Hunger & Thirst Flashcards
Isreal Kamakawiwo’ole nickname
izzy
What was Izzy’s highest weight
757
What age did Izzy die
38
When and where did Izzy die
Medical center Honolulu in 1997
What was izzy famous for singing
somewhere over the rainbow
_____ _____ use our behavior to keep things balanced
homeostatic systems
Main homeostatic mechanism
negative feedback systems
In homeostatic systems, if a desired _____ ____ is deviated from, compensatory action begins
set point
In homeostatic systems, if a desired set point is deviated from, ______ ______ begins
compensatory action
Where is
“ill eat when i’m hungry
ill drink when in dry
if the moonshine dont kill me
ill live till i die”
from?
Im a Rambler
______ ______ is stimulated by low extracellular/intravascular volume
hypovolemic thirst
hypovolemic thirst is stimulated by low _____/_____ volume
extracellular
intravascular
_____ _____ is stimulated by high extracellular solute concentration
osmotic thirst
osmotic thirst is stimulated by _____ _____ _____ concentration
high extracellular solute
What is hypovolemic thirst?
A: Thirst caused by a loss of water volume from the body.
Q: Does hypovolemic thirst involve a change in fluid concentration?
A: No, fluid concentration stays the same; only volume is reduced.
Q: What can cause hypovolemic thirst?
A: Bleeding, vomiting, diarrhea, or excessive sweating.
Q: What detects the initial drop in blood volume during hypovolemic thirst?
A: Baroreceptors in blood vessels and the heart.
Q: What are baroreceptors?
A: Pressure sensors that detect changes in blood vessel stretch due to volume.
Q: How does the brain respond to baroreceptor signals during volume loss?
A: It activates thirst and a craving for salt.
Q: Why does the brain trigger salt craving in hypovolemic thirst?
A: To help retain water and restore electrolyte balance.
Q: What cardiovascular response helps maintain blood pressure during hypovolemia?
A: Arteries constrict to increase blood pressure.
Q: What hormone is released during hypovolemia?
A: Vasopressin (also called antidiuretic hormone, ADH).
What is Vasopressin also called?
antidiuretic hormone
What does ADH stand for?
antidiuretic hormone
Q: What does vasopressin do to blood vessels?
A: It constricts them to help raise blood pressure.
Q: How does vasopressin affect the bladder?
A: It reduces blood flow to the bladder to conserve water.
Q: What happens in vasopressin deficiency?
A: The kidneys send more water to the bladder, increasing urination.
Q: What symptom can vasopressin deficiency cause?
A: Chronic thirst due to excessive water loss in urine.
Q: What triggers the angiotensin cascade?
A: A drop in blood volume.
Q: What do the kidneys release when blood volume is low?
Renin
Q: What does renin do?
A: It initiates the formation of angiotensin II.
Q: What is the function of angiotensin II?
A: It raises blood pressure and stimulates thirst.
Q: What hormone signals the brain to start drinking behavior?
A: Angiotensin II.
Q: Where does angiotensin II act in the brain?
A: The subfornical organ (SFO).
Q: What is special about the subfornical organ?
A: It lacks a blood-brain barrier, allowing it to detect circulating signals.
Q: What does the subfornical organ do when it detects angiotensin II?
A: It signals other brain regions to trigger thirst and drinking.
What causes osmotic thirst?
A rise in blood osmotic pressure, usually due to excess salt.
What brain region detects osmotic pressure changes?
The OVLT (organum vasculosum of the lamina terminalis).
Q: What kind of neurons are in the OVLT?
A: Osmosensory neurons.
Q: How do OVLT neurons detect increased osmotic pressure?
A: Their membranes shrink, opening mechanically-gated Na⁺ channels.
Q: What happens when OVLT neurons are activated?
A: They signal the pituitary to release antidiuretic hormone (vasopressin).
Q: What is the function of antidiuretic hormone (ADH)?
A: It helps the kidneys conserve water and reduce urine output.
Q: Why do many diets fail?
A: The body reduces energy expenditure to resist weight loss.
Q: What happens to basal metabolic rate at the start of a diet?
A: It decreases to conserve energy.
Q: What effect does restricted food intake have in rats?
A: It can increase lifespan by up to 40%.
Q: Does restricted eating extend life in humans?
A: Probably not significantly.
Q: What is basal metabolic rate (BMR)?
A: The energy needed to fuel the brain, body, and maintain temperature.
Q: How much of a sedentary person’s energy use is BMR?
A: About 75%.
Q: What was common among dieting women who didn’t lose weight?
A: They had low BMRs.
Q: How much of BMR is influenced by heredity?
A: About 40%.
Q: Can physical activity affect BMR?
A: Yes, activity can increase BMR.
Q: What is the body’s main fuel for energy?
A: Glucose.
Q: What is glycogen?
A: Short-term stored glucose in the liver.
Q: What is glycogenesis?
A: The process of converting glucose to glycogen.
Q: What hormone triggers glycogenesis?
A: Insulin, released by the pancreas.
Q: What are lipids used for in the body?
A: Long-term energy storage in fat tissue.
Q: When is metabolic rate highest in life?
A: In the first year of life.
Q: How does metabolism change from age 1 to 20?
A: It gradually slows down.
Q: What happens to metabolic rate between ages 20 and 60?
A: It stays stable.
Q: What happens to metabolic rate after age 60?
A: It declines by about 1% per year.
Q: What does the brain monitor to regulate eating?
A: Insulin and glucose levels, along with other signals.
Q: What does the brain do with energy-related signals?
A: Integrates them to decide when to start or stop eating.
Q: Why is this integration important?
A: To maintain energy balance and prevent overeating or starvation.
Q: What produces and secretes leptin?
A: Fat cells.
Q: Where does leptin go after it’s released?
A: Into the bloodstream.
Q: What is leptin’s role in the brain?
A: It signals the brain about the body’s fat stores.
Q: What happens if there’s a leptin deficiency or insensitivity?
A: The brain gets a false low report of body fat.
Q: Are obese people leptin-deficient or leptin-resistant?
A: Leptin-resistant.
Q: What does overnutrition do to the hypothalamus?
A: It causes inflammation.
Q: What conditions are linked to hypothalamic inflammation?
A: Obesity, diabetes, and heart disease.
Q: What is ghrelin?
A: A hormone that stimulates appetite.
Q: Where is ghrelin released from?
A: Stomach and gut endocrine cells.
Q: When are ghrelin levels highest?
A: During fasting.
Q: What happens to ghrelin levels after eating?
A: They drop.
Q: What syndrome is associated with abnormally high ghrelin?
A: Prader-Willi syndrome.
Q: What does Prader-Willi syndrome cause?
A: Constant hunger and lack of satiety.
Q: How does Prader-Willi syndrome affect behavior?
A: People may eat excessively—even from garbage—due to extreme hunger.
Q: What brain region acts as the hunger control center?
A: The hypothalamus.
Q: What is the term for the hypothalamus’s role in regulating hunger?
A: “Hungerstat.”
Q: What happens if the lateral hypothalamus (LH) is lesioned?
A: The animal refuses to eat (aphagia).
Q: What happens if the ventromedial hypothalamus (VMH) is lesioned?
A: The animal becomes obese due to overeating (hyperphagia).
Q: What is the function of the lateral hypothalamus (LH)?
A: Stimulates hunger and eating.
Q: What is the function of the ventromedial hypothalamus (VMH)?
A: Signals fullness and inhibits eating.
Q: What happens to animals with VMH lesions?
A: They overeat and become obese.
Q: Do VMH-lesioned animals keep gaining weight indefinitely?
A: No, their weight stabilizes at a new, higher set point.
Q: What happens to VMH-lesioned animals during food restriction?
A: They return to their new, higher weight when food is available again.
Q: What happens to animals with LH lesions?
A: They initially stop eating (aphagia).
Q: Do LH-lesioned animals stay underweight?
A: No, they eventually resume eating.
Q: What happens to body weight after LH lesion recovery?
A: It stabilizes at a new, lower set point.
Q: What are the two main neuron groups in the hypothalamus that regulate hunger?
A: NPY/AgRP neurons and POMC/CART neurons.
Q: What do NPY/AgRP neurons produce?
A: Neuropeptide Y (NPY) and agouti-related peptide (AgRP).
Q: What is the function of NPY/AgRP neurons?
A: Stimulate appetite and lower metabolism → weight gain.
Q: What hormone activates AgRP neurons?
A: Ghrelin.
Q: What do POMC/CART neurons produce?
A: Pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART).
Q: What is the function of POMC/CART neurons?
A: Inhibit appetite and raise metabolism → weight loss.
Q: What happens when the VMH is lesioned?
A: It destroys the PVN, which ends hunger signals.
Q: What happens when the LH is lesioned?
A: It destroys the LHA, which normally causes hunger.
Q: How can overeating affect the brain?
Q: How can overeating affect the brain?
Q: What does hypothalamic inflammation do?
A: It inhibits neurogenesis and resets the body’s weight set point.
Q: What brain changes occur with high-calorie diets?
A: Hypothalamic scarring, microglial activation, and loss of POMC neurons.
Q: Why is losing POMC neurons harmful?
A: POMC neurons block eating and boost metabolism.
Q: Can the brain recover from diet-induced damage?
A: Yes—newborn hypothalamic cells can become POMC neurons if overeating stops.
Q: How does the body “talk” to the brain?
A: Through hormones, nutrients, and neural signals.
Q: What signals from the body help regulate hunger and energy?
A: Glucose, insulin, leptin, ghrelin, and more.
Q: What part of the brain listens to body signals?
A: The hypothalamus.
Q: Why is this communication important?
A: To maintain energy balance and survival.
Q: What are the two types of anorexia nervosa?
A: Restricting type and Binge-Eating/Purging type.
Q: What are the key diagnostic features of anorexia nervosa (DSM-V)?
A: Refusal to maintain healthy weight, intense fear of gaining weight, and body image disturbance.
Q: What is the lifetime prevalence of anorexia nervosa in women?
A: About 1 in 200.
Q: What is the lifetime prevalence of anoriexia in men?
A: About 1 in 2,000.
Q: How severe is anorexia nervosa compared to other psychiatric disorders?
A: It has the highest mortality rate.
Q: How does Louise Glück’s poem describe the onset of anorexia?
A: As a quiet fear of death that becomes dedication to hunger, reflecting deep psychological and societal pressures.
Q: What is the key feature of bulimia nervosa?
A: Recurrent episodes of binge eating.
Q: What follows binge eating in bulimia?
A: Recurrent inappropriate compensatory behaviors (e.g., vomiting, laxatives, excessive exercise).
Q: How often must bulimia symptoms occur for diagnosis?
A: At least twice a week for 3 months (DSM-V).
Q: What are physical symptoms of anorexia?
A: Thinning bones, brittle hair and nails, dry/yellowish skin.
Q: What are other signs of anorexia?
A: Anemia, muscle weakness, lethargy.
Q: What are cardiovascular symptoms of anorexia?
A: Low blood pressure, slow breathing and pulse.
Q: What are other systemic signs of anorexia?
A: Severe constipation, drop in body temp, and amenorrhea (loss of menstruation).
Q: Do eating disorders often co-occur with other psychiatric conditions?
A: Yes, very frequently.
Q: What percentage of women with anorexia or bulimia had childhood anxiety disorders?
A: 40%.
Q: What percentage experienced depression?
A: 90%.
Q: In a study of 246 women with eating disorders, how many attempted suicide?
A: 30%.
Q: What was the mortality rate in that group?
A: 5% died.
Q: Who is Allegra Versace in the context of eating disorders?
A: A public figure known to have struggled with anorexia, highlighting its impact even among high-profile individuals.
Q: What brain region is larger in teen girls with anorexia and linked to disgust?
A: The insula.
Q: What brain region is larger in anorexia and linked to self-restraint or guilt?
A: The orbitofrontal cortex.
Q: What age group was surveyed in the KEDS study?
A: Students in grades 5 to 8.
Q: How many students were included in the KEDS study?
A: 3,175 students.
Q: What percentage of students in KEDS study reported dieting?
A: 30%.
Q: What percentage in KEDS study reported fasting?
A: 10%.
Q: What percentage in KEDS study reported vomiting to lose weight?
A: 5%.
Q: What percentage in KEDS study reported using diet pills?
A: 2%.
Q: Who was Israel Kamakawiwo’ole?
A: A Hawaiian singer known for his ukulele medley of “Somewhere Over the Rainbow” and “What a Wonderful World.”
Q: When did Israel Kamakawiwo’ole live?
A: 1959–1997.
Q: What health issue contributed to Israel Kamakawiwo’ole’s early death?
A: Complications related to extreme obesity.
Q: What is the most important part of obesity treatment?
A: Eating less—creating a daily 200-calorie deficit.
Q: What’s the key mindset shift for weight loss?
A: Eat until you’re not hungry, then stop.
Q: Why is reducing calories hard to maintain?
A: It requires a long-term lifestyle change.
Q: What two supports are critical for success?
A: Self-monitoring and social support.
Q: What type and amount of exercise helps with weight loss?
A: Strenuous aerobic activity for over 200 minutes per week.
Q: Does light exercise like walking alone work for significant weight loss?
A: No, more intense activity is needed, along with calorie restriction.
Q: What class of drugs is used in new obesity treatments?
A: Glucagon-like peptide-1 (GLP-1) agonists.
Q: Name two GLP-1 agonist medications for obesity.
A: Mounjaro and Ozempic.
Q: How do GLP-1 agonists help with weight loss?
A: They reduce appetite, slow stomach emptying, and improve insulin sensitivity.
Q: What is an added benefit of GLP-1 drugs like Ozempic?
A: They also help manage type 2 diabetes.
