Week 3 Problem Concepts Flashcards Preview

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Flashcards in Week 3 Problem Concepts Deck (141):
1

Fxn and Location of Simple Squamous Epithelium

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

2

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

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

3

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

Function: absorption
location: GI tract

4

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

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

5

function and location of stratified squamous epithelium

Protection

Skin (keratinized), vagina, oral cavity, esophagus

6

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

Protection and conduit

large ducts exocrine glands, anorectal jxn

7

function and location of transitional epithelium

distension

bladder

8

holocrine secretions

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

9

apocrine secretions

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

10

merocrine secretions

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

11

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

multicellular, simple coiled tubular (serous secretions)

12

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

multicellular, simple tubular, mucus secretions

13

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

mutlicelllar, compound acinar, serous secretions

14

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

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

15

what is an apical pulse?

listen to the pulse with stethescope

16

what is a peripheral pulse

palpate or feel the pulse

17

what is eosin? what does it reveal?

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

18

what is hemtoxyln dye? what does it reveal?

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

19

epidermis: composition, originates?

keratinized stratified squamous epithelium. originates from ectoderm

20

dermis: composition, originates?

composed of connective tissue, mesoderm

21

what are the layers of the dermis?

superficial: papillary layer, loose areolar connective tissue

deep: reticular layer, dense irregular connective tissue

22

what is connective tissue?

cells in an ECM

23

what is the ECM

ground substance and protein fibers

24

what are the types of connective tissue?

Specialized: Bone, cartilage, blood

Connective tissue proper:
dense: regular, irregular
loose: reticular, areolar, adipose

25

how do you calculate the incidence rate?

Incidence/sum of disease-FREE person time

26

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

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 people*2.5 yrs)

27

what is the relationship between prevalence and incidence?

P=(incidence)(duration)

28

which AA is a precursor for heme?

Gly

29

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

Nitrogen balance= Nitrogen consumed-nitrogen excreted

positive nitrogen balance, negative nitrogen balance, nitrogen equilibrium

30

what is cachexi? symptoms? treatment?

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

31

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

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

32

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

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

33

what is the cause of homocystinuria? treatment?

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

34

why is homocysteine accumulation bad?

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

35

what is the cause of Acute lymphatic leukemia?

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

36

what is the treatment for Acute Lymphatic Leukemia

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

37

what is chemical score of a protein?

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

38

what is the protein digestivility corrected AA score?

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

39

what is the biological value of a protein?

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))

40

what is net protein utilization?

similar to BV but the denominator is only N diet

41

what is the protein efficiency ratio?

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

42

how do you calculate protein digestibility?

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

43

what are PEM disorders?

Protein Energy Metabolism Disorders

44

what are the two PEM disorders discussed?

Kwashiorkor disease:

Marasmus disease

45

what is Kwashiorkor disases?

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)

46

what is marasmus disease?

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

47

what is an available vs. unavailable carb?

available: carb we can use (starch)

unavailable: carb we cant digest (cellulose)

48

what are the three main lipids in our diet?

sterols, phospholipids, gylcerides

49

what are the essential FAs?

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

50

what are the three behavior treatments related to classical conditioning?

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

51

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

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

52

what is the estimated average requirement? EAR

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

53

what is the upper tolerable intake level?

UL: the highest nutrient intake w/o adverse effects

54

what is adequate intake?

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

55

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

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

56

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

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

57

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

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

58

what is role of PYY? produced? long or short

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

59

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

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

60

define metabolic syndrome

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

what is the role of white adipose tissue?

storage of triglycerides, insulate/protect body, endocrine fxn

62

role of LPL and HSL?

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

63

what are adipokines?

endorcine hormones produced by adipocytes

64

what are the main adipokines?

leptin, adiponectin, IL-6, angiotensinogen

65

role of adiponectin, main site of production.

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

produced in visceral, decreased production in obesity

66

role of IL-6, produced?

recurit macrophages, visceral

67

role of angiotensinogen? produced

signals RAS to increase BP, visceral

68

define obesity

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

69

describe adipose dysfuncrion

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

70

what occurs as adipocytes enlarge?

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

71

Insulin nomrally suppresses what?

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

72

Insulin is suppressed by what?

FFAs, TNF-alpha

73

what is the RQ of carbs, protien, lipids?

carbs: 1.0
protein: 0.8
lipids: 0.7

74

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

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

75

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

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

what is the role of calcitrol

stimulated by PTH to increase Ca absorption in intestines

77

how does Vit D defic manifest in adults? kids?

adults: osteoporosis
kids: rickets

78

Vit D toxicity?

hypercalemia, calcium deposits in heart and kidney

79

Vitamin A active forms?

Retinol, retinoic acid

80

fxns 2, of Vit A

Retinol: visoin
retinoic acid: gene expression-->proliferation and differentiation

81

Vit A def conditions (3)?

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

82

how does retinol work?

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

83

Vitamin E fxn:

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

84

Vit K funciton

coagulation and bone growth

85

how does Vit K work?

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

86

What is VKDB

Vit K deficiency bleeding: seen in newborns with sterile guts

87

where is VIt K obtained?

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

88

B1 AKA

Thiamin

89

B2 AKA

Riboflavin

90

B3 AKA

Niacin

91

B7 AKA

Biotin

92

B9 AKA

Folic Acid

93

What are teh B vitamins?

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

94

what is the active from of B1

TPP

95

fuxn of thiamin?

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

96

thiamin def should be correlated with...

Berberi Disease (decrease in NS fxn)

97

Riboflavin function?

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

98

Function of Niacin

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

99

Niacin Defic

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

100

B5 fxn

CoA precursor

101

B6 important role?

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

102

Biotin role?

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

103

Folic acid role?

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

104

B12 role

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

105

Vitamin C AKA

ascorbic acid

106

Ascorbic Acid role

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

107

Vit C def?

scurvy: failure to cross-link collagen

108

Important vitamins?

Zn, Fe, Se, I

109

importance of Zn

essential in fxn of enzymes and TFs

110

importance of Se

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

111

Se defic?

Keshan Disease

112

Arsenate Poisoning

"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

Aresnite Poisoning

PDH complex is inhibited, pyruvate accumulates

114

Lactic acidosis? cause?

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

115

What is Chronic Hemolytic Anemia? what are two causes

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

116

what occurs in Pyruvate Carboxylase Defic?

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

how can you treat PC defic? (3)

biotin, glucose, citrate

118

PDH Defic results in?

lactic acidosis, decrease Acetyl-CoA, decreased ATP

119

how does dichloroacetate treat PDH defic?

inhibits the kinase that deactivates PDH

120

What does CN poisoning do?

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

121

what does rhodanase do?

liver enzyme that detoxifies CN in our diet

122

what does MERRF stand for

Myoclonic Epilepsy and Ragged Red Fiber Disease

123

MERRF cause? presents as?

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

124

Leber's Optin Neuropathy cause? symptoms?

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

125

Leber's Optic Neuropathy treatment

Idebenone: bypass Complex I of ETC

126

MCAD Defic cause? results in? triggered?

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

127

MCAD treatment

avoid fasting, high carb dier

128

CPT II defic

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

129

Jamaican Vomiting Syndrome. Cause? effect?

eating unripe akee fruit. produces MCPA which inhibits FA oxidation

130

Propionly CoA Carboxylase Def cause? result?

cant break down odd chain FA. organic acidemia

131

Peroxisomes breakdown what 2 FAs?

VLCFA, branched FA

132

why is accumulation of VLCFA and Branched FA bad?

neurotoxic

133

X-linked adrenoleukodystrophy cause?

cant transport VLCFA

134

Zellweger syndrome cause

no peroxisomes produced

135

Adult refsum disease

branched FA accumulates due to loss of alpha-oxidation

136

how is nitrogen removed from AA?

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

what is hyperammonemia? why is it bad? cause?

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

138

Congenital Hyperammonemia: cause? occurs when?

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

Acquired heyperammonemia: cause

liver damage (alcoholic, hep, fatty liver disease)

140

what is hepatic encephalopathy

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

141

what are some treatments (2) for hyperammonemia?

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

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