Hunger & Thirst Flashcards
1
Q
Isreal Kamakawiwo’ole nickname
A
izzy
2
Q
What was Izzy’s highest weight
A
757
3
Q
What age did Izzy die
A
38
4
Q
When and where did Izzy die
A
Medical center Honolulu in 1997
5
Q
What was izzy famous for singing
A
somewhere over the rainbow
6
Q
_____ _____ use our behavior to keep things balanced
A
homeostatic systems
7
Q
Main homeostatic mechanism
A
negative feedback systems
8
Q
In homeostatic systems, if a desired _____ ____ is deviated from, compensatory action begins
A
set point
9
Q
In homeostatic systems, if a desired set point is deviated from, ______ ______ begins
A
compensatory action
10
Q
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?
A
Im a Rambler
11
Q
______ ______ is stimulated by low extracellular/intravascular volume
A
hypovolemic thirst
12
Q
hypovolemic thirst is stimulated by low _____/_____ volume
A
extracellular
intravascular
13
Q
_____ _____ is stimulated by high extracellular solute concentration
A
osmotic thirst
14
Q
osmotic thirst is stimulated by _____ _____ _____ concentration
A
high extracellular solute
15
Q
What is hypovolemic thirst?
A
A: Thirst caused by a loss of water volume from the body.
16
Q
Q: Does hypovolemic thirst involve a change in fluid concentration?
A
A: No, fluid concentration stays the same; only volume is reduced.
17
Q
Q: What can cause hypovolemic thirst?
A
A: Bleeding, vomiting, diarrhea, or excessive sweating.
18
Q
Q: What detects the initial drop in blood volume during hypovolemic thirst?
A
A: Baroreceptors in blood vessels and the heart.
19
Q
Q: What are baroreceptors?
A
A: Pressure sensors that detect changes in blood vessel stretch due to volume.
20
Q
Q: How does the brain respond to baroreceptor signals during volume loss?
A
A: It activates thirst and a craving for salt.
21
Q
Q: Why does the brain trigger salt craving in hypovolemic thirst?
A
A: To help retain water and restore electrolyte balance.
22
Q
Q: What cardiovascular response helps maintain blood pressure during hypovolemia?
A
A: Arteries constrict to increase blood pressure.
23
Q
Q: What hormone is released during hypovolemia?
A
A: Vasopressin (also called antidiuretic hormone, ADH).
24
Q
What is Vasopressin also called?
A
antidiuretic hormone
25
What does ADH stand for?
antidiuretic hormone
26
Q: What does vasopressin do to blood vessels?
A: It constricts them to help raise blood pressure.
27
Q: How does vasopressin affect the bladder?
A: It reduces blood flow to the bladder to conserve water.
28
Q: What happens in vasopressin deficiency?
A: The kidneys send more water to the bladder, increasing urination.
29
Q: What symptom can vasopressin deficiency cause?
A: Chronic thirst due to excessive water loss in urine.
30
Q: What triggers the angiotensin cascade?
A: A drop in blood volume.
31
Q: What do the kidneys release when blood volume is low?
Renin
32
Q: What does renin do?
A: It initiates the formation of angiotensin II.
33
Q: What is the function of angiotensin II?
A: It raises blood pressure and stimulates thirst.
34
Q: What hormone signals the brain to start drinking behavior?
A: Angiotensin II.
35
Q: Where does angiotensin II act in the brain?
A: The subfornical organ (SFO).
36
Q: What is special about the subfornical organ?
A: It lacks a blood-brain barrier, allowing it to detect circulating signals.
37
Q: What does the subfornical organ do when it detects angiotensin II?
A: It signals other brain regions to trigger thirst and drinking.
38
What causes osmotic thirst?
A rise in blood osmotic pressure, usually due to excess salt.
39
What brain region detects osmotic pressure changes?
The OVLT (organum vasculosum of the lamina terminalis).
40
Q: What kind of neurons are in the OVLT?
A: Osmosensory neurons.
41
Q: How do OVLT neurons detect increased osmotic pressure?
A: Their membranes shrink, opening mechanically-gated Na⁺ channels.
42
Q: What happens when OVLT neurons are activated?
A: They signal the pituitary to release antidiuretic hormone (vasopressin).
43
Q: What is the function of antidiuretic hormone (ADH)?
A: It helps the kidneys conserve water and reduce urine output.
44
Q: Why do many diets fail?
A: The body reduces energy expenditure to resist weight loss.
45
Q: What happens to basal metabolic rate at the start of a diet?
A: It decreases to conserve energy.
46
Q: What effect does restricted food intake have in rats?
A: It can increase lifespan by up to 40%.
47
Q: Does restricted eating extend life in humans?
A: Probably not significantly.
48
Q: What is basal metabolic rate (BMR)?
A: The energy needed to fuel the brain, body, and maintain temperature.
49
Q: How much of a sedentary person’s energy use is BMR?
A: About 75%.
50
Q: What was common among dieting women who didn’t lose weight?
A: They had low BMRs.
51
Q: How much of BMR is influenced by heredity?
A: About 40%.
52
Q: Can physical activity affect BMR?
A: Yes, activity can increase BMR.
53
Q: What is the body’s main fuel for energy?
A: Glucose.
54
Q: What is glycogen?
A: Short-term stored glucose in the liver.
55
Q: What is glycogenesis?
A: The process of converting glucose to glycogen.
56
Q: What hormone triggers glycogenesis?
A: Insulin, released by the pancreas.
57
Q: What are lipids used for in the body?
A: Long-term energy storage in fat tissue.
58
Q: When is metabolic rate highest in life?
A: In the first year of life.
59
Q: How does metabolism change from age 1 to 20?
A: It gradually slows down.
60
Q: What happens to metabolic rate between ages 20 and 60?
A: It stays stable.
61
Q: What happens to metabolic rate after age 60?
A: It declines by about 1% per year.
62
Q: What does the brain monitor to regulate eating?
A: Insulin and glucose levels, along with other signals.
63
Q: What does the brain do with energy-related signals?
A: Integrates them to decide when to start or stop eating.
64
Q: Why is this integration important?
A: To maintain energy balance and prevent overeating or starvation.
65
Q: What produces and secretes leptin?
A: Fat cells.
66
Q: Where does leptin go after it's released?
A: Into the bloodstream.
67
Q: What is leptin’s role in the brain?
A: It signals the brain about the body's fat stores.
68
Q: What happens if there’s a leptin deficiency or insensitivity?
A: The brain gets a false low report of body fat.
69
Q: Are obese people leptin-deficient or leptin-resistant?
A: Leptin-resistant.
70
Q: What does overnutrition do to the hypothalamus?
A: It causes inflammation.
71
Q: What conditions are linked to hypothalamic inflammation?
A: Obesity, diabetes, and heart disease.
72
Q: What is ghrelin?
A: A hormone that stimulates appetite.
73
Q: Where is ghrelin released from?
A: Stomach and gut endocrine cells.
74
Q: When are ghrelin levels highest?
A: During fasting.
75
Q: What happens to ghrelin levels after eating?
A: They drop.
76
Q: What syndrome is associated with abnormally high ghrelin?
A: Prader-Willi syndrome.
77
Q: What does Prader-Willi syndrome cause?
A: Constant hunger and lack of satiety.
78
Q: How does Prader-Willi syndrome affect behavior?
A: People may eat excessively—even from garbage—due to extreme hunger.
79
Q: What brain region acts as the hunger control center?
A: The hypothalamus.
80
Q: What is the term for the hypothalamus’s role in regulating hunger?
A: "Hungerstat."
81
Q: What happens if the lateral hypothalamus (LH) is lesioned?
A: The animal refuses to eat (aphagia).
82
Q: What happens if the ventromedial hypothalamus (VMH) is lesioned?
A: The animal becomes obese due to overeating (hyperphagia).
83
Q: What is the function of the lateral hypothalamus (LH)?
A: Stimulates hunger and eating.
84
Q: What is the function of the ventromedial hypothalamus (VMH)?
A: Signals fullness and inhibits eating.
85
Q: What happens to animals with VMH lesions?
A: They overeat and become obese.
86
Q: Do VMH-lesioned animals keep gaining weight indefinitely?
A: No, their weight stabilizes at a new, higher set point.
87
Q: What happens to VMH-lesioned animals during food restriction?
A: They return to their new, higher weight when food is available again.
88
Q: What happens to animals with LH lesions?
A: They initially stop eating (aphagia).
89
Q: Do LH-lesioned animals stay underweight?
A: No, they eventually resume eating.
90
Q: What happens to body weight after LH lesion recovery?
A: It stabilizes at a new, lower set point.
91
Q: What are the two main neuron groups in the hypothalamus that regulate hunger?
A: NPY/AgRP neurons and POMC/CART neurons.
92
Q: What do NPY/AgRP neurons produce?
A: Neuropeptide Y (NPY) and agouti-related peptide (AgRP).
93
Q: What is the function of NPY/AgRP neurons?
A: Stimulate appetite and lower metabolism → weight gain.
94
Q: What hormone activates AgRP neurons?
A: Ghrelin.
95
Q: What do POMC/CART neurons produce?
A: Pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART).
96
Q: What is the function of POMC/CART neurons?
A: Inhibit appetite and raise metabolism → weight loss.
97
Q: What happens when the VMH is lesioned?
A: It destroys the PVN, which ends hunger signals.
98
Q: What happens when the LH is lesioned?
A: It destroys the LHA, which normally causes hunger.
99
Q: How can overeating affect the brain?
Q: How can overeating affect the brain?
100
Q: What does hypothalamic inflammation do?
A: It inhibits neurogenesis and resets the body’s weight set point.
101
Q: What brain changes occur with high-calorie diets?
A: Hypothalamic scarring, microglial activation, and loss of POMC neurons.
102
Q: Why is losing POMC neurons harmful?
A: POMC neurons block eating and boost metabolism.
103
Q: Can the brain recover from diet-induced damage?
A: Yes—newborn hypothalamic cells can become POMC neurons if overeating stops.
104
Q: How does the body "talk" to the brain?
A: Through hormones, nutrients, and neural signals.
105
Q: What signals from the body help regulate hunger and energy?
A: Glucose, insulin, leptin, ghrelin, and more.
106
Q: What part of the brain listens to body signals?
A: The hypothalamus.
107
Q: Why is this communication important?
A: To maintain energy balance and survival.
108
Q: What are the two types of anorexia nervosa?
A: Restricting type and Binge-Eating/Purging type.
109
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.
110
Q: What is the lifetime prevalence of anorexia nervosa in women?
A: About 1 in 200.
111
Q: What is the lifetime prevalence of anoriexia in men?
A: About 1 in 2,000.
112
Q: How severe is anorexia nervosa compared to other psychiatric disorders?
A: It has the highest mortality rate.
113
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.
114
Q: What is the key feature of bulimia nervosa?
A: Recurrent episodes of binge eating.
115
Q: What follows binge eating in bulimia?
A: Recurrent inappropriate compensatory behaviors (e.g., vomiting, laxatives, excessive exercise).
116
Q: How often must bulimia symptoms occur for diagnosis?
A: At least twice a week for 3 months (DSM-V).
117
Q: What are physical symptoms of anorexia?
A: Thinning bones, brittle hair and nails, dry/yellowish skin.
118
Q: What are other signs of anorexia?
A: Anemia, muscle weakness, lethargy.
119
Q: What are cardiovascular symptoms of anorexia?
A: Low blood pressure, slow breathing and pulse.
120
Q: What are other systemic signs of anorexia?
A: Severe constipation, drop in body temp, and amenorrhea (loss of menstruation).
121
Q: Do eating disorders often co-occur with other psychiatric conditions?
A: Yes, very frequently.
122
Q: What percentage of women with anorexia or bulimia had childhood anxiety disorders?
A: 40%.
123
Q: What percentage experienced depression?
A: 90%.
124
Q: In a study of 246 women with eating disorders, how many attempted suicide?
A: 30%.
125
Q: What was the mortality rate in that group?
A: 5% died.
126
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.
127
Q: What brain region is larger in teen girls with anorexia and linked to disgust?
A: The insula.
128
Q: What brain region is larger in anorexia and linked to self-restraint or guilt?
A: The orbitofrontal cortex.
129
Q: What age group was surveyed in the KEDS study?
A: Students in grades 5 to 8.
130
Q: How many students were included in the KEDS study?
A: 3,175 students.
131
Q: What percentage of students in KEDS study reported dieting?
A: 30%.
132
Q: What percentage in KEDS study reported fasting?
A: 10%.
133
Q: What percentage in KEDS study reported vomiting to lose weight?
A: 5%.
134
Q: What percentage in KEDS study reported using diet pills?
A: 2%.
135
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."
136
Q: When did Israel Kamakawiwo'ole live?
A: 1959–1997.
137
Q: What health issue contributed to Israel Kamakawiwo'ole’s early death?
A: Complications related to extreme obesity.
138
Q: What is the most important part of obesity treatment?
A: Eating less—creating a daily 200-calorie deficit.
139
Q: What’s the key mindset shift for weight loss?
A: Eat until you're not hungry, then stop.
140
Q: Why is reducing calories hard to maintain?
A: It requires a long-term lifestyle change.
141
Q: What two supports are critical for success?
A: Self-monitoring and social support.
142
Q: What type and amount of exercise helps with weight loss?
A: Strenuous aerobic activity for over 200 minutes per week.
143
Q: Does light exercise like walking alone work for significant weight loss?
A: No, more intense activity is needed, along with calorie restriction.
144
Q: What class of drugs is used in new obesity treatments?
A: Glucagon-like peptide-1 (GLP-1) agonists.
145
Q: Name two GLP-1 agonist medications for obesity.
A: Mounjaro and Ozempic.
146
Q: How do GLP-1 agonists help with weight loss?
A: They reduce appetite, slow stomach emptying, and improve insulin sensitivity.
147
Q: What is an added benefit of GLP-1 drugs like Ozempic?
A: They also help manage type 2 diabetes.
148
