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Foundations 1 > Week 3 Problem Concepts > Flashcards

Week 3 Problem Concepts Flashcards

1
Q

Fxn and Location of Simple Squamous Epithelium

A

Diffusion! located: alveoli, bowman’s capsule, endothelium

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2
Q

Fxn (3) and Location of Simple Cuboidal Epithelium (3)

A

Absorption, Secretion, minimal protection. Location: small ducts of exocrine glands, thyroid follicles, kidney tubules

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3
Q

Function (1) and location (1) of Simple columnar Epithelium

A

Function: absorption
location: GI tract

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4
Q

Function (3) and location (2) of pseudostratified epithelium

A

Fxn: absorption, secretion, transport
Location: vas deferens/epididymis, bronchial tree

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5
Q

function and location of stratified squamous epithelium

A

Protection

Skin (keratinized), vagina, oral cavity, esophagus

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6
Q

function (2) and location (2) of stratified cuboidal epithelium AND stratified columnar epithelium

A

Protection and conduit

large ducts exocrine glands, anorectal jxn

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7
Q

function and location of transitional epithelium

A

distension

bladder

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8
Q

holocrine secretions

A

A mode of exocrine secretion in which the cell dies and releases its contents

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9
Q

apocrine secretions

A

a mode of exocrine secretion in which a cell releases a vesicle with its contents

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10
Q

merocrine secretions

A

a mode of exocrine secretion in which a cell exocytoses its contents (most common)

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11
Q

what type of exocrine gland is a eccrine sweat gland? secretion type?

A

multicellular, simple coiled tubular (serous secretions)

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12
Q

what type of exocrine gland is the intestinal gland? secretion?

A

multicellular, simple tubular, mucus secretions

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13
Q

what type of exocrine gland is the pancreatic gland? secretion type?

A

mutlicelllar, compound acinar, serous secretions

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14
Q

what four steps should you follow prior to taking vital signs?

A

wash your hands, introduce yourself and verify patient, tell the patient about the procedure and ask if they have any questions, ask if the patient has done anything (meds, exercise, pain) that will alter vitals

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15
Q

what is an apical pulse?

A

listen to the pulse with stethescope

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16
Q

what is a peripheral pulse

A

palpate or feel the pulse

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17
Q

what is eosin? what does it reveal?

A

an acidic dye that binds to positively charged molecules (cytoplasm, collagen, muscle fibers)

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18
Q

what is hemtoxyln dye? what does it reveal?

A

a basic dye that binds to negatively charged molecules. DNA/RNA. Hematoxylin and Eosin (H&E) are commonly used together

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19
Q

epidermis: composition, originates?

A

keratinized stratified squamous epithelium. originates from ectoderm

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20
Q

dermis: composition, originates?

A

composed of connective tissue, mesoderm

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21
Q

what are the layers of the dermis?

A

superficial: papillary layer, loose areolar connective tissue
deep: reticular layer, dense irregular connective tissue

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22
Q

what is connective tissue?

A

cells in an ECM

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23
Q

what is the ECM

A

ground substance and protein fibers

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24
Q

what are the types of connective tissue?

A

Specialized: Bone, cartilage, blood

Connective tissue proper:

dense: regular, irregular
loose: reticular, areolar, adipose

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25
Q

how do you calculate the incidence rate?

A

Incidence/sum of disease-FREE person time

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26
Q

what is disease free person time? how can it be measured?

A

the amount of time (in years) that each subject was without a disease. You can either add up the total years (most exact), you can average the number of people and multiply by years (500,000 people 1 yr), or you can average the number of years and multiply by people (100 people2.5 yrs)

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27
Q

what is the relationship between prevalence and incidence?

A

P=(incidence)(duration)

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28
Q

which AA is a precursor for heme?

A

Gly

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29
Q

how do you calculate nitrogen balance? what are the three nitrogen balance terms?

A

Nitrogen balance= Nitrogen consumed-nitrogen excreted

positive nitrogen balance, negative nitrogen balance, nitrogen equilibrium

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30
Q

what is cachexi? symptoms? treatment?

A

a hyper-catabolic state in which protein and AA (Gln) are degraded (negative nitrogen balance). Symptoms: weight loss, seen in cancer renal disease and burns.
Treat: anabolic steroids

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31
Q

what is Phenylkeonuria (PKU) caused by? (2)

A

lack of Phe Hydroxylase which results in no Tyr being formed OR a lack of phe hydroxylase cofactor (tetrahydrobiopterin)

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32
Q

why is PKU a problem. how can you treat it?

A

Tyr becomes essential AA, Phe metabolites accumulate (neurotoxic).
Treat: supplement Tyr, avoid Phe (artificial sweeteners)

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33
Q

what is the cause of homocystinuria? treatment?

A

Recall: Met gives rise to homocysteine. Homocysteine and Ser combine to form Cystathionine via Cystathionine Synthetase. Cystathionine is converted to Cys via cystathionase.

Homocystinura (an accumulation of homocystine) is caused by a defect in Cystathionine synthetase

Treat: decrease Met, supplement Cys

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34
Q

why is homocysteine accumulation bad?

A

disrupts collagen cross-linking (stroke, heart attack), Cys becomes essential

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35
Q

what is the cause of Acute lymphatic leukemia?

A

most common cause of childhood cancer! Asn not produced in WBCs due to a defect in Asn synthetase (Asp–>Asn via Asn Synthetase)

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36
Q

what is the treatment for Acute Lymphatic Leukemia

A

Provide body with L-Asparaginase which converts Asn to Asp. this will kill the defective cells as their only source (diet) of Asn will deplete

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37
Q

what is chemical score of a protein?

A

compares the AA content of a test protein to an egg protein. (CS=(mg AA/g test)/(mg AA/g egg protein))x100. The AA with the lowest % is reported as the CS of that protein

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38
Q

what is the protein digestivility corrected AA score?

A

similar to CS, but instead of egg use the requirement for a 2-5 yr old. then you multiply the lowest score (not percentage) by the protein digestibility. PDCAAS=((mg AA/g test)/(mg AA/g requirement))–>figure our which AA is the lowes–>multiply by digestibility

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39
Q

what is the biological value of a protein?

A

tells you how much of a protein is retained in the body

=(N diet-(N urine-N0 urine)-(N poop-N0 poop))/(Ndiet-(Npoop-N0 poop))

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40
Q

what is net protein utilization?

A

similar to BV but the denominator is only N diet

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41
Q

what is the protein efficiency ratio?

A

weight gain over a period/total weight of protein ingested over that period

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42
Q

how do you calculate protein digestibility?

A

(N diet-(Npoop-N0poop))/Ndiet

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43
Q

what are PEM disorders?

A

Protein Energy Metabolism Disorders

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44
Q

what are the two PEM disorders discussed?

A

Kwashiorkor disease:

Marasmus disease

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45
Q

what is Kwashiorkor disases?

A

PEM disorder caused by severe protein deficiency. Often seen when a second baby is born and the older child is no longer given breast milk (in developing countries)

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46
Q

what is marasmus disease?

A

PEM disorder. Protein-calorie malnutrition (less severe than kwashiorkor but with a more starved appearance)

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47
Q

what is an available vs. unavailable carb?

A

available: carb we can use (starch)
unavailable: carb we cant digest (cellulose)

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48
Q

what are the three main lipids in our diet?

A

sterols, phospholipids, gylcerides

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49
Q

what are the essential FAs?

A

omega 6 (linoleic acid) and omega 3 (linolenic acid)

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50
Q

what are the three behavior treatments related to classical conditioning?

A

aversive conditioning, systematic desensitization, exposure w/o learning incompatible response

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51
Q

what is the DRI? goal? what are the values?

A

Daily dietary reference intake for groups of people.
Goal is to prevent nutrient deficiencies AND prevent over-nutrition (RDA only prevents deficiencies)

Values; estimated average requirement, tolerable upper intake level, atequate intake

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52
Q

what is the estimated average requirement? EAR

A

requirements that meet needs of 50% of a group (this is the average in which RDA values are based)

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53
Q

what is the upper tolerable intake level?

A

UL: the highest nutrient intake w/o adverse effects

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54
Q

what is adequate intake?

A

somewhere between RDA and UL (amount to sustain good health)

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55
Q

what are four hormones that regulate appetite? they all act on what?

A

Leptin, orexin, PYY, ghrelin. all act on the hypothalamus

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56
Q

what is the role of leptin? produced? long or short term?

A

produced in SubQ adipose. decrease appetite, increases energy expenditure (increase lipid oxidation and lipolysis), long

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57
Q

what is role of ghrelin? produced? long or short?

A

stimulates appetite when you think about a meal and releases hormones. produced in stomach. short

58
Q

what is role of PYY? produced? long or short

A

produced in intestines. decrease appetite and slow movement of food in gut. short

59
Q

what is role of orexin? produced? long or short?

A

increase appetite, decrease REM, increase wakefulness. Produced in lateral pituitary. short

60
Q

define metabolic syndrome

A

a group of conditions (increase BP, increase visceral fat, increase cholesterol, increase glucose) that act together to increase risk of CVD, obesity and diabetes

61
Q

what is the role of white adipose tissue?

A

storage of triglycerides, insulate/protect body, endocrine fxn

62
Q

role of LPL and HSL?

A

LPL: stores FFAs in adipose
HSL: liberated FFAs from adipose

63
Q

what are adipokines?

A

endorcine hormones produced by adipocytes

64
Q

what are the main adipokines?

A

leptin, adiponectin, IL-6, angiotensinogen

65
Q

role of adiponectin, main site of production.

A

this is a good adipokine, anti-atherosclerotic, increases glucose uptake, insreases insulin sensitivity (breakdown of FFAs)

produced in visceral, decreased production in obesity

66
Q

role of IL-6, produced?

A

recurit macrophages, visceral

67
Q

role of angiotensinogen? produced

A

signals RAS to increase BP, visceral

68
Q

define obesity

A

a chronic low grade inflammatory state due to increased size of adipocytes and icreased macrophages

69
Q

describe adipose dysfuncrion

A

a hyper-secretory state of adipose tissue caused by increased visceral adipose tissue.

70
Q

what occurs as adipocytes enlarge?

A

Increase release of bad adipokines–>release FFAs–>recruit macrophages–>macrophages invade and release TNF-a–>TNF-A increases FFAs, cylce repeats.

71
Q

Insulin nomrally suppresses what?

A

inhibits FFA release (inhibit HSL) and promotes FFA storage (promotes LPL)

72
Q

Insulin is suppressed by what?

A

FFAs, TNF-alpha

73
Q

what is the RQ of carbs, protien, lipids?

A

carbs: 1.0
protein: 0.8
lipids: 0.7

74
Q

what is BMR (basal metabolic rate) for men and women?

A

men: 1.0 kcal/hour/kg
women: 0.9 kcal/hour/kg

75
Q

what is active form of Vit D? how is it produced?

A

Calcitriol. Pro-vitamin activated with light to form Vit D3. Vit D3 undergoes two hydroxylation events (in liver then in kidney) an form calcitrol. Vitamin D3 also obtained from diet.

76
Q

what is the role of calcitrol

A

stimulated by PTH to increase Ca absorption in intestines

77
Q

how does Vit D defic manifest in adults? kids?

A

adults: osteoporosis
kids: rickets

78
Q

Vit D toxicity?

A

hypercalemia, calcium deposits in heart and kidney

79
Q

Vitamin A active forms?

A

Retinol, retinoic acid

80
Q

fxns 2, of Vit A

A

Retinol: visoin

retinoic acid: gene expression–>proliferation and differentiation

81
Q

Vit A def conditions (3)?

A

Night blindness, skin lesions, Xerophthalmia: blindness (gross eye abnormalities)

82
Q

how does retinol work?

A

trans retinal binds opsin (forming rhodopsin complex), when light strikes retinol it becomes all cis

83
Q

Vitamin E fxn:

A

anti-oxidant for PUFA, no major fxn. often used in lotions and oils to increase shelf life

84
Q

Vit K funciton

A

coagulation and bone growth

85
Q

how does Vit K work?

A

important cofactor for carboxylation reactions. once carboxylated, the proteins bind calcium

86
Q

What is VKDB

A

Vit K deficiency bleeding: seen in newborns with sterile guts

87
Q

where is VIt K obtained?

A

gut bacteria (50%), diet (50%)

88
Q

B1 AKA

A

Thiamin

89
Q

B2 AKA

A

Riboflavin

90
Q

B3 AKA

A

Niacin

91
Q

B7 AKA

A

Biotin

92
Q

B9 AKA

A

Folic Acid

93
Q

What are teh B vitamins?

A

B1, B2, B3, B5, B6, B7, B9, B12

94
Q

what is the active from of B1

A

TPP

95
Q

fuxn of thiamin?

A

B1: important cofactor for metabolic enzymes (PDH complex, PP pathway)

96
Q

thiamin def should be correlated with…

A

Berberi Disease (decrease in NS fxn)

97
Q

Riboflavin function?

A

B2: converted to FAD and FMN (easily destroyed by light (conjugated))

98
Q

Function of Niacin

A

B3: converted to NAD and NADP (can be made from Try)

99
Q

Niacin Defic

A

Pellegra: 3 D’s: dermatitis, dementia, diarrhea

100
Q

B5 fxn

A

CoA precursor

101
Q

B6 important role?

A

PLP is a coenzyme for >100 enzymes. W/o B6 all AA essential

102
Q

Biotin role?

A

B7: conenzyme in carboxylation reactions (pyruvate carboxylase, propionyl-CoA carboxylase)

103
Q

Folic acid role?

A

B9, functions in single carbon transfer reactions (AA, purine, thymidine synthesis)

104
Q

B12 role

A

Met (coenzyme for Met synthetase), needs Tranport (IF) to get into blood

105
Q

Vitamin C AKA

A

ascorbic acid

106
Q

Ascorbic Acid role

A

anti-oxidant, aids in hydroxylaiton (important in collagen)

107
Q

Vit C def?

A

scurvy: failure to cross-link collagen

108
Q

Important vitamins?

A

Zn, Fe, Se, I

109
Q

importance of Zn

A

essential in fxn of enzymes and TFs

110
Q

importance of Se

A

forms selenoproteins that play a role in preventing oxidative damage, disulfide bond homeostasis and thyroid hormone metabolism

111
Q

Se defic?

A

Keshan Disease

112
Q

Arsenate Poisoning

A

“ate Pi” Arsenate is incorporated with G3P instead of Pi causing a loss of 1,3BPG and therefore a loss of ATP (1,3BPG–>3 PG produces ATP)

113
Q

Aresnite Poisoning

A

PDH complex is inhibited, pyruvate accumulates

114
Q

Lactic acidosis? cause?

A

buildup of lactate that decreases pH. can be caused by lack of O2, Pyruvate buildup, increase in NADH/NAD ratio

115
Q

What is Chronic Hemolytic Anemia? what are two causes

A

Anemia cuased by excessive hemolysis. Seen in G6PD and PK deficiency of RBCs (causes morphology changes that and hemolysis by spleen)

116
Q

what occurs in Pyruvate Carboxylase Defic?

A

pyruvate accumulates (lactic acidosis), hypoglycemia, decrease in myelin sheath, decrease in neurotransmitter. Mainly due to a decrease in oxaloacetate being produced, an important precursor in many reactions

117
Q

how can you treat PC defic? (3)

A

biotin, glucose, citrate

118
Q

PDH Defic results in?

A

lactic acidosis, decrease Acetyl-CoA, decreased ATP

119
Q

how does dichloroacetate treat PDH defic?

A

inhibits the kinase that deactivates PDH

120
Q

What does CN poisoning do?

A

blocks complex IV of ETC (binds iron), massive lactic acidosis

121
Q

what does rhodanase do?

A

liver enzyme that detoxifies CN in our diet

122
Q

what does MERRF stand for

A

Myoclonic Epilepsy and Ragged Red Fiber Disease

123
Q

MERRF cause? presents as?

A

mtDNA mutation DNA that codes for tRNALys. Muscle twitching, clumps of diseased mito appear (stain red)

124
Q

Leber’s Optin Neuropathy cause? symptoms?

A

mutation in complex I of ETC. Acute blindness due to degeneration of optic nerve

125
Q

Leber’s Optic Neuropathy treatment

A

Idebenone: bypass Complex I of ETC

126
Q

MCAD Defic cause? results in? triggered?

A

cant break down MCFA. results in hypoketonic, hypoglycemic. tirggered by prolonged fasting.

127
Q

MCAD treatment

A

avoid fasting, high carb dier

128
Q

CPT II defic

A

CPT II transports FA into mito. Rhabdomylosis: muscle breakdown and release of Mb

129
Q

Jamaican Vomiting Syndrome. Cause? effect?

A

eating unripe akee fruit. produces MCPA which inhibits FA oxidation

130
Q

Propionly CoA Carboxylase Def cause? result?

A

cant break down odd chain FA. organic acidemia

131
Q

Peroxisomes breakdown what 2 FAs?

A

VLCFA, branched FA

132
Q

why is accumulation of VLCFA and Branched FA bad?

A

neurotoxic

133
Q

X-linked adrenoleukodystrophy cause?

A

cant transport VLCFA

134
Q

Zellweger syndrome cause

A

no peroxisomes produced

135
Q

Adult refsum disease

A

branched FA accumulates due to loss of alpha-oxidation

136
Q

how is nitrogen removed from AA?

A
  1. Amino transferase move amino from AA to alpha-ketogluterate to form Glu
  2. Glu can either give up the ammonia or make other AA
  3. Ammonia is carried by Ala or Gln in the blood
  4. LIver detoxifies Ammonia into urea using urea cycle (5 enzymes, 3ATP)
137
Q

what is hyperammonemia? why is it bad? cause?

A

Increased blood ammonia, bad because ammonia can cross blood-brain barrier and cause coma/death, caused by liver defect

138
Q

Congenital Hyperammonemia: cause? occurs when?

A

defective urea cycle enzyme (present at birth). the earlier enzymes will have a greater impact (CPSI). occurs after birth becuase urea cycle not present in utero

139
Q

Acquired heyperammonemia: cause

A

liver damage (alcoholic, hep, fatty liver disease)

140
Q

what is hepatic encephalopathy

A

loss of brain fxn as a result of liver damage. Seen in half of individuals with acquired liver damage

141
Q

what are some treatments (2) for hyperammonemia?

A

decrease protein (supplement essential AA), find alternate pathway (Na Benzoate or Na Phenylbutyrate can comples with AA and make them readily excreted)

Foundations 1 (65 decks)

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