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Foundations 1 > Foundations 1 Test Misc Week 3-4 > Flashcards

Foundations 1 Test Misc Week 3-4 Flashcards

1
Q

when is beta-oxidation triggered?

A

fasting, exercise, after a fat rich meal

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2
Q

What is ketogensis? where does it occur? when does it occur?

A

production of ketone bodies that occurs in the liver when there are high levels of acetyl-CoA

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3
Q

which type of epithelium can be ciliated?

A

pseudostratified (located in airways)

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4
Q

which type of epithelium can contain micro-villi?

A

simple columnar (located in GI tract)

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5
Q

eccrine sweat glands are what type of gland?

A

simple coiled tubular gland

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6
Q

mucous secretions of intestinal glands are what type of gland?

A

simple tubular glands (multicellular), also contain unicellular goblet cells

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7
Q

the exocrine pancreas is what type of gland?

A

compound acinar

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8
Q

which type of medical imaging gives you the best tissue contrast?

A

MRI

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9
Q

which medical imaging technique(s) us X-rays?

A

radiography and CT

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10
Q

which medical imaging technique gives the worst resolution

A

Nuclear medicine (used to view anatomy and physiology in real time with gamma rays)

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11
Q

which imaging technique has many artifacts?

A

Ultra sound

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12
Q

which imaging technique uses radiofrequency waves

A

MRI

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13
Q

what is ECM composed of?

A

Ground substance (glycoproteins, glycoaminoglycans) and protein fibers (collagen)

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14
Q

what are the layers of integument from keratin to muscle?

A

keratin–>epidermis (stratified squamous)–>dermis (connective tissue)–>hypodermis/subQ/superficial fascia (fat, blood, nerves)–>deep fascia–>muscle

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15
Q

incidence vs prevelence

A

incidence: number of new cases
prevalence: total number of cases

P=I*D

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16
Q

what is incidence rate?

A

IR=incidence/sum of DISEASE FREE person time

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17
Q

what are the essential AA?

A

PVT TIM HLL

Phe, Val, Tyr, Thre, Ile, Met, His, Lys, Leu

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18
Q

A positive nitrogen balance is seen in what two cases?

A

Pregnancy and growth

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19
Q

what is PKU? cause? signs?

A

A decrease in Tyr production due to Phe hydroxylase defici (Phe–>Tyr) or lack of Phe Hydroxylase cofactor (tetrahydrobiopterin). Tyr becomes essential and neuro-toxic Phe metabolites accumulate. Mental retardation, musty body odor

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20
Q

Cachexia: cause? seen in? treatment?

A

excessive protein and AA (Gln) degradation (negative nitrogen balance). seen in cancer and burns. Treatment: steroids, Gln supplement

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21
Q

Protein Quality

A

Complete: maintain growth and life
Partially Complete: maintain life not growth
Incomplete: not maintain life

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22
Q

what is the sparing effect?

A

some nutrients can spare other nutrients from being used. Carbs spare protein use, Tyr spares Phe use, Cys spares Met use

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23
Q

Homocystinuria: what is it? causes?

A

accumulation of homocysteine due to a mutation in cystathionine synthase (homocysteine–>cystathionine).Homocysteine disrupts collagen cross-linking causing strokes and heart attacks, Cys becomes essential

Note: Met–>homocysteine–>cystathionine–>cys

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24
Q

Acute Lymphatic Leukemia: cause? treatment?

A

Asn-synthase deficiency in WBCs (Asp-x->Asn). L-Asparaginase (Asn–>Asp) is used to treat and starve these cells of dietary Asn

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25
Q

what does the biological value of a protein tell you?

A

how much dietary protein is retained in the body (accounts for protein lost in urine and feces)

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26
Q

what is the best measure of the completeness of a protein?

A

PDCAAS (protein digestibility corrected AA score): compares the amount of AA in each protein to the requirements for a 2-5 year old

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27
Q

what are the three dietary lipids

A

(sterols, phospholipids, glycerides)

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28
Q

what is a reason a nutrient (biotin/B7) would not have a RDA? what do you do if this is the case?

A

insufficient research. go by Adequate intake levels

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29
Q

what is the RDA?

A

intake of food fro a group (men/women/age) that meets 97.5% of the needs of individuals within that group

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30
Q

what is DRI?

A

dietary requirements (EAR, tolerable upper level, adequate intake) with a goal of preventing nutrient defficeincies and preventing over-nutrition

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31
Q

Is hip-waist ratio or BMI better for determining risk of heart attacks?

A

hip-waist ratio had a stronger correlation

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32
Q

what are the hormones that regulate appetite? Role? produced? short or long-term

A

Decrease appetite:
Leptin: adipocytes, long term, increase energy utilization
PYY: intestines, short-term, slows gastric emptying

Increase Appetite:
Orexin: lateral hypothalamus, supppress REM, increase wakefulness
Ghrelin: stomach, short term when you think about food

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33
Q

what is metabolic syndrome

A

cluster of conditions (increases visceral obesity, increasesd bp, increased cholesterol) that increases the risk for CVD and diabetes

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34
Q

impact of insulin on TG of adipocytes

A

Promotes LPL (storage of FFAs into TGs)

Inhibits HSL (release of FFAs)

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35
Q

what are adipokines? what is the relationship between adipokine levels and visceral obesity?

A

adipokines are the hormones produced by adipocytes; as obesity increases, adipokine levels increase (except adiponectin)

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36
Q

what is the role of adiponectin?

A

anti-atherosclerotic effects, enhance insulin sensitivity, increase glucose uptake

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37
Q

Obestiy is…

A

a crhonic low grade inflammatory state due to increase size of adipocytes and increased macrophages

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38
Q

how does increased adipocyte size/number increase insulin resistance?

A

Adipocytes enlarge and produce more IL-6, leptin that recruits tissue macrophages and increases FFAs. Increased FFAs and TNF-alpha (released by macrophages) produces insulin resistance

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39
Q

what is RQ of fats, proteins, carbs

A

Carbs 1.0
Fats: .7
protein: .8

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40
Q

describe the energy source over a a 2 hour intense workout

A

0-10 min: only glycogen within smooth muscle

10-20: muscle glycogen and liver glycogen

> 20 min: muscle, liver, and FAs

> 2hours: FAs with near glycogen depletion in muscle and liver

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41
Q

what percent of our total energy goes into basal metabolic rate?

A

50-70%

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42
Q

B1 defic: moderate, severe

A

moderate: Wernickes-Korsakoff (chronic alcoholic)

Severe: beriberi

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43
Q

vitamin(s) defic that results in sores at corner of mouth (cheilosis) and tongue issues (Glossitis)

A

B2 and B6 deficiency

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44
Q

B5 AKA

A

Pantothenate

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45
Q

B6 AKA

A

Pyridoxine

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46
Q

B12 deficiency

A

Megaloblastic and pernicious anemia

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47
Q

what are the only 2 vitamins not rich in plants?

A

B12 and D

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48
Q

Niacin is made from…

A

Trp

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49
Q

what is the fetal origins hypothesis? what was the kidney example?

A

fetal experiences “program” future disease. embryo kidney functional capacity was limited by some insult (malnutrition, lack protein, increased glucocoritcoids) and the embryo adapted by slowing kidney growth (decreased nephrons). once the baby was born the kidney had to work harder which led to the death of more kidney. this lead to an increased BP and poor kidney fxn. Adaptions of fetus of fetus to insult became maladaptive later in life

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50
Q

compare the mid brain and front brain: which develops faster? what are their roles?

A

Mid brain: develops quickly, controls emotions (amygdala)

front brain: develops gradually, keeps impulses of mid brain at bay (has trouble keeping up with mid brain early in development and in the teens)

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51
Q

what is the role of the hypothalamus and hippocampus? how do they interact

A

hypothalamus: maintains homeostasis, activates stress response
hippocampus: memory center

hippocampus terminates stress response of the hypothalamus

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52
Q

describe brain growth over the life-span

A

0-3: rapid growth

3-25 moldable brain where 1/2 of the neurons are pruned away

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53
Q

what did the dutch famine experiment show?

A

increased disease seen in (adult) children of malnourished mothers

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54
Q

what did the Carolina Abecedarian study show?

A

high quality pre-school (health care, nutrition, cognitive stimulation) had long lasting positive impact on kids (better graded, better health)

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55
Q

what are the four US probe types? what are their general roles?

A
  1. Linear: superficial
  2. Phased Array: abdomen and cardiac
  3. Curvilinear: abdomen
  4. Endoluminal: vaginal, rectal, oral
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56
Q

what is the attenuation of air? what does that mean?

A
  1. it means that little US signal will return after passing through air (all the waves are absorbed)
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57
Q

what is the most abundant AA in circulation; this is also used to treat cachexia

A

Gln (non-essential made from Glu+ ammonia, but it can become depleted). Nitrogen shuttle!

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58
Q

how much extra kcal/day should a lactating mother consume?

A

500-700 kcal/day for milk.

59
Q

compare the diet of infants to the diet of adults

A

Infants: higher kcal/kg of body weight, higher fat, lower protein

adults; more carbs and proteins

60
Q

what is the single most common nutrient deficiency in the US?

A

iron

61
Q

what is koilonychia

A

spoon shaped nails due to iron deficiency

62
Q

what age group do we see individuals become picky eaters

A

toddler (1-3)

63
Q

what type of cell jxn are intermediate filaments found in?

A

desmosomes

64
Q

what are the four classes of intermediate filaments

A

Vimentin: connective tissue and muscle
neurofilaments: nerve cells
keratins: in all epithelial cells
nuclear lamins: progeria!!

65
Q

what are the uses of taxol, colchicine, and vinblastine?

A

all anti-cancer drugs that prevent cell division.

taxol: stabilizes MT
vinblastine/colchicine: prevent MT polymerization

66
Q

what is congenital myopathy? cause

A

muscle weakness caused by a lack of muscle-specific actin

67
Q

GLUT4 vs GLUT2

A

GLUT4: the only insulin sensitive glucose transporter. seen in membranes of muscle, liver and adipose cells

GLUT2: found in beta-cells of pancreas, detects rising glucose levels

68
Q

what is the structure of pre-proinsulin?

A

signal peptide–B–C–A

69
Q

how is insulin stored

A

in vesicles around w/ 3 (ab/ab insulin dimers) around a Zn ion

70
Q

GLUT4 is released via..

A

receptor mediated endocytsosis (Insulin>RTK>IRS-1>PI-3K>GLUT4 exocytosed

71
Q

what is myotonic dystrophy? what can it lead to?

A

muscle wasting/weakness that can lead to diabetes

72
Q

HLA status and type II diabetes

A

HLA gene complex codes for the antigens presented by cells. the DR locus has correlations to T1DM.

DR3: increase risk for T1DM (antibodies produced against beta cells)

DR4: increase risk for T1DM (antibodies produced against insulin)

DR2: protective role associated with T1DM

73
Q

we discussed two genes found through the GWA study that were thought to play a role in increased risk for type II diabetes, what were they

A

TCF7L2: codes for TF in Wnt pathway (proglucagon synthesis), homozygous carriers 2x increased risk for T2DM

FTO gene: set of genes associated with obesity (methylation of RNA that preferentially produce fat); secondary risk of diabetes

74
Q

MODY disorders affect what type of cell?

A

beta cells!

75
Q

what is meant when diabetes is called a complex disease?

A

influenced by biological, behavioral and environmental factors

76
Q

by the time of T2DM diagnosis how would you describe the function of beta cells?

A

their function is already 50% impaired

77
Q

values for normal, and diabetic fasting glucose

A

normal: 70-100 mg/dL
diabetes: >125 mg/dL
between=IFG, pre-diabetes

78
Q

when should you begin screening of diabetes?

A
  1. BMI>25 w/ an additional risk factor

2. over 45 yo

79
Q

total cholestrol should be below? LDL cholesterol?

A

total: below 200mg/dL
LDL: below 100 mg/dL

80
Q

how does sulfonurea work?

A

increases intracellular calcium and promotes insulin release from beta cells (effective monotherapy for MODY T2DM)

81
Q

how does metformin work?

A

decreases gluconeogenesis of the liver and reduces insulin resistance (very effective monotherapy for T2DM)

82
Q

how do SGLT2 inhibitors work?

A

prevent glucose reabsorption in the kidneys

83
Q

how do TZD (pioglitazone) work?

A

decrease insulin resistance of skeletal muscle and fat

84
Q

what are the diabetes ABCs?

A

complications associated with diabetes (increased A1C, increased BP, increased cholesterol)

85
Q

what effect do catecholamines have on the liver

A

Increase: glycogen degradation, gluconeogensis

decrease: FA synthesis, glycogen production, glycolysis

86
Q

what effects do catecholamines have on skeletal muscle?

A

Increase: glycolysis, gycogen breakdown, TG utilization

Decrease: glycogen production

87
Q

what effect do catecholamines have on adipose?

A

Increase: lipolysis
decrease: storage of FAs (TG production)

88
Q

what explains the alternate responses of liver and skeletal muscle to catecholamines?

A

Same signaling pathway (E/NE–>GPCR–>Adenyl cyclase–>cAMP–>PKA–>phosphoryaltes F-2,6-BPase AKA PFK-2.

however phosphorylation of PFK-2 in liver deactivates it (creates less F-2,6-BP and thus less glycolysis)

phosphorylation of PFK-2 in skeletal muscle acitavates it (creates F-2,6-BP and promotes glycolysis)

89
Q

what are the effects of cortiosol (glucocorticoids) on the liver?

A

Increase: glycogen production, gluconeogensis

90
Q

what are the effects of cortisol in skeletal muscle?

A

Increase: protein degradation

91
Q

what are the effects of cortisol in skeletal muscle:

A

increase: Lipolysis (increase FFAs, insulin resistance)

92
Q

ethanol consumption activates which pathways? what is the result?

A

actiavtes ADH pathway (cytosol of liver) when at low levels and MEOS pathway when at excessively high levels (ER of liver). Produces an abundance of NADH, and acetyl-CoA, and ATP

Effects:

  • hypoglycemia (no need to produce glucose at liver, inhibited glycolysis)
  • lactic acidosis: high NADH/NAD+ drives lactate production
  • Hyperlipidemia: FA oxidation cannot occur without NAD+
93
Q

T2DM is characterized by hyperglycemia; what can cause hyperglycemia? 5

A
  1. decreased insulin (progressive B-cell dysfunction)
  2. impaired insulin signaling (insulin resistance)
  3. accelerated gastric emptying
  4. elevated glucagon
  5. impaired incretin effect
94
Q

how quickly are incretins degraded?

A

very quickly; half-life is in minutes. would not expect increased levels over an hour after a meal (degraded by DPP-4)

95
Q

GLP-1: found? produced? role?

A

produced by Gut-L cells of distal ileum and colon. increase insulin, decrease glucagon, increase insulin sensitivity, increase beta cell size, slow gastric emptying, cardio/neuro protection

96
Q

Exenatide and Liraglutide are type of…

A

GLP-1 mimics used to treat T2DM. Require daily SubQ injections and cause weight loss

97
Q

vildaliptin and sitaglipitn are types of…

A

DPP-4 inhibitors used to treat T2DM. daily pills that are weight neutral

98
Q

what are teh CRH? what are their normal sequence of activation?

A

Glucagon–>Catecholamines (short-acting)–>Glucocorticoids and GH (long acting)

99
Q

what is hypoglycemia induced autonomic failure

A
  • T1DM over 5 years has lost ability to secrete glucagon
  • recurring hypoglycemic events result in progressive desensitization NE/E receptors. this results in the body becoming “numb” to the effects of NE/E
100
Q

what causes DKA?

A

most common in T1DM:

hyperglycemia occurs but because of lack of insulin the cells cannot uptake glucose–>the body thinks it needs more glucose so it releases CRH that increase glycogen degradation and gluconeogenesis–> when this fails the cells break down FAs (poorly)–>this results in the accumulation of ketone bodies. Hyperglycemia and ketonemia increases the fluid lost in the urine. Severe dehydration occurs, tachycardia, respiratory distress, coma

101
Q

a patient has been diagnosed with polycistic ovary syndrome… how should you advise them?

A

increased risk of insulin resistance (diabetes)

102
Q

early in T2DM progression what will be elevated?

A

insulin (hyperinsulimeia) to try and compensate for increased glucose. beta cells will eventually fail to compensate

103
Q

what are two endocrine disorders associated with diabetes? how?

A

Cushing’s syndrome: increased cortisol leads to chronic hyperglycemia and beta cell dysfunction

Acromegaly: increased GH, induces hyperglycemia–>B cells will eventually fail to keep up

104
Q

According to the diabetes prevention program, what is the best way to prevent pre-diabetes from turning into T2DM

A

exercise! legacy effect (16% reduction in risk for every kg lost)

105
Q

Primary Ciliary Dyskinesia: cause? effects?

A

an autosomal recessive disease affecting motile cilia due to a loss of dynein (NOT primary cilia). results in impaired mucocilary elevator, infertility in males (flagella), situs inversus

106
Q

autosomal dominant polysystic kidney disease: cause?

A

large cytsic kidneys formed due to lack of polycystin (important in primary cilia/non-motile cilia)

107
Q

what are the two cellular adhesion molecules we discussed

A

Cadherins (Ca dependent, lateral domain)

integrins (basal domain)

108
Q

what are the four juncitons found in the lateral domain of epithelial cells; from most apical to most basal

A
  1. Zonula occludins (tight jxn)
  2. Zonula adherins (intermediate jxn)
  3. Macula adherins (desmosomes)
  4. Gap junctions
109
Q

Zonula occludens: role and important proteins

A

separates the apical and basal surfaces. Occludin and claudin

110
Q

zonula adherins: role and important proteins

A

connects adjacent cells. cadherins, actin, catenins

111
Q

macula adherins: role and important proteins

A

spot welds adjacent cells to resist shear force. Desmo-, plakoglobins, keratin

112
Q

Gap junctions important proteins

A

Connexin, connexon

113
Q

two types of junctions seen in the basal surface of epithelial cells

A

focal adhesions

hemidesmosomes

114
Q

focal adhesions: role and important proteins

A

attach cell to BM, communication form ECM to cell

Integrin, fibronectin, collagen, laminin

115
Q

Hemidesmosomes: role and important proteins

A

Role: connect cell to ECM

protein: BP230, Collagen XVII, collagen VII, integrins

116
Q

Pemphigus Vulgaris: cause? blister type? nikolsky?

A

antibodies produced against desmosomes that causes a loss of the lateral domain in epithelial cells. flaccid blisters (easily popped, often just open sores). Nikolsky +. Net-like IF

117
Q

Bullous Pemphigoid: cause? blister type? nikolsky?

A

body creates antibodies against BP230 or collagen XVII, loss of hemidesmosomes and basal domain. tense blisters. nikolsky -

118
Q

Dystrophic Epidermolysis Bullosoa: cause

A

inherited defect in collagen VII (Hemidesmosomes) that causes skin to fall off and esophageal issues

119
Q

the smooth ER is important in detox of…

A

ethanol and barbiturates

120
Q

drugs metabolized by CYP2C9

A

phase I metabolism of warfarin (VKORC1, CYP2C9), phenytoin, tolbutamide

121
Q

drugs metabolized by CYP2D6

A

antipsychotic, anti-depressant, metprolol, tamoxifen (pro-durg)

122
Q

what are the 4 metabolizer groups of the many CYP2D6 alleles?

A

ultrarapid
efficient
intermediate
poor

123
Q

a person is a UM for a drug, how do you alter their dose? normal drug and pro drug

A

increase dose of normal drug

decrease for pro-drug

124
Q

the FDA recommends genetic testing prior to? requires it?

A

recommends to avoid ADRs: G6PD deficiency, HLA-B1502, HLA-B5701, TPMT deficiency

requires to improve efficacy: trastuzumab (HER2), maravicor (HIV), imatinib (GI tumors)

125
Q

a person with ____ has an increase risk of ADRs (hemolytic anemia) when taking rasburicase, uricemia, primaquin, dapsone

A

G6PD defic

126
Q

a person with ____ has an increased risk of ADRs (steve-johnson syndrome) when taking carbamazepine

A

HLA-B*1502

127
Q

a person with ____ has an increased risk of ADRs when taking abacavir

A

HLA-B*5701

128
Q

what is the role of TPMT?

A

phase II inactivation of thiopurines (immunosuppressant).

129
Q

individuals with _____ have an increased risk of leukopenia when taking azathiorprine

A

TPMT-deficiency

130
Q

imatinib is more effective when

A

treating C-KIT-positive GI tumors

131
Q

Maravicor is more effective when….

A

treating CCR5-tropic HIV-1 infection

132
Q

how do anabolic steroids work

A

induce muscle hypertrophy by re-inducing fetal geen expression of contractile proteins and increase their synthesis

133
Q

what is chronic granulomatous disease caused by?

A

mutation in more than 400 genes in 1 of 5 NADPH oxidase enzymes. frequent life threatening fungal and bacterial infections occur (no HOCl is produced)

134
Q

what is the role of peroxisome

A

degradation of VLCFA and branched FA

production of plasmogelens (found in lipid membranes of brain, heart, neutrophils)

AA degradation

production of bile acids (liver)

135
Q

what are the effects of ADA deficiency?

A

(converts adenosine to inosine). high dATP levels inhibit ribonucleotide reductase which stops cell division. immune cells are particularly effected by this. causes SEVERE COMBINED IMMUNODEFICIENCY

136
Q

what causes gout? treatment?

A

excessive nucleotide (purine) degradation produces an abundance of Uric acid which leads to uric acid crystals in joints; gout. caused by decreased HGPRT activity (guanine–>GMP) or by increased PRPP synthase activity (more nucleotides=more degradation).

allopurinol is used to treat gout because it is a suicide inhibitor of XO.

137
Q

what is lesch-nyhan syndrome caused by? symptoms?

A

absent HGPRT (high levels of guanine) lead to very high levels of uric acid. gout-like symptoms AND agressive/self-mutalive behavior

138
Q

what is the role of ribonucleotide reductase?

A

converts NDP to dNDP

139
Q

what is hydroxyurea?

A

a cancer therapy that inhibits ribonucleotide reductase and therefore stops production of dNTP and halts proliferation

140
Q

what is the role of thymidylate synthase?

A

dUMP–>dTMP (only way that dTMP is made)

141
Q

what is fluorouracil (5-FU)?

A

blocks thymidylate synthase activity. cancer therapy.

142
Q

what is the role of DHF reductase?

A

converts DHF to THF so it can be used to aid thymidylate synthase in the creation of dTMP.

143
Q

what is methotrexate?

A

inhibits DHF reductase. cancer therapy

Foundations 1 (65 decks)

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