Physiology Exam 1

energy generation

units from nutrient breakdown enter metabolic pathways to produce acetyl-CoA to fuel citric acid cycle and create ATP

urea is produced from

protein breakdown and then excreted

aerobic metabolism location

mitochondria; primary pathways in CAC and oxidative phosphorylation

main substrates of aerobic metabolism

glucose, fatty acids, amino acids

end products of aerobic metabolism

CO2, H2O, 36 ATP, long term energy supply, essential for normal function in tissues with high demand (ex. heart, brain)

anaerobic metabolism

location in cytoplasm, pathway in glycolysis, main substrate glucose

end products of anaerobic metabolism

lactic acid (lactate), short/high-intensity activities, low energy yield, lactic acidosis can occur

breakdown of molecules

catabolism (relsearing energy)

synthesis of molecules

anabolism (requies energy)

damage to lipid bilayer

• ex. during hypoxia or toxic injury → loss of cell integrity and cell death

• lipid peroxidation is implicated in diseases like atherosclerosis and neurodegenerative disorders

what is fluidity of membrane influenced by

composition of lipids (ex. cholesterol)

adhesions

link cells and mediate signals

cadherins

mediate cell-cell adhesion

• crucial for tissue integrity

integrins

facilitate cell-extracellular matrix (ECM) interactions and signal transduction

what can disruption of adhesion molecules lead to

cancer metastasis

• loss of cadherin expression allows cancer cells to detach and invade surrounding tissues

physiological signaling

membrane receptors (ex. G-protein coupled, tyrosine kinase) transduce external signals

• relevance → insulin resistance; overactivation of HER2 receptors=uncontrolled cell growth in breast cancer

impaired ion trasnport causes what

hyperkalemia (K+) in renal failure and hypokalemia leading to arrhythmias

clinical significance of transport mechanisms

defective transport in familial hypercholesterolemia causes elevated cholesterol and atherosclerosis

CO2 byproduct

from cellular respiration in mitochondria

creatinine byproduct

from muscle creatine phosphate; filtered by kidneys, excreted in urine

lactic acid byproduct

produced in muscles during anaerobic respiration; converted in liver or excreted

ketone bodies byproduct

from fat metabolism during fasting/carb restriction; excreted in urine or used for energy

ammonium (NH4+) byproduct

from amino acid deamination; liver converts to urea for excretion

bilirubin byproduct

from hemoglobin in aged RBCs; liver processes, excreted in feces

uric acid byproduct

from purine (nucleic acid) breakdown by liver; excreted in urine

carbon monoxide (CO) byproduct

low-level byproduct of heme metabo.ism; exhaled in low concentrations

water byproduct

cellular metabolism byproduct; excreted via urina, sweat, breath

diseases leading to heat accumulation

hyperthyroidism-excessive metabolic rate leads to increased heat generation

malignant hyperthermia-anesthesia-induced disorder causing uncontrolled heat production

diseases leading to accumulation of CO2

• COPD

• respiratory acidosis - lung dysfunction or respiratory muscle failure

diseases leading to accumulation of urea

• chronic kidney disease (CKD) - decreased ability of kidneys to excrete urea →uremia

• liver cirrhosis - impaired conversion of ammonia to urea → hyperammonemia

diseases leading to accumulation of creatinine

• chronic kidney disease (CKD) - inefficient clearance of creatinine by kidneys=elevated levels

• rhabdomyolysis - rapid muscle breakdown relesease creatinine into bloodstream

diseases leading to accumulation of lactic acid

• lactic acidosis - in shock, sepsis, vigorous exercise from anaerobic respiration

• mitochondrial disorders - imparired oxidative phosphorylation leads to increased lactate production

diseases leading to accumulation of ketone bodies

• diabetic ketoacidosis (DKA) - uncontrolled diabetes results in excess ketone production

• prolonged fasting or starvation - ketone bodies accumulate as byproduct of fat metabolism for energy

diseases leading to accumulation of ammonium

• hepatic encephalopathy - liver failure leads to accumulation of ammonia in blood

• urea cycle disorder - inherited enzyme deficiencies prevent conversion of ammonia to urea

diseases leading to accumulation of bilirubin

• liver cirrhosis - reduced liver function causes bilirubin buildup → jaundice

• hemolytic anemia - increase breakdown of RBCs releases excess bilirubin

diseases leading to accumulation of uric acid

• gout - crystallization of uric acid in joints due to overproduction or reduced excretion

• tumor lysis syndrome - rapid breakdown of tumor cells causes elevated uric acid levels

ICF % of body weight

40% contained within cells

ECF % of body weight

20% of body weight divided into 5% plasma and 15% interstitial fluid (buffer zone)

clinical example of fluid distribution

fluid resusciation in shock patients aims to expand ECF volume to improve perfusion and oxygen delivery

ECF ionic compostion

high in Na+, chloride Cl-, bicarbonate HCO3-

ICF ionic composition

K+, phosphate, protein

clinical relevance of ICF and ECF

hyperkalemia in acidosis arises as H+ shifts into cells in exchange for K+, elevated serum K+ levels → cardiac arrhythmias

functions of Na+/K+ ion pump

• maintains resting membrane potential

• regulates cell volume

• supports secondary active transport (Na+ gradient powers co-transport of other molecules)

ECF and ICF osmotic balance

osmotic shifts maintain equilibrium

• if plasma proteins drop, water moves into interstitial space → edema

• hypoalbuminemia → low oncotic pressure causes fluid shift into interstitial space → peripheral edema or ascites

oncotic pressure

osmotic pessure exerted by plasma proteins that attract water into blood vessels

Starling forces

oncotic pressure is key part of Starling equation, determining fluid exchange between capillaries and tissues

• arterial end = higher hydrostatic pressure pushes fluid out

• venous end = ocnotic pressure draws fluid back into bloodstream

albumin

large, impermeable protein that remains in capillaries and creates concentration gradient that drives water back into vessels to maintain blood volume and pressure

ICF homeostasis

metabolic reactions within cells

ECF homeostasis

facilitates transport of nutrients waste products, electrolytes between organs and tissues

dehydration

loss of ECF volume

• tachycardia, hypotension, dry mucous membranes

• corrected with isotonic fluids

CNS and endocrine interaction

CNS neuronal signaling and hormonal control

• hypothalamus and pituitary gland are central

hypothalamic-pituitary axis

hypothalamus releases hormones (ex. TRH, CRH, GnRH) that regulate pituitary gland

• pituitary gland secretes hormones (ex. TSH, ACTH, etc.) that impact metabolic balance, stress response, growth

autonomic nervous system (ANS)

CNS regulates homeostasis through ANS with SNS and PNS

group 1 hormonal pathways (steroids and thyroid)

enter cells and directly influence gene expression to maintain long-term homeostasis

group 2 hormonal pathways (peptide and protein hormones)

bind to surface receptors, triggering quick responses through second messengers (ex. cAMP) to adjust to immediate changes

sympathetic

• increase HR and BP

• bronchodilation

• digestion and urinary inhibition

• stimulates glucose release from liver

• dilates pupil

• redistributes blood to muscles

• NT: norepinephrine

parasympathetic nervous system

• constrict pupils

• stimulate digestion and urinary

• promote energy storage (ex. glycogen synthesis)

• bronchoconstriction

• saliva and mucus production

• MT: acetylcholine

hypothalamus activation in sympathetic

• activates adrenal medulla to release NE and epi

  • impulses activate skeletal muscles and smooth muscles

• stimulates adrenal cortext

  • pituitary gland releases ACTH

  • ACTH stimulates adrenal cortex to secrete hormones, including cortisol

adrenergic receptors (SNS)

• alpha-1: vasoconstriction, mydriasis

• alpha-2: inhibits NE release, insulin modulation

• beta-1: increases HR and cardiac contraction

• beta-2: promotes bronchodilation, vasodilation, glycogenolysis

cholinergic receptors

respond to acetylcholine

• nicotinic receptors (Nn, Nm) - stimulate muscle contraction at NMJ

• muscarinic receptors (M1 to M5)

  • M1: CNS and gastric acid secretion

  • M2: reduces cardiac rate and contraction

  • M3: smooth muscle contraction, gladular secretion, vasodilation

behavioral adaptions

conscious decisions to maintain internal balance, contrasting with automatic physiological responses

physiological homeostasis

involuntary, autonomic (ex. insulin release), involves internal body adjustments

pancreatic beta cells monitor

high blood glucose; release insulin

pancreatic alpha cells monitor

low blood glucose; release glucagon

what does glucose primarily fuel

• brain - only glucose

• muscle - rapid energy during energy

• RBCs - only glucose due to lack of mitochondria

glucose’s pathophysiological role in hyperglycemia

osmotic diuresis, neuropathy, vascular damage

glucose’s pathophysiological role in hypoglycemia

confusion, seizures, coma

insulin impacts for high blood sugar

stimulates glycogen formation in liver and stimulates glucose uptake from blood into fat & muscle cells

thermoregulation components (37 celsius, 98.6 farenheit)

• sensor - peripheral skin and central brain receptors

• control center - hypothalamus evaluates and responds to temperature signals

• effectors - execute responses via skin vessels and sweat glands

• heat - vasodilation and sweating

• cold - vasoconstriction and shivering, brown fat → heat production

normal thermoregulation clincial correlations

physical exercise (evaporative cooling, cutaneous vasodilation)

cold (shivering, thermogenesis in brown fat, peripheral vasoconstriction)

fever (increased hypothalamic setpoint, heat generation through muscle tone & shivering, post-fever sweating)

patholgical thermoregulation clinical correlations

hypothermia - shivering, reduced peripheral circulation

hyperthermia - heat dissipation mechanisms overwhelmed, sweating becomes ineffective, heat stroke risk

fever hypothalamic set point

• greater than or equal to 38 degrees celcius

• triggered by pyrogens releasing PGE2

• vasoconstriction and shivering to reach new set point

• slows pathogen growth, boosts immune response, protects cells

central neural control of breathing

pons and medulla - govern respiratory rhythm and depth of ventilation

chemoreceptors

• peripheral chemoreceptors (carotid and aortic bodies) - monitor arterial oxygen levels (PaO2), CO2, pH

• central chemoreceptors (medulla) - respond to elevated CO2 and decreased pH in cerebrospinal fluid

respiratory muscles and lungs

diaphragm and intercostals - facilitate inspiration and expiration

lungs

acidosis

occurs when too many H+ ions accumulate in blood (too acidic, low pH)

alkalosis

occurs when reduction of H+ ions or excess bicarbonate (HCO3-) (too basic, high pH)

bicarbonate buffer

HCO3- combines with H+ to form carbonic acid (H2CO3), which breaks down into CO2 and water (CO2 is removed by lungs)

kidney role in pH

remove extra H+ by excreting into urine and make new bicarbonate to neutralize acid

normal blood pH range

7.35-7.45

regulation of respiratory rate

central - respond to CO2 and pH changes

peripheral - react to low O2 levels

factors influencing RR

exercise, emotions, medications, altitude

clinical importance of perfusion

excessive pressure can damage vasculature while inadequate perfusion can lead to ischemia and tissue hypoxia

regulatory mechanisms of blood flow

vasoconstriction, vasodilation, vascular permeability

healthy BP range

between 90/60 mmHg and 120/80 mmHg

what is HR’s role in homeostasis

maintains consistent blood flow and pressure, adjusts to physiological demands (slep, exercise, stress)

feedback mechanisms of HR

baroreceptors sense BP changes and modulate HR

chemoreceptors detect blood chemistry (O2, CO2) and influence HR

BP homeostasis

body regulates BP via neural, hormonal, renal mehcnisms to ensure perfusion meets metabolic demands of different tissues (including reflex arcs and circulating hormones like adrenaline)

what are the two primary factors of BP regulation

cardiac output - volume of blood the heart pumps per minute

systemic vascular resistance - resistance to blood flow within all blood vessels

long-term adjustments of BP

• fluid balance - kidneys regulate blood volume and urine content

• RAAS - activates with reduced kidney blood flow to increase blood volume and resistance

• endothelial function - controls vessel constriction/dilation, influencing vascular resistance

response mechanisms for BP

• baroreceptors - aorta and carotid arteries; sense reduced vessel stretch from low BP and signal brain to increase HR and induce vasoconstriction to restore pressure

• volume receptors - heart and veins, receptors detect reduced venous return and activate compensatory mechanisms (ex. thirst stimulation) to increase fluid intake and blood volume

• kidneys - detect decreased perfusion and release renin to activate RAAS (promotes water and sodium retention) and increase BP and blood volume

• chemoreceptors - carotid and aortic bodies; detect low O2 or high CO2 levels from decreased perfusion; trigger increased respiratory rate and cardiac output to enhance O2 delivery and circulation

non-pathological HR and BP for homeostasis

exercise , sleep, stress

pathological HR and BP for homeostasis

dehydration, bleeding, infection

pathological breathing for homeostasis

asthma (RR increase but airway constriction, O2 decrease, CO2 increase), pneumonia (RR increases to enhance gas exchange, O2 may drop bc alveolar filling), opiod overdose (RR decreases, O2 decrease, CO2 increase)