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67 Cards in this Set

  • Front
  • Back

Negative Feedback (Testosterone)

1. Stress inhibits GnRH neurons in the hypothalamus from producing GnRH


2. LH receptors on the anterior pituitary don't receive GnRH so LH decreases


3. LH receptors in the testes don't receive LH so testosterone decreases


4. Stressor goes away so GnRH neurons create GnRH and are not inhibited by testosterone


5. anterior pituitary responds to GnRH and produces high levels of LH


6. testes receive high levels of LH and produce high levels of testosterone


7. androgen receptors on the hypothalamus and anterior pituitary receive high levels of testosterone and decrease levels of GnRH and LH


8. Testes receive low levels of LH and reduce testosterone levels



Opposing systems (glucose)

Homeostasis: 90 mg/100 mL


1. Eat a meal so glucose levels rise


2. Beta cells release insulin


3. Liver and muscle cells take up glucose and store as glycogen


4. glucose levels return to homeostasis


5. fast, glucose levels decrease


6. alpha cells in the pancreas releases glycogen


7. liver breaks down glycogen into glucose and releases it to the blood system


8. glucose levels rise to homeostasis

Positive feedback (labor)

Positive Feedback Loop #1


1. Fetus stimulates placenta to make prostaglandins


2. prostaglandins stimulate uterus to contract


3. contractions stimulate uterus to make more prostaglandins


Positive Feedback Loop #2


1. fetus pushes on pressure receptors on the cervix and causes dilation and the release of oxytocin from neurosecretory cells


2. oxytocin stimulates uterus to contract


3. contractions cause baby's head to push on the cervix more


**Estrogen produced by the placenta creates prostaglandins and oxytocin receptors on uterus



oral cavity

salivary amylase breaks carbs like glycogen down into polysaccharides and disaccharides

stomach

-G cells produce gastrin producing hormones


-ECL cells, parental cells, and chief cells produce acetylcholine


-gastrin stimulates histamine release from ECL cells into ECF


-Gastrin/histamine/ACh stimulate chief cells and parental cells which secrete HCl (gastric juice)


-HCl breaks down proteins to expose greater surface area for pepsin (enzyme) to break down polypeptides


-chief cells secrete pepsinogen which turns into pepsin by acidic conditions, and pepsin turns pepsinogen into move pepsin (+)


-Goblet cells relate mucus to protect stomach


-smooth muscles mix food through churning every 20 seconds

Small Intestine (duodenum)

-pyloric sphincter squirts acid chyme into duodenum, and acid chyme stimulates S cells to secrete secretin into blood system


-Secretin tells pancreas to secrete alkaline sodium bicarbonate to raise pH for enzymes


-Secretin tells I cells to release CCK into blood stream which stimulates gall bladder and pancreas (secretin + CCK inhibit gastrin and gastric juice)


-Amino acids and fatty acids also secrete CCK


-CCK tells gall bladder to release bile to emulsify fats for simpler absorption, pancreas to release inactive peptide digesting enzymes/amylase/lipase


-molecules absorbed across epithelium of duodenum, jejunum, ileum

Acid hydrolysis

unfolds and exposes proteins to enzyme attack (only in the stomach)

Enzyme Hydrolysis

cleaves food molecules at specific sites

Fatty acid digestion

bile released by the gall bladder emulsifies fats so that enzyme hydrolysis can occur by lipase. Fats turn into glycerol and fatty acids so that they can be absorbed

protein digestion

Pancreas releases inactive peptide digesting enzymes through the bile duct and activate in the duodenum. Dipeptidases help the peptide digesting enzymes break up proteins into amino acids so they are more easily absorbed

Carbohydrate digestion

Pancreas secretes amylase to break sugars and polysaccharides into simpler sugar molecules. Then disacchridases complete digestion right before absorption

Fatty Acid absorption

They are synthesized into chylomicron particles which are exocytosed from enterocytes basolateral membrane, transported through fatty acid transporters, and taken to blood circulation at the point where veins drain into the heart by lacteals (lymph vessels) in the lymphatic system.

Everything but fatty acid absorption

-Leave small intestine through the epithelial cells and enter into he capillaries. The capillaries cary it to the hepatic portal vein which takes it to the liver BEFORE it goes into blood circulation.


-ATP drives Na+ out of the cell and K+ into the cell so the inside of the cell is more negative. Then diffusion drives Na+ back into the cell with glucose and amino acid molecules "piggy backing" into the cell and leave through GLUT 2 or amino acid cotransporter with help from water.

Water absorption

Most of the water (80%) is absorbed by helping other molecules get absorbed. Water absorption is enabled by aquaporin 3


90% water absorption in the large intestine

Path of Deoxygenated blood through the heart

1. Deoxigniated blood comes to the heart through the vena cava and lymphatic fluid comes from another vein


2. Blood enters the right atrium and goes through the right AV valve which is open at rest into the right ventricle, the right atrium contracts to get all of the blood through


3. The right ventricle (22 mmHg, 75 mL) contracts to shut AV valve and pumps blood through the right semi-lunar valve through the pulmonary artery to the lungs

Path of oxiginated blood through the heart

1. oxygenated blood comes from the lungs through the pulmonary vein to the left atrium


2. Blood goes through the left AV valve to the left ventricle (120 mmHg, 75 mL) when left atrium contracts


3. Left ventricle contracts to shut AV valve and pumps blood through the left semi-lunar valve and though the aorta to the rest of the body

Systematic Circulation

Heart pumping blood to and from the body

Pulmonary Circulation

Heart pumping blood to and from the lungs

Path of blood in circulation

arteries, small arteries, capillaries, capillary beds, small veins, veins

Diastolic Blood pressure

pressure in the arteries when left ventricle relaxes

Systolic blood pressure

pressure in the arteries when left ventricle contracts

Heart Rhythm

-atria and ventricles synced up


-SA node generates Ca++ in atria so they contract


-myocardial cells drive Na+ out of cell and K+ into cell creating negative charge to -70 mV


-Then Na+ channels open and they flood cell back to -50 mV (depolarization)


-That causes Ca++ channels to open and myocardial cells contract


-Ca++ channels only open for so long, and the signal takes .1 seconds to get to the AV node from the SA node

Sympathetic Nervous System

-Releases more norepinephrine onto SA node which accelerates heart rate because of faster opening of Na+ and Ca++ channels


-NE binds to beta adrenergic receptors on Na+ channels increasing Na+ channels as SA node hyper polarizes


-More Na+ channels means less time before Ca++ channels open

Parasympathetic Nervous System

-release acetylcholine onto SA node which decelerates heart rate b because opens K+ channels so K+ escapes SA node cells causing hyper polarization


-Less K+ channels means more time for Ca++ channels to open


-Heart rate, heart force, and systolic blood pressure are reduced

Blood Pressure increase and decrease

Increased: stimulates PNS to slow heart rate


Decreased: stimulates SNS to increase heart rate


Opposing systems

Fluid Exchange

-Arterial Blood goes through capillaries at 32 mmHg, but outside is 22 mmHg so lose 10 mmHg


-Resistance from the capillaries causes it to drop 7 mmHg to 15 mmHg


-eventually veins bring blood back at 22mmHg


-3 mmHg are lost and sent to lymphatic system for immune system


-arterial end: diffusing out of capillary


-venous end: diffusing into capillary

Osmolarity

High: higher concentration (more dissolved solutes)


Low: lower concentration (less dissolved solutes)


Osmosis flows from higher osmolarity to lower osmolarity

Blood Pressure in kidneys

Forces blood through Bowman's capsule into excretory nephron (filtration)


-high blood pressure can damage filtration and reabsoption

Path of blood

Renal artery, kidney, renal vein

Glomerulus

Filtration: urea/fluid and nutrients go out of the blood

Proximal tube

Secretion: drugs, toxins, specifically transported from blood to filtrate


Reabsorption: water, salt, nutrients

Loop of Henle

Reabsorption: water in descending, salt in ascending


Distal Tube

Reabsorption: salt

Collecting Duct

Reabsorption: water, salt, urea

Bowman's capsule

Filtration: permeable to water, urea, salt, small nutrients (but not large nutrients)

Reabsorption in kidney

-(See digestion)


-As the Loop of Henle gets deeper, it becomes hyperiosmotic so it loses more water


-The capillary countercurrent allows the most efficient reabsorption of water and salt

Nonspecific immune system: skin

openings have mucus with lysozyme which attack bacterial walls but viruses can get past mucus

Internal defenses

-Phagocytosis


-damaged or infected cells give off pro-inflammatory signals called cytokines and chemokines that attract neutrophils


-mast cells mature at infected site, bind to pathogen, and release histamine


-pluripotent stem cells release monocytes which mature into macrophages to phagocytose pathogens and repair tissues or dendritic cells to phagocytose pathogens and take them to lymph vessel


-Inflammatory response: platelettes create clotting which reduces blood flow


-Redness/heat: histamine released by mast cells trigger pre-capillary arteries to dilate which increases local blood and fluid flow


Capillaries become more permeable allowing more things in


-Neutrophiles come then macrophages and dendritic cells


-macrophages release cytokines to tell bone marrow to make more neutrophils and monocytes


-extracellular fluid goes through lymphatic system where, in lymph nodes, pathogens encounter the specific immune system

Production of lymphocytes

pluripotent stem cells produce them in bone marrow


-if they mature in bone marrow, b cells


-if they move to thymus to mature, t cells


-B cells and T cells are found in spleen, lymph nodes and other lymphatic organs

B Cell Activation

-activation: rapid mitotic division


-B cells' antigen receptors capture pathogen so that lysozyme can digest it


-digested fragments bind to MHC class II molecules and the cell goes to other cells


-t cell will bind once b cell is at cell membrane, bound t cell to b cell is an immune synapse


-t cell secretes cytokines


-b cells activate and create plasma cells that secrete antibodies and memory cells

Humoral Immune system engaged

-activation produces antibodies similar to b cells


-IgM: on the surface of B cells and help binding to antigen to multiply b cell response


-IgG: smaller so can go everywhere


-Binding of antibodies inactivates antigen because IgG blocks binding site by coating cell surface and IgM agglutinates the antigen


-antibodies also help macrophages phagocytose

MHC class I

-on surface of all cells


-binds to cytotoxic t cells with help from CD8+


-virus


-presents smaller molecules made inside the cell

MHC class II

-on surface of dendritic cells, macrophages, b cells and neutrophils


-bind to helper t cell with help from CD4+


-bacteria


-presents larger molecules made outside the cell

Other activation

-Helper and cytotoxic t cells get activated too in order to create memory t cells for secondary immune response


-binding of t cell activates it so it produces cytokines

AIDS

-HIV binds to CD4+ sites by forming an immune synapse in order to infiltrate host genome by reverse transcribing DNA


-antibodies can't get rid of it because it is part of the t cell, by cytokines can destroy it, but only for a few weeks


-HIV mutates until immune system can't detect it, destroys helper and cytotoxic t cells which destroys lymphatic system and lymph nodes

ACTH

-receptors protrude through adrenal cortex cell membrane


-ACTH binds to receptor and reconfigures the molecule which triggers second messenger cascade (Amplification) to activate cortisol or stimulate transcription-based synthesis of a new product

Cortisol

-steroid


-cortisol binds to glucocorticoid receptor found in cell cytoplasm or nucleus and initiates transcription


-cortisol binds to glucocorticoid receptor found on cell membrane and changes the configuration which triggers a second messenger cascade (application) which can release synthesized product of initiate synthesis of new product

Hypothalamus

interface between stimulus and response


-stimulus: environmental or physiological response


-response: feedback systems or maintenance of homeostasis

Posterior Pituitary

-attached to hypothalamus by neurosecretory cells that make ADH and oxytocin


-Releases hormones synthesized in the hypothalamus


-releases oxytocin that goes to the uterus during labor for a positive feedback loop

Anterior Pituitary

-not part of brain


-hormones released at base of hypothalamus regulate anterior pituitary hormones that are synthesized and released into circulatory system


-neurosecretory cells synthesize neural peptides that are carried to anterior pituitary by portal vessels

Stress Response: ACTH

-Adrenal glands secrete cortisol under stress to break down glucose from the liver


-Hypothalamus releases CRH to stimulate anterior pituitary to secrete ACTH from corticotrope cells


-ACTH stimulates adrenal gland to secrete cortisol


-cortisol tells anterior pituitary to stop releasing ACTH and hypothalamus to stop secreting CRH

Stress Response: Neural Regulation of adrenal medulla

SNS neurally stimulates adrenal medulla to secrete epinephrine


-epinephrine causes stimulation of metabolic rate, glycogen breakdown to glucose liver, release of fatty acids, increase in heart rate, and diversion o blood from gut/skin/kidneys to muscles/brain

Diabetes

-Chronic stress results in prolonged elevations of blood glucose levels therefore elevated insulin levels


-Harder and harder to initiate insulin secretion until insulin can't be secreted anymore


-Obesity also causes diabetes because high concentrations of fatty acids in blood results in high levels of insulin which reduces insulin activity


-Diabetes causes damage to nerve cells, blood vessels (causing heart disease), and increased urination

Type I diabetes

DNA malfunction so pancreas doesn't secrete insulin

Type II diabetes

insulin sensitivity decreases so even though there is a high level of insulin and glucose, body doesn't respond properly

Male Reproduction Function and Anatomy

-Testes in scrotum and contain seminiferous tubules that make sperm


-Between seminiferous tubules are Leydig Cells that produce testosterone


-Sperm mature (being able to fertilize egg) by going through epididymus for 20 days


-Then sperm propelled out through vas deferens into ejaculation duct


-Urethra contracts and semen expelled through tip of penis


-Sperm + seminal fluid is semen. seminal fluid is an energy substrate for sperm to transport through female in a viable state

Male Reproduction hormonal regulation

-hypothalamus releases from GnRH to stimulate anterior pituitary to release FSH and LH from gonadotropes


-LH stimulates synthesis and secretion of testosterone from Leydig cells in the testes


-testosterone inhibits release of GnRH from hypothalamus



Female Reproduction Function and anatomy

-oocytes surrounded by follicles that secrete estrogen and then more follicles


-One follicle matures 14 days after menstruation each month


-fimbria's cilia waft oocyte that was gathered by fimbria out into the oviduct


-oocyte moves down uterus


-fertilized egg plants in uterine wall, unfertilized egg travels down into vagina through cervix and 14 days later the endometrium lining is shed

Oogenesis

Development of oocyte


-oogonia are developed before birth and then mature until puberty into oocytes


-Once a month FSH stimulates an oocyte to grow and secretes estradiol


-Rising estrogen increases GnRH which increases LH (+)


-14 days later LH induces ovulation and remaining follicle cells turn into corpus luteum which produces progesterone

Female Reproduction Hormonal Regulation

-GnRH release from hypothalamus releases LH and FSH from anterior pituitary


-FSH stimulates follicles to grow and secrete estradiol


-One follicle develops FSH and LH receptors so it becomes dominant follicle and keeps growing, when FSH decreases because of estradiol, other follicles undergo apoptosis


-estradiol rises which stimulates LH and GnRH to rise (+) so that oocyte is released from follicle


-High levels of LH turn follicles into corpus luteum which undergoes apoptosis in 14 days


-progesterone decreases and causes arterial spasms so endometrium sheds due to lack of blood


-in pregnancy HCG saves corpus luteum

Afferent Neuron

Sensory Neuron: tells CNS about stimulus

Efferent Neuron

Motor Neuron: send messages from CNS to muscles to respond to stimulus

Interneurons

create faster response to stimulus because just relays to the spinal cord or brain, reflex

Action Potential

1. Resting state (-70 mV): no ion flow because Na+ and K+ channels closed

2. Threshold (-50 mV): neuron receives stimulus so some Na+ channel opens and depolarizes.


3. Depolarization (+40 mV): If depolarizes to -50 mV, all Na+ gates open no matter the stimulus


4. Repolarizing Phase: at +40 mV, Na+ channels close and K+ ions open causing the charge to drop again, and at -50 mV, K+ channels close too


5. Undershoot (-75 mV): K+ channels stay open too long to compensate, so the charge gets too low, K+ leak channels bring it back -70 mV


-Na+ channels won't open until at -70 mV when the Na+ inactivation gate is open

Self Propagation

If action travels along neuron due to triggering, then it is a signal

-domino effect because can only go one way due to the refractory period

Saltatory Conduction

Mylenation increases action potential by 150 times because the action travels over mylenation from + node of Ranvier to next - node of ranvier.

Neurotransmission at the synapse

Pre synaptic neuron depolarizes from an action potential causing Ca++ channels to open releasing a lot of Ca++ and causing synaptic vesicles within synaptic terminal to fuse with the cell membrane of the terminal


-synaptic vesicles contain neurotransmitter molecules that are released into synaptic cleft and bind to receptors on Na+ gated channels of post synaptic neuron


-Post synaptic neuron depolarizes if Na+ ions cause it to cross threshold


-Then neurotransmitter degrades and closes na+ channels which stops signal