Lecture Notes Flashcards

General Review

• All PBLs + their SAQs
• Progress tests
• Peerwise
• Kahoots FunMed

Collagen Types

• Type 1: Bone
• Type 2: Cartilage

Hypertonic Solutions

E. coli

• Gram-negative bacterium that causes stomach ulcers.
• Triple therapy: 1 PPI + 2 antibiotics.

Antibodies and Their Functions

• IgA: Dimer; secretions (tears, gastric, mucous, colostrum, breastmilk).
• IgE: Monomer; allergies, asthma, antiparasitic activity.
• IgG: Monomer; crosses placenta.
• IgD: Monomer
• IgM: Pentamer; made first in an immune response.

Cancer, Oncogenes, and Tumor Suppressor Gene (TSG) Mutations and Conditions

• Edwards syndrome, etc. - Know the numbers.
• Xeroderma pigmentosum – nucleotide excision repair.
• Constitutional mismatch repair deficiency syndrome (CMMRD) – mutations in MutS + MutL enzymes?
• Inherited BRCA2 repair-associated mutations – homologous recombination repair.
• Edwards syndrome – trisomy 18.
• Patau syndrome – trisomy 13.
• Down syndrome – trisomy 21 (classic, Robertsonian translocation 14+21, mosaic - mildest).
• Klinefelter – 47, XXY.
• Turner – 45, XO.
• P16, p21, p27: CDK1 proteins, G1/S transition.
• P53: Tumor suppressor, G1/S + G2/M.
• Rb (retinoblastoma protein): Tumor suppressor.
• BRCA1+2: Tumor suppressor, DNA double-strand break repair by regulation of homologous recombination.
• Proto-oncogene to oncogene: Gain of function.
• Tumor suppressor gene mutation: Loss of function.

Methylation

• Most commonly cytosine.

Types of Joints

• Fibrous: Suture (skull), Gomphosis (teeth), Syndesmosis (between tibia and fibula).
• Cartilaginous: Primary (synchondroses – epiphyseal plate, costochondral joints), Secondary (symphyses – pubic, intervertebral disc).
• Synovial: Condyloid (metacarpal-proximal phalanx, radius-carpal bones), Planar (between tarsal bones, clavicle-scapula [acromion]), Saddle (thumb), Hinge (elbow), Pivot (C1-C2), Ball and socket (hip, shoulder).

RAAS and Hypertension

• RAAS → hypertension → all the receptors e.g., baroreceptors, chemoreceptors etc. → hypertension drugs and when to give.
• Sympathetic: Increases HR and MAP.
• Parasympathetic: Decreases HR and MAP.

Neural Control of BP – Baroreceptor System (Fast)

• Sensors: In carotid sinus, aortic sinus, arterial baroreceptors.
• Arterial pressure ↑ → ↑ vascular wall tension → PIEZO channels activated: Inflow of Na^+, Ca^{2+} → membrane depolarization → Action Potentials generated → medullary cardiovascular center.
• Nerve endings in carotid sinus → sinus nerve → joins glossopharyngeal/vagus → afferent fibers of these nerves synapse in brainstem (in Nucleus of Solitary tract).
• If BP is ↑: NTS (+) nucleus ambiguus → parasympathetic outflow → vagus nerve → heart (SA node) → ↓ HR + ↓ CO = ↓ MAP.
• If BP is ↓: NTS (+) vasomotor center → sympathetic outflow → reticulospinal tract → heart → vasoconstriction + ↑ HR → ↑ peripheral resistance = ↑ MAP.

RAAS, JGA, Aldosterone, and ANP

• Hypertension treatment:
  • Under 55 or have type II diabetes: ACE inhibitors (if cough, ARBs).
  • Over 55 or Afro-Caribbean (+ no diabetes): Calcium channel blockers.

Asthma and Asthma Drugs

• Beta 2 agonist.
  • Short-acting beta agonist: Salbutamol.
  • Long-acting beta agonist: Salmeterol.

Adrenergic Receptors

• A1 (specific agonist - phenylephrine): Smooth muscle contraction – vasoconstriction, ↑BP.
• A2 (specific agonist - clonidine): Inhibits norepinephrine release + insulin release.
• B adrenergic receptors.
  • B1: ↑ HR.
  • Bronchodilation.

Review of SNS

• Sympathetic division
  • Preganglionic neurons use: ACh
  • Postganglionic neurons use: norepinephrine (in PNS = ACh)

SNS Functions

• Pupil dilation
• Inhibits salivation
• Relaxes bronchi
• Accelerates BP
• Inhibits peristalsis + secretion
• Activates glucose production + release
• Secretion of adrenaline and noradrenaline
• Inhibits bladder contraction
• Stimulates orgasms

Location of Sympathetic Ganglia

• Cell bodies: lateral horn of spinal cord: T1-L1.
• Postganglionic neurons cell bodies  ganglia + project to target organs.
• Pre + post ganglionic neurons synapse in: paravertebral ganglia of sympathetic chain, prevertebral ganglia.

Adrenoreceptors

• Stimulatory effect: alpha 1, beta 1
  • Alpha 1: vasoconstriction
  • Beta 1: increase HR
• Inhibitory effect: alpha 2, beta 2
  • Alpha 2: (-) SNS activity
  • Beta 2: bronchodilation + vasodilation

Lung Volumes

• Tidal volume: Amount of air you move in + out of lungs during rest.
• Forced vital capacity: Max. volume of air in and out of lungs in a single respiratory cycle.
• Inspiratory reserve volume: Volume of air you can draw into your lungs.
• Expiratory reserve volume: Volume of air you can expel from lungs.
• Residual volume: Volume of air left in lungs after max. exhalation.
• Forced vital capacity = inspiratory reserve volume + tidal volume + expiratory reserve volume.

Inspiration and Expiration Muscles

• Forced inspiration: Elevate ribs and move sternum up.
  • Diaphragm: contracts, moves down + external intercostal muscles contract: ribcage expands (quiet breathing) + accessory muscles – pec. Minor + major, serratus anterior.
• Forced expiration.
  • Internal intercostals + accessory muscles – anterior abdominal muscles + quadratus lumborum.
  • Diaphragm: relaxes, moves up, ribcage: down and in.

Recoil and Compliance

• Higher recoil = less compliance.
• Compliance: Ease at which lung expands under pressure  normally lungs are very compliant.
  • Reduced compliance:
    • Pulmonary fibrosis.
    • Collapse of lung.
    • ↑ in pulmonary venous pressure.
  • Increased compliance:
    • Emphysema.
    • Age.

Causes of Edema

• JV(NFP)= K[(Pc – Pi) – σ(Πc- Πi)]

• Increased capillary hydrostatic pressure.

• Decreased plasma oncotic pressure.

• Increased capillary permeability.

• Obstruction of the lymphatic system.

Preload and Afterload

• Preload: Degree of tension/load on the ventricular muscle when it begins to contract at the end of diastole  preload index: End Diastolic Volume: volume of blood in ventricles at the end of diastole (↑EDV → ↑ preload → ↑ active tension → ↑ contraction).
• Frank-Starling law: Changes in preload → changes in stroke volume.
• Afterload: Load that heart must eject blood against (↑ afterload → ↑ stroke volume).

Partial Pressures of Gases and Volume Graph

• Partial pressure of a gas: In a mixture of gases, each constituent gas has a partial pressure, which is the notional pressure of that constituent gas if it alone occupied the entire volume of the original mixture at the same temperature.
• Partial pressure of oxygen:
  • ↓ in blood and ↑ in alveoli → oxygen flows from alveoli into blood.
• Partial pressure of CO2:
  • ↑ in blood and ↓ in alveoli → CO2 flows from blood into alveoli.
• High altitude:
  • ↓ oxygen partial pressure → ↓ partial pressure of inspired air → ↓ partial pressure of alveolar air → ↓ hemoglobin saturation in lungs → altitude sickness.

Gas Laws

• Laplace: The smaller the radius of a vessel → the more pressure it can withstand (aneurysms).
• Frank-Starling law: Force developed in a muscle depends on the extent its stretched (changes in preload → changes in stroke volume).
• Boyle's: Pressure of a given quantity of a gas is inversely proportional to the volume that contains it (alveoli expand → pressure inside them ↓ → air goes out).
• Poiseuille's: Small changes in radius of a vessel (r^4) → big changes in flow.

FEV1/FVC Ratio

• Ratio of forced expiratory volume in 1 sec / forced vital capacity.
• Values above 70-80%: Normal.
• In airflow limitation (i.e., asthma), ratio drops.

ECG Intervals and Chest Leads

• Chest leads:
  • V1: 4th ICS to right of sternum.
  • V2: 4th ICS to left of sternum.
  • V3: between V2 and V4.
  • V4: 5th ICS midclavicular line.
  • V5: level with V4 at left anterior axillary line.
  • V6: level with V5 at midaxillary line.
• ECG intervals:
  • P wave: Less than 0.08 sec (2 small boxes).
  • P-R interval: 0.12-0.20 sec (3-5 small boxes).
  • QRS complex: 0.08-0.12 sec (2-3 small boxes).
  • Q-T interval: 0.35-0.43 sec – dependent on HR.

Heart Stab Wound

• Stabbed anteriorly, most likely is right ventricle → takes up most of anterior space of heart.

Arteries and Veins

• Arteries: Thickest: tunica media.
• Veins: Thickest: tunica adventitia.

ADH and Blood Osmolarity

• Blood osmolarity ↑ → subfornical organ senses → (+) hypothalamus: paraventricular + supraoptic nuclei → post pituitary produced ADH.
• ADH:
  • Additional aquaporins on collecting duct.
  • ↓ urine output volume.
  • More concentrated urine.
  • ↑ permeability of collecting duct to urea → water reabsorption.
  • Sodium reabsorption in thick ascending loop of Henle by ↑ activity of NKCC → ↑ osmolarity of medullary interstitial fluid: water reabsorbed from collecting ducts.

Immune System and IL-4

• Increase in IL-4: allergies and asthma.

MET

Micronutrients and Deficiencies

• Water-soluble can act as coenzymes.
• Vitamin A: Eye things.
• Vitamin D: Rickets, osteomalacia.
• Vitamin E: Peripheral neuropathy.
• Vitamin K: Coagulopathy.
• Vitamin C: Scurvy.
• Vitamin B1: Beri-beri, Wernicke’s/Korsakoff syndrome.
  • Wernicke's encephalopathy: horizontal nystagmus, cerebellar ataxia, ophthalmoplegia → Korsakoff syndrome: irreversible mental impairment.
• Vitamin B2: Angular stomatitis.
• Vitamin B3: Pellagra.
• Vitamin B6: Neuropathy, anemia.
• Vitamin B9: Anemia.
• Vitamin B12: Anemia.

Absorption Phases:

1. Luminal phase: Ingested food broken down by acid - stomach, alkali - small intestine + enzymes by gastric + small bowel mucosa + pancreas.
2. Mucosal phase: Pre-digested nutrients taken up by brush border membrane of enterocytes + enter intestinal cells.
3. Post-absorptive phase: Transport of absorbed nutrients via lymphatics + portal circulation to body.

GORD (Gastro-Oesophageal Reflux Disease)

• Movement of stomach contents from fundus to distal esophagus.
  • Causes:
    • Lower esophageal sphincter (LOS) → relaxed → allows passage of acid.
    • Excessive reflux of normal gastric juice: ↑ frequency of transient LOS relaxations.
    • Hiatal hernia.
    • Hypersensitivity of esophageal pain-sensing nerves.
  • Treatment:
    • PPIs.
    • Antacids: Gaviscon – sodium alginate and potassium hydrogen carbonate.
    • Surgery.

IBS, IBD, and Crohn's Disease

• IBS: Umbrella term for functional gastrointestinal diseases (FGID), pathogenesis unknown, defined set of symptoms.
  • FGIDs in upper GI: GORD, dyspepsia, bloating, pain, etc.
  • FGIDs in lower GI: Abdominal pain, constipation, motility diarrhea.
• IBD: Collective term that refers to chronic inflammation of the lower GIT (large intestine, anus): Crohn’s, ulcerative colitis – unknown cause.
• Crohn’s Chronic inflammatory condition that can affect the whole GIT but often found localized to small bowel (some parts of large).
  • Active symptoms: Abdominal pain, fatigue, fever, blood in stool, inflammatory diarrhea.
  • Damage to epithelium and ↑ levels of uncontrolled inflammation → can lead to changes in bowel epithelium → scaring → bowel obstruction, ulcers, fistulas.
• Ulcerative colitis Chronic inflammatory condition that is restricted to the colon.
  • Damage to colonic epithelium leading to ulcer-like appearance of mucosa.
    • Can lead to: perforation of the colon, severe bleeding, dehydration, systemic inflammation, colon cancer.
  • Treatment: mild/moderate symptoms – anti-inflammatory drugs (corticosteroids), severe symptoms – immunosuppressants, biological therapies.

Diarrhea

• Osmotic: Lactose intolerance, malabsorption.
• Secretory: E. coli (enterotoxins), cholera.
• Inflammatory: Crohn’s.
• Motility: Lower GI FGIDs.

Gastric Secretion Cells + Feedback Control

• Gastric epithelial cells:
  • Surface mucus cell: secretes mucus, trefoil peptides, bicarbonate.
  • Mucus neck cell: stem cell compartment.
  • Parietal cell: secrete HCL, IF.
  • ECL: histamine.
  • Chief cells: pepsinogen, chymosin, lipase.
  • G cells: hormones – gastrin.
  • D cell: somatostatin.
• Stimulation of acid secretion.
  • Parietal cells + ECL in corpus body (connected to ENS).
    • ACh: causes contractions → binds to M3 receptor → (+) parietal cells (acid) + ECL (histamine) → histamine also stimulates HCL secretion.
    • Gastrin – ‘the booster’ CCK2 receptor (gastrin receptor)  both in ECL + parietal cells. Infront of pyloric sphincter → we can sense number of digested protein → (+) G cells: gastrin → blood → CCK2 in ECL + parietal.
    • D cell/somatostatin – ‘the break’. D cell: release somatostatin → inhibits acid production. Somatostatin receptors: parietal + ECL. ENS connected to D cell: allows for inhibition.
    • D cells: have a paracrine function as well → endocrine function: goes through blood to stomach. D cell is (+) by excess acid. ENS (connected to vagus → when stressed → stomach acid) → (+) G cells → gastrin + inhibit D cell.
      • Parietal cells.
        • Gastrin receptors, M3 receptors, histamine receptors → (+) and ↑ HCL.
        • Somatostatin receptor, prostaglandin → (-) and ↓ HCL.

Vitamin B12 Absorption

• Saliva: Releases haptocorrin.
• Stomach (parietal cells): Releases IF.
• B12 binds with haptocorrin in the mouth → allows it to travel to duodenum → B12 binds with IF → goes to terminal ileum and is absorbed → in the enterocytes.
• B12 binds to transcobalamin II → blood stream.

Celiac Disease

• Autoimmune disease of small intestine.
• Gluten component destructive to the small intestine: gliadin → recognized by CD4 T cells.
• Genes: HLA-DQ2, or HLA-DQ8.
• Test: IgA anti-tTG (IgA anti-tissue transglutaminase) antibodies.
• Need to test for both IgA and IgA anti-tTG antibodies because: if patient doesn’t produce IgA the test → false negative.
• Histology.
  • Villous atrophy: villi flattening.
  • Crypt hyperplasia: increase in cells lining crypts.
  • Intraepithelial lymphocytosis: ↑ in lymphocytes number within epithelial cells lining SI.

Cori Cycle

• Gluconeogenesis in fasting and exercise.
• In muscle: glucose → lactate during anaerobic respiration.
• In liver: lactate → oxidized back to glucose by gluconeogenesis.
• Glucose → muscle to work.
• Cori cycle: interaction between liver and muscle.
• Only works if pyruvate is conserved (not converted to acetyl CoA).
• Fatty acids: supply the energy + prevent conversion of pyruvate to acetyl CoA by inhibiting PDC complex.

Body Fluid Compartments

• Body water content:
  • Infant: 80%.
  • Adult male: 60%.
  • Adult female: 50%.
• Extracellular fluid (15% body weight):
  • Mainly: Na^+, Cl^-$
  • A bit of K^+, HCO_3^-
• Intracellular fluid (40% body weight):
  • Mainly: K^+, PO_4^{3-}
  • A cell is an island with a banana tree, surrounded by sea.

Cholera

• Crypt enterocytes.
  • B subunit: facilitates entry of the A subunit into cells.
  • A subunit: activates adenylate cyclase → converts ATP to cAMP.
• ↑ cAMP levels → (+) CFTR protein → secretion of Cl^- into intestinal lumen (chloride channels stuck in open position) → osmotic imbalance: draws water and Na^+ into intestine → secretory diarrhea.

Gut Homing – Gut as an Immune Organ

• Paneth cells: secrete antimicrobial peptides – they’re in the crypts of Lieberkühn of the SI.
• Peyer’s patches: organized lymphoid follicles that contain large amounts of T cells, B cells, and APCs.
• M cells (microfold): above Peyer’s patch – transport antigens/bacteria across epithelium allowing APCs to access gut content.
• Most common APC: Dendritic cells.
• Gut homing.
  • Vitamin A → retinoic acid – acts as a transcription factor for T cells.
  • T cells make: CCR9 receptor + α4β7 → helps them find way back to gut to tell them to make antibodies against something.
  • Endothelial cells express: MadCAM.
  • MadCAM binds to α4β7.
  • Enterocytes release: cytokine CCL25.
  • CCR9 receptors sense CCL25.

Biochem

• Review Formosa’s thing again.

Metabolic Insight into Disease

• Carbohydrate metabolism
  • Glycogen storage disease (GSD) type I – Von Gierke’s.
    • Autosomal recessive.
    • 3 types/gene defects:
      • GSD IA: G6PC gene → glucose-6-phosphatase.
      • GSD IB: SLC37A4 or "G6PT1" → the G6P transporter.
      • GSD IC: SLC17A3 or SLC37A4 → G6P transporters.
    • G6PC deficiency: Liver glycogen stores → unable to produce glucose to be sent via blood; Prevent gluconeogenesis in liver + kidney from other sources (pyruvate).
  • GSD type VI: Her’s disease.
    • Autosomal recessive
    • Deficiency in liver: glycogen phosphorylase (PYGL gene) → ↓ in livers ability to breakdown glycogen.
  • GSD type V: McArdle’s disease.
    • Autosomal recessive.
    • Deficiency in muscle: glycogen phosphorylase (PYGM gene) → exercise causes immediate depletion of energy stores: they can’t access energy stored in glycogen.
      • Second wind: improved tolerance towards exercise as new (extra-muscular) fuels are delivered to the exercising muscles via the blood: fatty acids, glucose, and amino acids.

SGLT1 and SGLT2

• SGLT1 – small intestine, SGLT2 – kidney and nephron.

AMPK

• Activates catabolic processes.

Glycemic Index

• Glycemic Index: Measure of how quickly a given food that contains carbohydrates causes blood sugar/glucose levels to rise → reflects how easily (or not) a given food is digested to release glucose in the blood.
  • Low GI index foods → complex carbohydrates that are not so easy to break down, and thus release lower blood glucose over a prolonged period of time.
  • High GI index foods → quickly digested and absorbed, resulting in a rapid spike of blood glucose.

Cholesterol

• Acetyl CoA → cholesterol via HMG-CoA reductase; statins inhibit HMG CoA reductase.
• Chylomicrons – formed in gut during digestion; carry fats/cholesterol from GI to peripheral tissue, Apo C2: allows the chylomicron to give its triglycerides to peripheral cells, ApoE: allows the chylomicron remnant to be taken up by the liver to deliver fatty acids and cholesterol。
• VLDL – formed in liver (from excess energy + chylomicron leftovers) → triglycerides to peripheral tissues.
• IDL – formed from VLDLs that have had triglycerides partially absorbed from peripheral tissue.
• LDL – remnants of VLDL + IDL which go back to circulation to take cholesterol to cells, Apo B100 binds to LDL receptors on the surface of target cells and allows receptor-mediated endocytosis to occur – process by which cholesterol is taken up by target cells.
• HDL – cholesterol from peripheral cells to liver as cholesterol esters for VLDL + LDL.
• LOCO

Insertion and Attachment Points

• Know the main insertion and attachment points  know biceps, triceps and rotator cuff muscles

• Corocoid process

  • Short head of biceps brachii
  • Coracobrachialis
  • Pectoralis minor

• Rotator cuff

  • Greater tuberosity
    • Supraspinatus
    • Infraspinatus
    • Teres minor
  • Lesser tuberisity
    • Subscapularis

• Biceps brachii long head  supraglenoid tubercle

• Greater trochanter

  • Gluteus minimus
  • Gluteus medius
  • Piriformis
  • Obturator Externus
  • Obturator internus

• Lesser trochanter

  • Iliopsoas

• Ischial tuberosity

  • Hamstrings

Rotator Cuff Muscles

• Supraspinatus – suprascapular nerve: first 0-15 degrees of shoulder abduction.
• Infraspinatus – suprascapular nerve: lateral rotation of arm.
• Teres minor – axillary nerve: lateral rotation of arm.
• Subscapularis – upper + lower subscapular nerves: medial rotation of arm.

Long Thoracic Nerve Damage

• Winged scapula.

Palsies

• Brachial Plexus
  • Superior Cord Injury – Erbs Palsy C5-C6
    • Neonatal: shoulder stretching during delivery
    • Sensory: loss of sensation in lateral aspect of arm
    • Motor: deltoid, infraspinatus, biceps brachii
  • Inferior Cord Injury – Klumpke Palsy C8-T1
    • Neonatal: limp pulled
    • Paralysis of lumbricals
    • Claw hand
    • Possible horner’s syndrome (ptosis, miosis, anhidrosis)
• Anterior Cord Branches
  • Musculocutaneous: paralysis of coracobrachialis, biceps, brachialis
  • Median Paralysis of most digit flexors + thenar muscles (long term: thenar wasting)
    • Causes: supracondylar fracture (high) → hand of benediction, compression of wrist (low) → carpal tunnel
  • Ulnar Paralysis of intrinsic muscles of hand (not LLOAF) → claw hand
    • Cause: medial epicondyle fracture
• Posterior Cord Branches
  • Axillary Paralysis of deltoid, loss of sensation over lateral arm
    • Causes: shoulder dislocation, humerus surgical neck fracture
  • Radial Paralysis of wrist + finger extensors, weakened elbow extension → wrist drop
    • Causes: mid-shaft humerus fracture
• Lower Limb
  • Femoral Nerve Palsy L2-L4
    • Paralysis of quadriceps
    • Sensory loss anterior thigh and medial leg
    • Causes: pelvic fractures, anterior hip dislocation
  • Tibial Nerve Palsy L4-S3
    • Paralysis of plantar flexors
    • Sensory loss of back of leg and sole of foot
    • Causes: tibia fracture, tarsal tunnel compression
  • Sciatic Nerve Injury L4-S3
    • Foot drop
    • Loss of achilles reflex
    • Wasting of hamstrings, calf muscles, dorsiflexors
    • Cause: posterior hip dislocation

Reflexes

• Biceps C5/C6
• Triceps C7/C8
• Knee L3/L4
• Achilles S1/S2

LLOAF

• All hand muscles innervated by ulnar apart from these muscles → median nerve
• Lateral two Lumbricals
• Opponens pollicis
• Abductor pollicis brevis
• Flexor pollicis brevis

Synovial Fluid

• Type I synoviocytes: mostly dormant macrophages
• Type II synoviocytes: fibroblast-like cells, produce: hyaluronic acid, lubricin
• Glucoronic acid + n-acetyl-glucosamine → hyaluronic acid
• Non-newtonian properties
• Rheopectic: with ↑ time of stress → viscosity ↑
• Thixotropic: with ↑ stress over time → viscosity ↓

Dermatomes

• C6: Thumb
• C7: Middle finger
• C8: Little finger
• T4: nipple
• T10: umbilicus
• L3: knee
• L5: Big toe
• S1: Little toe

Bone Remodelling

• Sclerostin (-) bone formation
• PTH (+) bone formation – counteracted by calcitonin
• RANKL + OPG
• ↓ serum Ca^{2+} à PTH release from parathyroid à osteoblast/osteocyte-induced formation of RANKL à osteoclast (+)

Blood Vessels

• Median cubital vein: take blood from
• Retrograde blood supply: scaphoid, neck of femur

Cervical Vertebrae

• C1: atlas
• C2: axis

Cranial Nerves

• Where they enter, what they do, sensory or motor or both, lesions in all of them

Cranial Nerve Damage Symptoms

• CNI: olfactory - Anosmia
• CNII: optic - Blindness, no pupillary light reflex
• CNIII: oculomotor - Down + out, ptosis, dilated pupil
• CN IV: trochlear - Up + in
• CN V: trigeminal - Jaw deviates to side of lesion, loss of motor function
• CN VI: abducens - Look in
• CN VII: facial - LMN lesion – ipsilateral facial weakness, bell’s palsy, dry eyes/mouth, impaired taste. UMN lesion – contralateral facial weakness, forehead sparing
• CN VIII: vestibulocochlear - Hearing + balance  Romberg test
• CN IX: glossopharyngeal - Swallowing difficulties * uvula to contralateral side
• CN X: vagus * uvula to contralateral side. UMN damage: paralysis of vocal cords, strained phonation (recurrent laryngeal) + swallowing difficulties. LMN unilateral: palate drops, vocal fold paralysis, weak pharynx – difficulty swallowing. LMN bilateral: not compatible with life
• CN XI: accessory - Trapezius and sternocleidomastoid issues: can’t shrug shoulders
• CN XII: hypoglossal - Tongue wasting and tongue goes to ipsilateral side of lesion

Skin Sensory Receptors

• Root hair plexus: Very sensitive mechanoreceptors for touch
• Free nerve ending: temperature, mechanical stimuli = pain – Αδ + C fibers
• Meissner corpuscle: discriminatory touch, sensitive for shape + texture changes, moderately rapid - Αβ
• Pacinian corpuscle: vibration and deep pressure (pain), rapid - Αβ
• Ruffini ending: skin stretch + sustained pressure/ movement, slow - Αβ
• Merkel disc: pressure, position (deep static touch features), slow – Αβ

Nerve Fibers

Tracts

• Mainly their functions and where they decussate
• Descending – function, decussation
  • Corticospinal (Pyramidal): voluntary, discrete, skilled movements
    • Anterior: axial muscles – spinal cord
    • Lateral: distal muscles – medullary pyramids
  • Rubrospinal: (+) flexor muscles, (-) extensor muscles
  • Vestibulospinal: (+) extensor muscles, (-) flexor muscles
  • Reticulospinal: regulation of voluntary movement + reflex activity – no decussation
• Ascending
  • Dorsal column (DCML): discriminative touch, proprioception, vibration, light touch, pressure – medulla
    • Gracile fasciculus: lower limb
    • Cuneate fasciculus: upper limb
  • Spinocerebellar: unconscious information from: muscles, joints, skin, subcutaneous tissue – no decussation
  • Spinothalamic: pain, temp, light touch, pressure – spinal cord at same level

Thirst and Hunger

• Circumventricular organs (CVOs): surround 3rd and 4th ventricles  serve as communication between blood, brain parenchyma, and CSF.

Thirst

• Determined by plasma osmolality → sensed by osmoreceptor cells of subfornical organ and OVLT region (wall of 3rd ventricle – adjacent to hypothalamus).
• Thirst induction
  • OVLT + subfornical organ sense hypertonic blood → (+) cells in median preoptic nucleus of hypothalamus.
  • The ↑ the activity of the median preoptic nucleus → the ↑ the thirst

ADH Release

• Subfornical organ (+) hypothalamic paraventricular and supraoptic nuclei → release ADH → posterior pituitary → blood.
• ADH effects on kidney

1. additional aquaporins on collecting duct → ↓ urine volume + ↑ urine concentration
2. ↑ permeability of collecting duct to urea → H_2O reabsorption + body retention ↑
3. Na^+ reabsorption in thick (ascending) loop of Henle by ↑ activity of Na/K/Cl cotransporter (NKCC2) → ↑ osmolality of medullary interstitial fluid → H_2O reabsorbed from collecting ducts

• Na+ balance impact H_2O balance

1. Na^+: most abundant in ECF + helps determine plasma osmolality
2. during heat stress → sweating: keep cool
3. heavy sweating → loss of H_2O + Na^+$$
4. ↓ blood volume + pressure detected by: baroreceptors in atrial walls, blood vessels, kidneys
5. Kidneys: RAAS → ↑ blood volume and pressure
6. baroreceptor + angiotensin II signals → CVOs in CNS
7. CVOs