimysium (surrounds fascicles/bundles of fibres), Endomysium (surrounds individual muscle fibres). Provide structural support, pathways for nerves and blood vessels and transmission of force to tendons.

What are small vs large motor units?

Small motor units: fewer muscle fibres, fine motor control (e.g. eye muscles). Large motor units: many muscle fibres, powerful contractions (e.g. quadriceps). Small units allow precision; large units generate greater force.