Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

nutritional aspects of disease > exam 1 > Flashcards

exam 1 Flashcards

1
Q

What are the primary circulating fuels of the body and their concentrations?

A

Glucose: 70-115 mg/dl, CHO(carbohydrate) in circulation

Triaclyglycerols: 100-250 mg/dL, bound and packaged in either GI derived chylomicrons or liver and gut derived VLDLs

Free-fatty acids: 20-200 mg/dL, non-esterified and bound to albumin, primary fuel in the fasted state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name steps to converting nutrient into acetyl CoA into another nutrient

A
  1. breakdown of large macromolecules to simple subunits
  2. breakdown of simple subunits to acetyl CoA accompanied by production of limited ATP and NADH
  3. complete oxidation of acetyl CoA to h20 and CO2 involved production of much NADH, which yields much ATP via electron transport
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the secondary circulating fuels?

A

amino acids, glycerol, lactate/pyruvate, ketone bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How many calories do we ingest every day?

A

9 kilocalories per day +/-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How to calculate BMI?

A

weight/(height^2)

kg/m^2

1kg = 2.205 lb
1 in = 2.54 cm
1m = 100 cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

obesity epidemic numbers

A

72.9% US adults obese/overweight
35.7% US adults obese
17-20% of children obese (up from 9% in last 20 years)

obese individuals spend $1,800 more each year on healthcare

300K+ annual deaths from obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name etiology of obesity

A 
genetics
metabolic and physiological
environment
appetite regulation
biochemical
endocrine
neuronal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

associated risks of obesity

A 
hypertension
stroke
diabetes
cancer
skin disorders
early death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name the classes of obesity and their numbers.

A

BMI 25-29.9 oberweight
30-34.9 obesity I
35-39.9 obesity II
40+ obesity III (morbidly obese)

body composition not accounted for in BMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

when does risk for mortality goes up in females for obesity regarding BMI?

A

once body fat percentages go below 12-14% for females, risk for mortality is as high as obese class I because hormone levels get completely disregulated in ameteria(loss of menses because body cannot support life)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

normal adipocyte number vs obesity

A

25-40x10^9 adipocyte normal
obese > 160x10^9 adipocytes

obeses adults shrink adipocyte cells but cannot lose them —Cellular apoptosis doesn’t occur until prolonged starvation because body resists cell breakdown despite lipid shrinking in adipose cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the difference in amount of calories in maintaining obesity in normal adults vs natural obese adults?

A

requires 2x amount of calories in normal individuals to maintain obesity but natural ones require 1/2 as many calories to maintain obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

normal body percentages

A

male: 10-25%, female: 18-32%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why do we need fat to live?

A

fuel for energy source, insulator to protect form the environment and amintain core body tmeperature, protection around soft tissues and hard tissues, myelin sheaths protects electrical current from moving beyond the acon for nueromusculasr communication, women need for pregnacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

fruit shpae vs type of obesity

A

pear > gynoid

apple > andoid (associated with disease like diabetes type II, high BP, cancer etc. Visceral stress)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Least invasive to most invasive measurements of body composition

A 
BMI
waist to hip ratio
waist to height ratio
hydrodensitometry* gold standard
bioelectrical impedance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Difference between Victoza and Saxenda?

A

Saxenda is marketed obesity drug, Victoza as diabetes type II drug; that’s why Saxenda is 4x more expensive (vanity drug)

Both are the same, Liraglutide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Saxenda an agonist for?

A

GLP-1 rececptor agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the BMI and conditions of the individuals who use Saxenda?

A

BMI >30 individuals OR

BMI>27 overweight and at least 1 weight-related condition (hypertension, type II diabetes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the dosage needed for Saxenda (Liraglutide)?

A

0.6 mg per day for 1 week, increasing 9.6 mg/day in weekly intervals until 3 mg/day dose is achieved

MUST walk up to this dose because side effect profile is too strong and patient cannot tolerate(will vomit and be nauseous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the dosage of Liraglutide in Saxenda versus Victoza?

A

Saxenda – 3mg/day

Victoza – 1.8 mg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is weight loss expected in Saxenda?

A

upward 8-10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the goal of weight management and treatment?

A

primary goal is to prevent further weight gain because diet and exercise are effective in preventing further gain once obesity is reached, but isa means of maintenance not treatment once an individual is obese

Reduce ->maintain->track in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the weight loss goals?

A

down 10% from weight baseline with moderate caloric deficit . (500-1000 kcal/day)
redcuce 1lb of body fat per week, which is essener

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

most metabolic pathways have a rate-limiting step. Why?

A

AKA committed step, to control metabolic flux, nonbidirectional processes to control the movement of substances in enzymatic sequences in regulation. typically expends the most energy in first enzymatic step to know you have enough energy to finish the rest of the sequence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the satiation signals?

A

CCK and serotonin (5-HT), peptide YY, GLP-1

accumulation of chemical inhibitory signals that eventually causes satiety within the meal for meal termination, largely arising form the GI tract. Meal initiation is primarily the result of an absence of satiating signals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

the gustatory system is postulated to be essential in what?

A

distinguishing palatable foods from non-palatable foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the sham feeding paradigm?

A

Rats can treat sucrose solutions and beverages accurately while humans cannot. they calorically compensate even if the sucrose concentration changes. they consume more with open fistula because the GI tract is responsible for those satiation signals. Without it, they continue to drink.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is responsible for the discrete balance of caloric consumption?

A

CNS, vagus nerve – a conduit of communication between brain and peripheral organs

nucleus tractus solitarus – first nucleus in brain that receives the communication signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is CCK and what does it do?

A

CCK is a satiety signal primarily derived from the GI tract and reduces the size of a meal acutely. Singularly only that meal. physiologically required for meal size control satiation signal. injections daily do not work because of chronic problems like pancreatitis and gallbladder stones, and tachyphylaxis (drug resistance) and toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

The OLETF and LETO rats difference?

A

OLETF rat lacks functional CCK1 receptor expression and the control rats LETO have the CCK receptor, but CCK does not alter feeding in the OLETF rat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Tie together CCK, GLP1 and PPG

A

CCK made from I cells in small intestine, PPG and GLP1 made from L cells

PPG and CCK make GLP1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the the GLP receptor agonists as a pharmacological treatment for obesity?

A 
Exendin-4 (half ife 2.5 hours)
and Liraglutide (half life 13 hours)

because unlike CCK, there are nonlife-threatening side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Why are Exendin-4 and Liraglutide FDA-approved?

A

approved for treating type II diabetes because resistant to enzyme degradation and reduced renal excretion, negligible risk of life-threatening adverse events

Incretin effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

L cell to incoming glucose load steps

A

L cells sense macronutrients and secrete GLP1, which on pancreatic beta cells and into circulation, which causes release of insulin secretion, body proactively causing release to deal with incoming glucose load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

how often do you take exendin-4 and liaglutide?

A

exendin-4 – twice daily
liraglutide – once daily

both produce comparable and pronounced suppressions in food intake and body weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Does exendin-4 treat obesity?

A

no, it treats diabetes and improves co-morbidity at least a bit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

difference in weight loss of liraglutide and exendin?

A

lirgalutide only drug approved to treat obesity, exendin treats diabetes

liraglutide meets 5-10% sustained weight loss but exendin does not. *liraglutide meets it but plateaus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is leptin

A

protein product of ob/ob gene found in animals
-controls appetite, body weight and obesity
acts in multiple nuclei within the brain to regulate energy balance
interacts with almost all neuropeptides known to be involved in energy balance and food intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how is leptin released into circulation?

A

Leptin is released into the circulation form adipocytes in proportion to the amount of energy (fat) storage; it acts as a catabolic hormone by decreasing appetite and increasing expenditure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Leptin and obesity and CSF relation?

A

Ratio of leptin in CSF to serum leptin is decrease in obese individuals

resistant leptin penetration in brain, CSF concentration of leptin is saturated, no longer responding in same magnitude but leptin causes suppressed food intake and body weight ONLY in lean individuals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Name the drugs that are approved for long term use in treating obesity.

A 
Orlistat (alli), 
Qsymia (phentermine/topiramate)
Lorcaserin (Belviq)
Saxenda (Liraglutide)
Contrave (Naltrexone/bupropion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the over the counter FDA obesity drug that is only drug that doesn’t affect the CNS?

A

Orlistat (Alli)

Gi lipase inhibitor and binds and inhibits function. Digests lips, specifically triglycerides because to absorb fats, you must break down into triglycerides first.

44
Q

What does ORLISTAT do?

A

prevents digestion of ingested fats, which goes into feces since digestion is repressed (malabsorption)

1/3 is in feces

5% weight loss at 6 months

45
Q

Orlistat side effects?

A

PRIMARILY GASTROINTESTINAL
–mild to moderate–

decreased absorption of fat-soluble vitamins
anal leakage common because fats are slippery
-oily spotting
-fatty/oily stool
-increased defecation
-flatus with discharge

You shart

occurs within 3 months of therapy

46
Q

What is lorcaserin (belviq)?

A

serotonin receptor agonist to act in CNS as appetite suppressant –>activation of hypothalamic POMC neurons

5-6% weight loss

not a strong drug in treating obesity

47
Q

Lorcaserin side effects (Belviq)?

A

headache, upper resp./sinus infections, nausea

48
Q

Is lorcaserin a strong drug to treat obesity?

A

no, weight loss lasts six months but then weight comes back

49
Q

What is Qsymia (phentermine /topiramate)?

A

appetite suppressant
Off target effects:

Phentermine through amphetamine
phenethylamine as psychostimulant

topiramate – as anticonvulsant and anti-addiction by activating GABA systme

14-15% weight loss

50
Q

What is Qsymia (phentermine /topiramate) side effects?

A

SEVERE

seizures
hallucinations
hostility
bizarre behavior
mood changes
numbness
nausea/diarrhea
51
Q

What is Contrave (Naltrexone/bupropion)?

A

opioid receptor anatagonist and re-uptake inhibitor of dopamine and noradrenaline

52
Q

side effects of Contrave (naltrexone/bupropion)?

A 
suicidal thoughts/actions
depression
anxiety
panic attacks
insomnia
fatigue
53
Q

Is contrave popular?

A

no, weight loss percentage not high over a year, just 5%

54
Q

weight loss by obesity drug percentages

A

Orlistat – 5% at 6months
Lorcaserin – 5-6% at 6 months but weight comes back (not strong drug)
Qysmia – 14-15% weight loss but severe side effects
Contrave – 5% weight loss over a year (not effective)
Liraglutide (Saxenda) – 8-10% safest and most popular FDA drug

55
Q

when to use obesity drug treatment?

A

only those at medical risk

BMI >30, >27 with co-morbidity

56
Q

whehn should weight loss surgery be used?

A

should be reserved for those patients who have failed in other attempts to lsoe weight and are suffering from the complications

less severely obese patients may be considered with at high risk with other co-morbid conditions

Produces the longest period of sustained weight loss

57
Q

What is Roux-en-Y gastric bypass surgery?

A

duodenum and jejunum surgically connected with new small stomach pouch with stomach left in peritoneal cavity , stomach almost completely bypassed from GI nutrient flow but left in peritoneal cavity

58
Q

Why is stomach left in peritoneal cavity in roux-en-y gastric bypass surgery?

A

endocrine hormones produced

intrinsic factors made in stomach, and without it you cannot absorb vitamin b12

59
Q

complications of roux-en-y gastric bypass surgery?

A 
severe nausea/vomiting
dumping syndrome
malabsorption of vitamin b12, folate, calcium, iron
dehydration
infection
behavioral/psychological changes
overabundance of GOp1, abundance of satiation signal
14-15 small meals per day
60
Q

other surgeries not used?

A

vertical banded and adjustable gastric band

61
Q

how does surgery work for metabolic physiology?

A

changes body but patietns can regain 75-100% of weight in about 3-5 years and overcome surgery options

62
Q

difference between type I and type II?

A

type I – insulin dependent diabetes, failure to produce insulin
autoimmune destruction of beta cells/absence of insulin because receptors are not there and body identifies cells as non-self (IDIOPATHIC UNKNOWN CAUSE), genetic predisposition +idiopathic virus(?) —>beta cell injury (autoimmune) and insulin dependent

type II – non insulin dependent
failure of receptors to regulate the hormone of signalling cascase
impairment, resistance, NOT AN ABSENCE

inadequate exercise +excessive food intake + genetic predisposition -> obesity -> insulin resistance

63
Q

characterizations of diabetes?

A

polyuria,polydipsia (excessive thirst) glucose concentraiton after at least 8 hours of fasting .126 mg/dL, and plasma glucose concentration >200 mg/dL 2 hours after oral glucose 75g intake (oral glucose tolerance test) and unexplained weight loss

genetic, metabolic, and acquired conditions that result in hyperglycemia

64
Q

alpha and beta cell difference? IMPORTANT

A

alpha – makes hormone glucagon is there is low blood glucose by breaking down stored glucose through glycolysis in liver into blood 70-155 mg/dL

beta– makes hormone insulin

65
Q

details about insulin’s functions

A

hormone produced by beta cells of pancreas to regulate blood glucose level in body

signal for the conversion of free glucose to glycogen and stores it in liver

promotes for glycogensis, lipogenesis, proteogenesis, nucleid acid synthesis

66
Q

beta cells in pancreas responsible for production of what hormone?

A

insulin

67
Q

insulin is required for glucose enter from where?

A

bloodstream because both have GLUT4 glucose receptor in cell and only way to get glucose in cell

68
Q

what is bad? refined or complex carbs?

A

refined

69
Q

how many people have diabetes?

A

5% Type I, 95% type II

7 million undiagnosed

70
Q

what makes Type I diabetes markered despite being idiopathic?

A

triggering event and beta cells go from injured to dead and cannot be re-expressed or replicated

71
Q

type II diabetes onset

A

stomach changes food into glucose ->glucose enters bloodstream -> pancreas makes insulin -> insulin enters bloodstream -> glucose can’t get into the cells up the body and build up in the blood vessels

72
Q

normal level of A1 C hemoglobin in individuals is what?

A

4-6%

73
Q

is A1C a diagnosable test?

A

no, it’s a measure of blood glucose and tests chronic state of blood glucose

74
Q

how to explain unexplained weight loss in type ii diabetes lack of insulin?

A

Body becomes a state of mobilizing stored fuels because body think its doesn’t have any fuels and breaks down the fat

Further exacerbation of the problem

75
Q

Cause of insulin inaction?

A

decreased receptors on cells!!!!!

Cells become saturated with glucose

other causes: abnormal b-cell secretory product, circulatory anti-insulin antibodies occurring years down that road and body targets cells for destruction

76
Q

When the Glut 4 glucose transporter cannot fuse with membrane, what happens?

A

low glucose flow into cell and then there are decreased receptors on cell

77
Q

Insulin dependent diabetes occurs how vs noninsulindependent

A

Type I

genetic predisposition + idiopathic virus? ->beta cell injury autoimmune destruction ->insulin dependent
less than 10% beta cells is diagnosis
TRIGGERING EVENT

Type II
Inadequate exercise + excess food intake + genetic predisposition -> Obesity ->Insulin resistance

78
Q

What mutation in what genes causes autoimmune diseases?

A

system that judges similarity of tissues is the Human Leukocyte Antigen (HLA)!!!!!

destruction of b-cell by immune system

proteins on cell surface display normality to immune system as a way to distinguish ‘self’ and ‘nonself’, where nonself antigens are targeted for destruction by killer T-cells

MUTATIONS IN proteins in CLASS II genes (HLA-DR and HLa-DQ regions) ASSOCIATED WITH TYPE I DIABETES AND OTHER AI DISEASES

79
Q

What are the two regions in class II genese with mutated proteins that put cell at risk of being identified as non self?

A

HLA-DR and HLA-DQ

80
Q

What causes the non self identification to occur?

A

Antigen changing shape slightly from single point mutations (lock and key example), where antibodies are created for it once macrophage notices this, which is why you can never re-express beta cells

Mutation in DQ and/or DR region will trigger autoimmune destruction of B-cells

81
Q

what is relationship between lipids and macrovascular disease?

A

proliferation of smooth muscle cells form lip filled plaques that migrate to do arterial occlusion
Fat builds up in arteries and palsma over the years for increased risk of CVD

LDL bad lipoprotein
HDL good lipoprotein

82
Q

what is the relationship between membrane structure and microvascular diseases?

A 
thickened basement membrane and capillary beds
*insulin-associated, not lipid*
angipathies
nephropathies
retinopathies
83
Q

the microvascular disease gangrene affected by diabetes how?

A

loss of nutrients call cell death as a chronic degenerative diseases, irreverisble glycosylation, micro-regional necrosis

84
Q

Altered glucose metabolism caused by hyperglycemia converts glucose to what and why is this a problem?

A

glucose to polyols

problem because they degrade slowly, which polyol accumulation alters function of peripheral nerves and increased protein glycosylation

85
Q

treatment for diabetes

A

insulin

hypoglycemic drugs like Metformin, which increases glucose absorption, decreases hypoglycemic risk, and Sulfonyl Ureas (Tolbudimine) that increase Glut II and increase sensitivity to glucose in B-cells

islet cell transplantation but human trials have failed

and exercise

86
Q

type II diabetes incretin hormone do what?

A

inhibit gastric emptying, reduce food intake and body weight, stimulate insulin response from beta cells in a glucose-dependent manner, inhibits glucagon secretion from alpha cells in a glucose -dependent manner

87
Q

Type II incretin hormones: alpha cells produce what? beta cells produce what?

A

alpha – glucagon pancreas
beta – insulin pancreas
glucose – liver

88
Q

GLP 1 and DDP-4 roles in glucose homeostasis

A

Following meal indigestion, incretin hormones GLP1 and GIP released from endocrine cells
Stimulate glucose-dependent insulin cells from pancreatic beta cells
Suppress glucagon release from pancreatic alpha cells

But incretin hormones GLP1 and GIP are degraded by enzyme DPP 4, inhibiting breakdown of incretin hormones and increading their levels to promote glycemic control

89
Q

How is Exendin-4 related to DDP-4?

A

it is resistant to degradation by the enzyme DPP-4 to enhance GLP1 and GIP incretin hormones

90
Q

What transporter cannot be blocked or no glucose goes into system?

A

SGLT2 transporter

91
Q

What does Glut 2 do?

A

increases beta cell sensitivity (insulin)

92
Q

one third rule, which is?

A

third of meal empties during meal, a third is intermeal interval and a third of meal is in stomach when second meal starts

93
Q

in diabetes, what occurs during gastric emptying?

A

carbs and hypoglycemia, not absorbed in stomach

94
Q

GERD occurs in what weak sphincter? what are the symptoms and what occurs>

A

cardiac sphincter location

Gastroesophageal reflux disease causes indigestion, acid regurgitation, sour stomach, chest pain

Stomach acid into esophagus because weak sphincter has less mucus to protect esophagus, acidity causing pain in that location because sensation is near the heart

95
Q

food that make heartburn worse

A

coffee
citrus products
spicy foods
ibuprofen

96
Q

therapy for heartburn and GERD?

A

elevation of ehad on bed
smaller meals
eat 3hr prior to sleep
antacids

97
Q

What are the GI diseases?

A

Crohn’s disease, ulcerative colitis, celiac disease

98
Q

What is Inflammatory bowel disease? (AI disease)

A

inflammatory disorders leading to damage of the GI tract, which casues painful and life-altering symptoms like rectal bleeding, diarrhea and cramping

largely dietary driven and intestinal motility

99
Q

nutritional deficiencies of IBD

A

mineral and trace element deficiencies, vitamin deficiencies, weight loss and malnutrition

100
Q

cause of IBD

A

enterocytes, acute attack
HLA Class II single point mutations
triggering event, body displays non-self and targeted for destruction by immune system – a creation of antibodies for our own enterocytes and possible impaired cytokine secretions by macrophages, critical for inflammatory responses to foreign bacterial agents

101
Q

Where does Crohn’s disease occur?

A

anywhere in GI tract, microscopic inflammation

102
Q

pathology and etiology of Crohns

A 
pathology:
malabsorption
abdominal pain
obstruction
abscesses
mucosal thickening
also causes impaired growth in 30% of patients
joint inflammation
skin ulcers

Etiology: unknown but suggested AI, genetic, dietary, thought to occur early in life nad have 15-20 year incubation

103
Q

ulcerative colitis

A

confine to colonic mucosa and 30% to rectum, cured by colectomy

104
Q

difference in location and treatment for ulcerative colitis and crohns

A

crohns: medication, surgery, nutrition, anywhere in GI tract, skipped areas

Ulcerative colitisL confined to colonic mucosa and 30% confined to rectum, cured by colectomy, only GI bleeding

105
Q

what occurs in both Crohns and ulcerative colitis?

A

increased risk of colorectal cner, extraintestinal manifestations, diarrhea, chronic relapse and varying degrees of severity

106
Q

short bowel syndrome cause of what?

A

crohns diseases and is nutritional and metabolic consequence of major resection of small intestine

107
Q

if you lose the ileum you cannot reabsrob what?

A

bile and b vitamin

nutritional aspects of disease (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions