Effective Flashcard Usage for Studying

Flashcards & Their Uses

• Flashcards are a study tool that helps with active recall and understanding
• They contain a question on one side and the answer on the reverse.
• Useful for reviewing definitions, key facts and processes, especially in courses like MEDI211
• Aids in strengthening long-term memory through active recall and spaced repetition

Effective Flashcard Usage

• Actively test yourself by attempting to answer before checking the reverse of each card.
• Sort cards by confidence level ("Know it," "Kinda know it," "Don't know it yet")
• Review "Know it" cards less often, "Kinda know it" regularly, and "Don't know it yet" frequently
• Short, frequent study sessions (15–20 minutes) are more effective than long cramming sessions
• Try to explain concepts in your own words to help you understand and apply the knowledge
• Shuffle cards to avoid memorizing the order
• Pair flashcards with spaced repetition tools like Anki or Quizlet

Homeostasis

• Homeostasis regulates cells' physical, chemical, and thermal status to maintain stable internal conditions for life.
• Essential components of a physiological regulatory system are the input signal, receptor, integrator, effector and outcome

Physiological Control vs Regulation

• Control modifies functions (heart rate), while regulation maintains variables (blood pressure) within a homeostatic range
• Blood pressure and oxygen are regulated variables maintained within narrow thresholds, supported by controlled organs like the lungs and heart
• Regulated variables have narrower thresholds (blood pressure), controlled variables fluctuate more widely (heart rate).
• Heat exposure can cause a need for both control and regulation: vasodilation (control) reduces regulated blood pressure, the body then increases heart rate (control) to normalize blood pressure.

Afferent vs Efferent Pathways

• Afferent pathways carry input signals from receptors to the integrator
• Efferent pathways carry output signals from the integrator to effector organs

Water Heater Analogy

• The central integrator in a water heater receives input from the thermometer and signals the gas flow to the heater.
• Feedback from the thermometer reduces heating once the target temperature is reached.

Feedback

• Feedback (usually negative) adjust output signals to maintain homeostasis by reversing or dampening changes.
• Negative feedback counteracts the original stimulus e.g. high blood glucose triggers insulin release, lowering glucose levels.
• Positive feedback amplifies the original stimulus e.g. oxytocin release during childbirth intensifies contractions.

Feedforward Control

• Feedforward control involves anticipatory signals from the brain to prime physiological systems before a change occurs
• It increases heart rate, ventilation, reduces skin blood flow, and initiates sweating before physical activity.

Control Definitions

• On-off control system is either fully on or off, and leads to fluctuating responses around a set point.
• Proportional control has responses that are proportional to the magnitude of the stimulus near its target range.
• On-off control causes fluctuations; proportional control maintains stability closer to the desired level.
• Redundancy is when multiple systems maintains critical parameters, in case one fails
• Equilibrium is a stable, well-regulated parameter maintained without energy expenditure
• Acclimatization is a body's adjustment to a new environment by setting a new equilibrium, e.g. increased breathing at high altitude.

Energy Metabolism

• It includes all chemical reactions by which the body obtains and spends energy from nutrients.
• Anabolic processes build substances (glycogen synthesis), while catabolic processes break them down (glucose breakdown).
• Oxidation involves losing electrons; reduction involves gaining electrons.
• Oxidation/reduction occur together; if one molecule is oxidized, another is reduced.
• In cellular respiration, glucose is oxidized to CO2, and oxygen is reduced to H2O
• Oxidation must be tightly controlled to prevent excessive heat production and tissue damage.
• Metabolic coupling is when one metabolic reaction depends on another
• An anabolic reaction requires ATP from a catabolic reaction.
• The First Law of Thermodynamics states that energy cannot be created or destroyed, only transformed. In a closed system, total energy is constant

Energy balance

• Positive energy balance is when energy intake is greater than expenditure, leading to weight gain.
• Negative energy balance is when energy intake is less than expenditure, leading to weight loss.

Macronutrients

• Carbohydrates provide 4 kcal/g.
• Fats provide 9 kcal/g.
• Protein provides 4 kcal/g.
• Alcohol provides 7 kcal/g.
• Glycogen (700g) can fuel metabolism for ~1.3 days
• 14kg of fat can fuel ~52 days of Resting Metabolic Rate (RMR).

Direct vs Indirect colorimetry

• Bomb calorimetry measures the energy content of food by burning it and measuring heat released
• Indirect estimates energy expenditure by measuring O2 consumption and CO2 production, reflecting cellular respiration.
• Respiratory Quotient (RQ) is the ratio of CO2 produced to O2 consumed, which indicates the type of fuel being metabolized.
• RQ is 1.0 for carbohydrates, 0.7 for fats, and 0.8 for proteins.
• The Second Law of Thermodynamics states that all chemical transformations lose some energy as heat, therefor no metabolic reaction is 100% efficient.
• Gibbs Free Energy (G) is available to do biological work/drive metabolic processes from total energy(E = G + TS)

Glucose Oxidation

• Bomb calorimeter releases 686 kcal as heat during glucose oxidation by contrast, the body stores 400 kcal as ATP and loses ~40% as heat.
• Resting Metabolic Rate (RMR) amount of energy (kcal/day) needed to sustain metabolism at rest.
• Approximately 2100 kcal/day for a 70kg human.
• Basal Metabolic Rate (BMR) is a clinical measure of metabolism under standard conditions
• Measured in the morning after fasting for 12 hours, resting for 1 hour, in a 25°C environment.
• Energy storage is vital due to sporadic intake and continous expenditure for bodies to work

Energy Storage

• Carbohydrates like glycogen are stored in the liver and muscles.
• Lipids, triglycerides, are stored in adipose tissue, liver, and muscles.
• Proteins structural/functional, not primary energy store.
• ATP stores energy from catabolism (ADP → ATP) and releases energy to fuel anabolic reactions (ATP → ADP).

Carbohydrate Groups

• Major dietary carbohydrate groups are monosaccharides and di/oligo/polysaccharides.
• Monosaccharides are absorbed directly, while di/oligo/polysaccharides must be broken down first
• Some polysaccharides are indigestible, like fiber.

Carbohydrate digestion

• Begins with salivary amylase in the mouth, continues with pancreatic amylase in the small intestine, and is completed by brush border enzymes (oligosaccharidases) which breakdown to monosaccharides.
• Monosaccharides are absorbed in the intestine via SGLT1 (Na+-glucose cotransporter), GLUT5 (fructose), and GLUT2 (basolateral exit)
• Glucose then enters blood for distribution via insulin
• Components of a triglyceride are 3 fatty acid chains and 1 glycerol backbone.
• Saturated fatty acids have no double bonds (all C-H) and unsaturated fatty acids have at least one C=C double bond.

Lipids

• Dietary lipids are emulsified by bile salts in the duodenum, forming micelles that contain monoglycerides and free fatty acids (FFAs)
• Micelles containing fatty acids/monoglycerides approach the acidic brush border which allows the fatty acids to diffuse via fatty acid transport proteins (FATPs) into enterocytes
• Inside enterocytes, FFAs and monoglycerides are re-esterified into triglycerides
• This is facilitated by chylomicrons with cholesterol and apoproteins, and exocytosed into lacteals
• Chylomicrons enter lymph and reach circulation via the thoracic duct
• Lipids are transported by lipoproteins eg. chylomicrons, VLDL, LDL, and HDL

Thoracic Duct

• Major lymphatic duct draining lipid-rich lymph from much of the body into venous circulation at the subclavian vein.
• Lipoprotein lipase (LPL) is an enzyme on capillary walls that hydrolyzes triglycerides in lipoproteins
• Insulin stimulates LPL activity.
• Glycerol in the liver can enter gluconeogenesis (→ glucose) or glycolysis (→ pyruvate).
• Lipid storage stops during fasting due to insulin level drops which limits LPL activity and halting lipogenesis.
• Protein has structural (skin, collagen, ligaments) and functional (enzymes, receptor, contractile proteins) roles
• Peptides enter via H⁺-cotransporters which get broken down by peptidases into amino acids
• Amino acids are transported into blood via AA transporters.
• Insulin release from pancreatic ẞ-cells is triggered by increased blood glucose and some amino acids

Insulin Actions

• Insulin receptor is a tyrosine kinase receptor composed of 2 extracellular a-chains and 2 intracellular B-chains with intracellular kinase domains.
• Insulin promotes glycolysis, glycogenesis, lipogenesis, protein synthesis it also, inhibits gluconeogenesis, glycogenolysis, lipolysis, and ketogenesis
• Insulin activates glucokinase and glycogen synthase whilst simultaneously inhibiting phosphorylase and glucose-6-phosphatase
• Insulin stimulates glycolysis and TCA cycle in carbohydrate metabolism, while inhibiting gluconeogenesis.
• Insulin converts excess pyruvate to acetyl-CoA → lipogenesis and inhibits ketogenesis by preventing free fatty acid oxidation preventing FFA entry into mitochondria.
• Insulin binds to IR increasing GLUT4 into membrane leading to glucose uptake. It also promotes protein as well as glycogen synthesis
• It promotes glucose uptake, lipogenesis, inhibits HSL and, activates LPL for triglyceride storage

Intracellular actions

• Hormone-sensitive lipase breaks down stored triglycerides into FFAs, insulin inhibits HSL activity.
• Insulin binds IR → TK activation → IRS phosphorylated → Activates PI & MAPK pathways →GLUT4 insertion, growth, glycogenesis, and lipogenesis.
• IRS helps activate PI pathway (GLUT4 insertion, protein synthesis) and MAPK pathway (DNA transcription, growth/repair)
• Overall it increases fat, glucose, protein synthesis whilst simultaneously decreasing gluconeogenesis, lipolysis, and proteolysis
• A kinase adds phosphate groups (usually from ATP) to substrates
• Activating or deactivating other proteins
• A phosphorylase breaks down molecules (e.g. glycogen) by adding inorganic phosphate without ATP.
• Phosphatase removes phosphate groups from a molecule, reversing kinase activity.

Glycogenolysis in Skeletal Muscle

• Epinephrine binds to B-adrenergic GPCRs activating the cAMP/PK pathway
• This then switches on glycogen phosphorylase turning glycogen into G-1-P
• Insulin inserts GLUT4, increasing glucose uptake, promoting glycogenesis and glycolysis
• It also increase lipogenesis, protein synthesis whilst inhibiting glycogenolysis, lipolysis, and proteolysis
• Glucagon and epinephrine bind to their receptors ( activate cAMP/PK pathway
• This activates glycogen phosphorylase which causes glycogen → G-1-P → G-6-P.
• G-6-P is converted to glucose by glucose-6-phosphatase in the liver then, it gets released into circulation

Overnight Fast State

• ~50% of hepatic glucose output comes from glycogenolysis
• ~50% from gluconeogenesis which is comprised of AAs, pyruvate, lactate, and glycerol.
• Epinephrine binds B-adrenergic GPCRs triggers cAMP/PK which then, activates hormone-sensitive lipase (HSL) converting triglycerides into FA + glycerol which stimulates lipolysis in adipocytes
• FFAs diffuse out of adipocytes and transports albumin to target tissues via blood stream
• HSL is inhibited by insulin, it is also by sympathetic stimulation, and growth hormone
• Glucagon secretion, is stimulated by fasting, low blood glucose, and amino acids. which activates pancreatic a-cells which releases glucagon.

Liver Metabolism

• Promotes glycogenolysis, gluconeogenesis, ketogenesis, lipolysis, and proteolysis.
• Glucagon inhibits liver glucose by inhibiting, glucokinase, glycogen synthase, and glycolysis enzymes.
• This shifts metabolism toward glucose production and fat oxidation.
• Glucagon shifts liver metabolism to produce and export glucose while preserving glucose for glucose-dependent tissues.
• The glucagon stimulates for fatty acid entry into mitochondria via carnitine carrier resulting in in acetyl-CoA that will turn into TCA or ketones if TCA is saturated.

Fasting State

• Insulin is limited and glucagon is increased resulting for fatty acid oxidation that exceeds TCA capacity and turns to ketone production for CNS fuel.
• OAA is diverted to gluconeogenesis resulting to acetyl-CoA that cannot enter TCA which leads to metabolic acidosis
• Glucose is low resulting in glucagon & epinephrine increase leading for hepatic glucose output.
• Insulin prevent hyperglycemia whilst glucagon prevents hypoglycemia.
• During Anaerobic conditions glucose becomes pyruvate with a total production of 2 ATP molecules. In Aerobic pathway pyruvate turns in acetyl-CoA result for TCA creation with great production of ATP.
• FFAs enters mitochondria go through B-oxidation to produce acetyl-CoA which turns to ketone synthesis.

Fatty Acids

• Disassembly in mitochondria converts them into 2-carbon units that turns to acetyl-CoA which enters TCA cycle for energy production. The B-Carbon serves at the the site of oxidation
• Amino acids are deaminated and converted Ammonia → urea (excreted)
• What do all macronutrients share as TCA cycle (accepts acetyl-CoA from carbs, lipids, proteins) produce NADH/FADH2 for electrons
• How is ATP produced mitochondria NADH/FADH2 donate electrons to ETC generates proton gradient synthesis thru oxidative phosphorylation.
• Substrate enzyme/inhibition
• Accumulation feedback
• Regulation
• Metabolism halts energy glycolysis lactate.

Energy vs ATP Regulation

• ADP availability to ATP turns catabolism.
• Fat helps create acetyl-CoA as glycogen via Oxidation
• Acetyl-CoA limits oxidation.
• The Glucokinase process glucose.
• Glucose 6 process
• Elevated increases secretion.
• Acids increase secretions.
• Glp signals
• Glucagon signals
• Cephalic and increases tone/hormone.
• Primaral beta and homeostasis via the glucose axis.

Hyper VS Hypo

• 2.5 and hypoglyemia, 10 kidneys glucose
• Intitator/recepter/mediator/outcome feedback
• Receptor regulation
• Muscles
• Hormone secretion.

Endocrine system

• It Communicates between cells for homeostasis, metabolism and balance.
• Are the three broad groups there is the Amines
• Acids.soluble or stored
• There secretes near cells calcium.

Peptide Blood

• In blood they are soluble
• Locations ontransmenrance receptors
• The give examples glucagon
• The synthesis cleave to processing, exocytosis.
• The inactive receptor sequencr r.e.r
• It signal removes or processing

Membrane Transduction

• They are membrane membrane.
• The cell bind effects nuclear
• Main receptors
• Receptor is an ion receptor receptor
• A recrptprs activate

GPCR signaling

• Hormone binds to activates via cycle
• It converts messenger.
• camp activation
• Activates.
• The type activation inhibits cAMP.
• Regulator subinits increases active.
• That is enzyme receptor

Second messengers

• binding insulin activated transfers regulation.
• It amplifies.

Steroid Hormones

• These are lipid based
• Synthesized adrenal and testes
• Cholestrol that has been synthesized
• Steroids diffuse.
• Bound albumin

Peptide Hormone Receptors

• Located nucleus which are intracellular.
• Bind r.a.a dna.
• Hormone that causes rna and replication and transfer.
• Hormones derived from Amino acids.
• That uses dopamine/serotnin
• water is membrane, lipids/receptors.
• membrane/messengers
• Stored colloids
• Binds activstes induction.
• blocks activates is a weaker
• without ligand and constitutive
• increase/high the opposite

Hormones

• subtyoes/dopmine different.
• By excretion/hormone.
• Half-life proteins half.lives.more
• higher rate
• R.I.A, HPLC.
• Antibodies/ measurable.
• receptor affinity/protein /adaptaton.
• Insulin restence etc

Hypothalamus, Pituitary & Related Hormones

• Hypothalamus main role is the integrator
• Pituaitry the gland is glandular pituitary is neural.
• Receprors the hypothalamas portal
• They relate though neurons

Anterior Pituitary Hormones

• Gnrh, crh, gihh, trh,lack prolactin
• vasopressin increases the insertion in kidneys.
• glands to produce.
• short the long th inhibits the

Female Hormones

• Gnrh leads to that follicle
• l.h is ovarian surge
• It leasd to menses cycles
• Pregnany/ estrogen affect brain signalling
• Sertoils

HGA

• Gnrh, the testosterone .
• Sert oli cells to production.
• Hormone stimulates cortex. Aldosterone for increasing pressure.

Muscle Metabolics

• Has atoblic and plasma to
• CRH the receptors is ghrh

Hormones affect cells

• It makes somatostin the production
• It released from liver
• Growth tissues for long term for cartilage
• Tr hormones thyroid by anterior
• Increases in cells
• Hormone increase hormones

Synthesis & Receptors

• Follicle for
• The release
• Hormone sequence
• Cells and membrane
• It to forline it and iodine

Released and Stimulate

• Are ty 4 the more has affinity
• Cell tissues regulators
• T1 receptors and affect
• It glycogenolysis the liver
• The proteins is.protolysis
• Lipolysis
• Increase simultanosely hormone
• T3 production
• Has hormone and milestones
• Hormones creintms

Thyroid & Growth Issues

• The hormone increase
• The increase state
• The is skeletal.
• thyroid for the
• Hashimoto hormone