Brainscape's Knowledge GenomeTM

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


See full index

Rapid Review Pathology > Chapter 8 - Nutritional Disorders > Flashcards

Chapter 8 - Nutritional Disorders Flashcards

0
Q

What is the most important factor determining the daily energy expenditure?

A

BMR most important factor determining DEE

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

Define recommended dietary allowance.

A

RDA: optimal dietary intake of nutrients for good health

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

What does BMR energy support?

A

BMR energy supports involuntary activities

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

What controls the BMR?

A

Thyroid hormones control the BMR

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

What is the most important factor affecting the BMR?

A

Lean body mass most important factor affecting BMR

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

How is the BMR affected in thyroid disorders?

A

BMR: ↓hypothyroidism, ↑hyperthyroidism

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

What is the thermic effect of foods?

A

Thermic effect of foods: energy expended in response to eating a meal

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

What do mature RBCs only use for fuel?

A

Mature RBCs only use glucose for fuel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where does CHO digestion begin? How much energy is produced by complete oxidation of glucose?

A

CHO digestion: begins in the mouth; 4 kcal/g

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does amylase do?

A

Amylase breaks down polysaccharides → disaccharides (lactose, maltose, sucrose)

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

What are the disaccharidases?

A

Disaccharidases: lactase, maltase, sucrase

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

What are the substrates and products of the disaccharidases?

A

Lactase converts lactose to galactose + glucose
Maltase converts maltose to two glucoses
Sucrase converts sucrose to fructose + glucose

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

What do the disaccharidases produce?

A

Disaccharidases: produce glucose, galactose, fructose

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

Amino acids are substrates for what?

A

AAs: substrates for gluconeogenesis

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

What do transaminases do?

A

Transaminases remove amine groups from AAs to produce an α-ketoacid

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

Describe the reactions performed by AST and ALT.

A

AST converts alanine to pyruvate; ALT converts aspartate to OAA

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

Where does protein digestion begin?

A

Protein digestion begins in stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does HCl digest protein?

A

HCl cleaves pepsinogen into pepsin

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

What does pepsin do?

A

Pepsin cleaves proteins into polypeptides

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

What do pancreatic proteases do?

A

Pancreatic proteases hydrolyze polypeptides to release AAs

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

What do AAs require for reabsorption?

A

AAs require functioning villi for reabsorption

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

What is a triglyceride?

A

TG major dietary lipid

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

FAs are the major energy source for what tissues?

A

FAs major energy source for all tissues except RBCs and brain

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

What are two plant sources of monosaturated fats?

A

Monounsaturated fats: olive oil, canola oil

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

What are two plant sources of polysaturated fats?

A

Polyunsaturated fats: soybean oil and corn oil

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

What are two plant sources of saturated fats?

A

Saturated fats: coconut oil, palm oil

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

Animal fats from adipose are what?

A

Animal fats from adipose are saturated

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

Animal fats from muscles/organs are what?

A

Animal fats from muscle/organs are polyunsaturated and monounsaturated

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

Name two essential fatty acids.

A

Essential FAs: linolenic (ω-3), linoleic (ω-6)

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

What is linoleic acid (ω-6) is required for?

A

Linoleic acid (ω-6) is required for arachidonic acid synthesis

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

What are the clinical findings associated with essential fatty acid deficiency?

A

↓Essential FAs: scaly dermatitis, hair loss, poor wound healing

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

Where does fat digestion begin?

A

Fat digestion begins in small intestine

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

What does pancreatic lipase do?

A

Pancreatic lipase hydrolyzes TGs to MGs and FAs

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

What do bile salts do?

A

Bile salts form micelles containing MGs, FAs, fat-soluble vitamins, CH esters

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

What does malabsorption of fats result in?

A

Malabsorption of fats produces fat soluble–vitamin deficiencies

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

Describe the process of fat digestion.

A

Fat digestion: pancreatic enzymes → bile salts/acids → intestinal cells (chylomicrons)

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

Describe the formation of chylomicrons.

A

Intestinal cells package resynthesized TG into chylomicrons

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

What is ApoB48 required for?

A

ApoB48 required for formation/secretion chylomicrons

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

What do chylomicrons contain?

A

Chylomicrons contain diet-derived TGs

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

How much energy does complete oxidation of FAs produce?

A

Complete oxidation FAs produces 9 kcal/g

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

Malnutrition best correlates with what?

A

Malnutrition correlates best with BMI

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

What is the BMI equation?

A

BMI = weight in kg/height in m2

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

What is protein-energy malnutrition defined as?

A

PEM is defined as a BMI <16 kg/m2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How are body fat stores evaluated?

A

Body fat stores: skinfold thickness, density, conductivity, DEXA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How are somatic protein stores in skeletal muscle evaluated?

A

Somatic protein stores in skeletal muscle evaluated with mid-arm circumference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How are visceral protein stores evaluated?

A

Visceral protein stores evaluated with serum albumin/transferrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is kwashiorkor?

A

Kwashiorkor: CHO intake > protein intake; total calories normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How are visceral protein stores affected in kwashiorkor?

A

↓Visceral protein; ↓serum albumin/transferrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What does excess carbohydrate intake spare in kwashiorkor?

A

Excess CHO intake spares protein breakdown as energy source

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How is plasma oncotic pressure affected in kwashiorkor? What clinical findings result from this effect?

A

Pitting edema/ascites characteristic of kwashiorkor; ↓plasma oncotic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How are apoB and VLDL levels affected in kwashiorkor? These changes result in what clinical finding?

A

Fatty liver due to ↓apoB synthesis and ↑VLDL synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the cause of diarrhea in kwashiorkor?

A

Diarrhea: loss of villi/disaccharidases; parasitic infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe the features of the anemia present in kwashiorkor.

A

Anemia multifactorial: RBC hypoplasia; iron/folic acid/vitamin B12 deficiencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe the cutaneous changes in kwashiorkor.

A

Flaky paint dermatitis; flag sign in hair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe how the immune system is affected in kwashiorkor.

A

Defective CMI: parasitic infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Describe the psychological disturbances in kwashiorkor.

A

Poor prognosis due to apathy, listlessness, and lack of appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is marasmus?

A

Marasmus: total calorie deprivation; ↓protein/CHOs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is common in marasmus?

A

Extreme muscle wasting is common in marasmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How are fat stores affected in marasmus?

A

Loss subcutaneous fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Secondary PEM is most common in whom?

A

2° PEM is most common in the elderly population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the clinical findings in secondary PEM?

A

Depletion subcutaneous fat/skeletal muscle; ankle/sacral edema; multiple nutrient deficiencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is anorexia nervosa?

A

Anorexia nervosa: self-induced starvation; 2° PEM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How do patients with anorexia nervosa view themselves?

A

Distorted body image

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How does the death rate compare to that of other psychiatric disorders?

A

Highest death rate among all psychiatric disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Use of what is common in anorexia nervosa?

A

Laxative abuse common; danger of laxative bowel and hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Who is affected by anorexia nervosa?

A

MC in teenage girls and young women

Common in athletics, modeling, ballet; history of sexual abuse common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How are GnRH levels affected in anorexia nervosa? What results from this effect?

A

2° Amenorrhea due to ↓GnRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How are FSH, LH, and estradiol levels affected in anorexia nervosa?

A

↓FSH, LH, estradiol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How is the bone affected in anorexia nervosa?

A

Osteoporosis due to hypoestrinism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is euthyroid sick syndrome?

A

Euthyroid sick syndrome: bradycardia, hypotension, cold intolerance, skin/nail changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the cardiovascular findings in anorexia nervosa?

A

Peripheral edema; ↑risk cardiac arrhythmias, sudden death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the laboratory findings in anorexia nervosa?

A

↓Serum GnRH, estradiol, FSH, LH

↑Growth hormone, cortisol (stress hormones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the most common cause of death in patients with anorexia nervosa?

A

MCC death is ventricular arrhythmia due to hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is bulimia nervosa?

A

Bulimia nervosa: bingeing with self-induced vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the epidemiology of bulimia nervosa?

A

Female dominant; more common than anorexia nervosa

75
Q

What are the complications of vomiting in bulimia nervosa?

A

Eroded enamel, parotid/salivary gland swelling; hematemesis (tear/rupture distal esophagus)

76
Q

What are the electrolyte abnormalities from vomiting in bulimia nervosa?

A

Vomiting: hyponatremia/hypokalemia; metabolic alkalosis

77
Q

What are the electrolyte abnormalities from laxative abuse in bulimia nervosa?

A

Laxative abuse: hyponatremia/hypokalemia; metabolic acidosis; hypomagnesemia, hypocalcemia

78
Q

What is the most common cause of death in patients with bulimia nervosa?

A

MCC death is ventricular arrhythmia due to hypokalemia

79
Q

How is obesity defined?

A

Obesity = BMI >30 kg/m2

80
Q

Describe the prevalence of obesity in terms of age.

A

Prevalence increases with age; declines after sixth decade

81
Q

Obesity is an independent risk factor for what?

A

Independent risk factor for ischemic heart disease

82
Q

Obesity is a major preventable cause of what in the U.S.?

A

Major preventable cause of death/disability in United States

83
Q

What are the cutaneous findings in anorexia nervosa?

A

Dry skin, brittle nails, sparse scalp hair, ↑lanugo hair on face, yellow skin (↑carotene)

84
Q

What is the most important risk factor for morbidity/mortality from obesity?

A

Abdominal visceral fat most important risk factor for morbidity/mortality

85
Q

What are the key hypothalamic centers?

A

Key hypothalamic centers: arcuate nucleus, paraventricular nuclei

86
Q

What is leptin? What is the effect of increased leptin levels?

A

Leptin: hormone secreted by adipose ↑Leptin → ↓food intake, ↑energy expenditure

87
Q

What is ghrelin? What is the effect of increased ghrelin levels?

A

Ghrelin: hormone secreted by stomach

↑Ghrelin → ↑food intake, ↓energy expenditure

88
Q

What is the effect of decreased or dysfunction of leptin?

A

↓/dysfunction leptin: ghrelin unopposed (↑appetite, ↓energy expenditure)

89
Q

What is the effect of insulin on TGs?

A

Insulin normally increases TG in adipose

90
Q

How are insulin levels and TGs stores affected in type II DM?

A

Type 2 DM: hyperinsulinemia ↑TG stores in adipose

91
Q

What is reabsorption of fat-soluble vitamins associated with?

A

Reabsorption of fat-soluble vitamins is associated with micelle formation for reabsorption of fats

92
Q

How does malabsorption of fat affect vitamin levels?

A

Malabsorption of fat leads to fat-soluble vitamin deficiencies

93
Q

Vitamin toxicities are more common with what vitamins?

A

Vitamin toxicities: fat-soluble > water-soluble

94
Q

What are the water-soluble vitamins used for?

A

Water-soluble vitamins cofactors for enzyme reactions (except folic acid)

95
Q

What are the clinical findings in β-carotenemia?

A

β-carotenemia: yellow skin, white sclera

96
Q

Where is the main storage site for vitamin A and how is it stored?

A

Liver is main storage site; stored as retinyl esters

97
Q

Why is retinoic acid important?

A

Retinoic acid: important in differentiation of epithelial tissue; growth/reproduction

98
Q

What is retinal and why is it important?

A

Oxidation product of retinol → used to synthesize rhodopsin → important in reduced light

99
Q

What are the functions of vitamin A?

A

Normal vision in reduced light (night vision)
Differentiation of mucus-secreting epithelium
Stimulates immune system
Stimulates growth/reproduction

100
Q

What are the causes of vitamin A deficiency?

A

Deficiency: diet lacking yellow/green vegetables; fat malabsorption

101
Q

What are the causes of vitamin A toxicity?

A

Toxicity: consuming liver from polar bears, whales, sharks, tuna
Toxicity: megadoses of vitamin A and Rx of acne with isotretinoin

102
Q

What are the clinical uses of vitamin A?

A

Clinical Rx: acne, APL, measles, hairy leukoplakia, retinitis pigmentosa

103
Q

What is preformed vitamin D in plants called and what is it converted to?

A

Ergocalciferol (plants) → cholecalciferol (vitamin D3)

104
Q

Describe the endogenous synthesis of vitamin D in the skin.

A

Photoconversion 7-dehydrocholesterol → cholecalciferol; 90% endogenously derived vitamin D

105
Q

Where does 25-hydroxylation of vitamin D occur? What enzyme performs this reaction?

A

25-Hydroxylation in the liver CYP-450 system

106
Q

What does PTH synthesize?

A

PTH synthesizes 1-α-hydroxylase in proximal tubules

107
Q

Where does 1-α-hydroxylation of vitamin D occur?

A

1-α-Hydroxylation in proximal tubules

108
Q

What is the active form of vitamin D?

A

1,25-(OH)2-D: active form of vitamin D

109
Q

What mediates feedback control of calcitriol synthesis?

A

Feedback control of calcitriol synthesis is calcium-mediated

110
Q

Describe the effect of decreased serum calcium on calcitriol synthesis.

A

↓Serum Ca2+ → ↑synthesis PTH → ↑synthesis 1-α-OHase → ↑synthesis calcitriol

111
Q

Describe the effect of increased serum calcium on calcitriol synthesis.

A

↑Serum Ca2+ → ↓synthesis PTH → ↓synthesis 1-α-OHase → ↓synthesis calcitriol

112
Q

What are the functions of calcitriol?

A

Calcitriol: bone mineralization; maintain serum Ca2+/PO43−
Calcitriol: stimulates macrophage stem cell conversion → osteoclasts

113
Q

Where are vitamin D receptors located?

A

Vitamin D receptors on osteoblasts/chondrocytes

114
Q

What does alkaline phosphatase do?

A

Alkaline phosphatase dephosphorylates pyrophosphate, an inhibitor of bone mineralization

115
Q

What is osteocalcin?

A

Osteocalcin is calcium-binding protein; important in bone mineralization

116
Q

What is the most common cause of vitamin D deficiency?

A

Renal failure MCC vitamin D deficiency

117
Q

What is the effect of inadequate sun exposure on vitamin D levels?

A

Inadequate sun exposure → ↓photoconversion to vitamin D3

118
Q

What is the effect of fat malabsorption on vitamin D levels?

A

Fat malabsorption → ↓micelle formation → ↓vitamin D/fat reabsorption

119
Q

What is the effect of chronic liver disease on vitamin D levels?

A

Chronic liver disease→↓25-hydroxylation

120
Q

What is the effect of induction of the liver CYP-450 system on vitamin D levels?

A

Induction liver CYP-450 system → ↑metabolism 25-(OH)-D → inactive metabolite

121
Q

What are two causes of vitamin D toxicity?

A

Toxicity: megadoses, sarcoidosis

122
Q

What are the functions of vitamin E?

A

Vitamin E: cell membrane antioxidant; prevents LDL oxidation

123
Q

What are the causes of vitamin E deficiency?

A

Vitamin E deficiency: fat malabsorption cystic fibrosis, abetalipoproteinemia

124
Q

What is a cause of vitamin E toxicity?

A

Vitamin E toxicity: megadoses vitamin E

125
Q

The majority of vitamin K is synthesized by what?

A

Vitamin K: majority synthesized by colonic bacteria

126
Q

What enzyme activates vitamin K?

A

Epoxide reductase activates vitamin K

127
Q

What enzyme is inhibited by coumarin derivatives?

A

Coumarin derivatives inhibit epoxide reductase

128
Q

What does vitamin K do?

A

Vitamin K: γ-carboxylates II, VII, IX, X; protein C and S

γ-Carboxylation activates vitamin K–dependent factors; allows them to bind calcium in fibrin clot formation

129
Q

What is the most common cause of vitamin K deficiency in a hospitalized patient?

A

Broad-spectrum antibiotics: MCC vitamin K deficiency in hospital

130
Q

When does bacterial colonization of the newborn bowel occur?

A

Newborns: lack bacterial colonization bowel until 5–6 days old

131
Q

How are newborns treated for vitamin K deficiency?

A

Newborns must receive IM injection of vitamin K

132
Q

Which fat-soluble vitamin is lacking in breast milk?

A

Breast milk lacks vitamin K

133
Q

How do coumarin derivatives and cirrhosis affect vitamin K activation?

A

Coumarin derivatives/cirrhosis decrease epoxide reductase

134
Q

What is the effect of fat malabsorption on vitamin levels?

A

Fat malabsorption ↓intestinal reabsorption fat-soluble vitamins

135
Q

What is thiamine important in?

A

Thiamine: important in ATP synthesis

136
Q

What are the functions of thiamine?

A

Thiamine: pyruvate dehydrogenase converts pyruvate to acetyl CoA
Thiamine: transketolase reactions

137
Q

What is the most common cause of thiamine deficiency in the U.S.?

A

Chronic alcoholism MCC thiamine deficiency in United States

138
Q

What is FAD used for?

A

FAD is cofactor for succinate dehydrogenase conversion of succinate to fumarate in CAC

139
Q

Where is FMN located and what is it important in?

A

FMN in ETC; important in ATP synthesis

140
Q

What are the active forms of niacin?

A

Niacin: NAD/NADP cofactors in oxidation-reduction reactions

141
Q

What type of reactions does NAD+ participate in?

A

NAD+ oxidation-reduction reactions are catabolic

142
Q

What type of reactions does NADP+ participate in?

A

NADP+ oxidation-reduction reactions are anabolic

143
Q

Corn-based diets are deficient in what?

A

Corn-based diets: deficient in tryptophan and niacin

144
Q

Tryptophan is used to synthesize what?

A

Tryptophan used to synthesize niacin/serotonin

145
Q

What are the causes of tryptophan deficiency?

A

Tryptophan deficiency: corn-based diet, Hartnup disease, carcinoid syndrome

146
Q

What are the three Ds of pellagra?

A

Three Ds of pellagra: dermatitis, diarrhea, dementia

147
Q

What are the functions of pyridoxine?

A

Pyridoxine: heme synthesis, transamination, neurotransmitters

148
Q

What are the causes of pyridoxine deficiency?

A

Pyridoxine deficiency: isoniazid (MCC), goat milk, chronic alcoholism

149
Q

What is the function of biotin?

A

Biotin: cofactor in carboxylase reactions

150
Q

Give two examples of carboxylation reactions.

A

Carboxylase reactions: pyruvate to OAA, propionyl CoA to methylmalonyl CoA

151
Q

What are the causes of biotin deficiency?

A

Biotin deficiency: eating raw eggs; antibiotics

152
Q

What are the sources of vitamin C?

A

Present in fruits/vegetables, liver, fish, milk

153
Q

What does vitamin C do?

A

Hydroxylates proline and lysine in RER of fibroblasts

154
Q

What does lysyl oxidase do?

A

Lysyl oxidase forms cross-links between hydroxylation sites on tropocollagen

155
Q

What is responsible for the tensile strength of collagen?

A

Cross-linking tropocollagen molecules increases tensile strength

156
Q

What is scurvy?

A

Scurvy: weak tensile strength of collagen; hemorrhage, poor wound healing
Scurvy: ↓synthesis structurally weak osteoid in bone; bone fragility, joint pain

157
Q

Describe the antioxidant properties of vitamin C.

A

Antioxidant: neutralizes hydroxyl FRs, regenerates vitamin E

158
Q

What does vitamin C do to iron?

A

Reduces nonheme iron (Fe3+) to heme iron (Fe2+)

159
Q

What is the heme iron state necessary for?

A

Heme iron (Fe2+) state: necessary for duodenal reabsorption; binds O2 in RBCs

160
Q

How does vitamin C affect tetrahydrofolate?

A

Keeps tetrahydrofolate (FH4) in reduced state; carrier for single-carbon functional groups

161
Q

What is the role of vitamin C in catecholamine synthesis?

A

Ascorbic acid: cofactor in conversion of dopamine to norepinephrine

162
Q

What are the causes of vitamin C deficiency?

A

Deficiency: diets lacking fruits/vegetables, smoking

163
Q

What is zinc a cofactor for?

A

Cofactor for metalloenzymes (e.g., collagenase)

164
Q

Why is zinc important in children?

A

Children: growth, spermatogenesis

165
Q

What are the causes of zinc deficiency?

A

Deficiency: alcoholism, diabetes, chronic diarrhea, acrodermatitis enteropathica

166
Q

What are the functions of copper?

A

Cofactor for ferroxidase, lysyl oxidase, tyrosinase

167
Q

What is the most common cause of copper deficiency?

A

MCC deficiency: TPN

168
Q

What is Wilson disease?

A

Wilson disease: defect in copper elimination in bile; ↓ceruloplasmin (binding protein)

169
Q

What are the clinical findings in Wilson disease?

A

Wilson disease: liver disease, Kayser-Fleischer ring, parkinsonism, dementia

170
Q

What are the lab findings in Wilson disease?

A

↓Total serum copper, ceruloplasmin; ↑serum/urine free copper

171
Q

What is the function of iodine?

A

Iodine used to synthesize thyroid hormone

172
Q

What is the cause of iodine deficiency?

A

Deficiency: ↓intake iodized table salt

173
Q

What are the functions of chromium?

A

Component of glucose tolerance factor to maintain normal serum glucose
Cofactor for insulin: facilitates binding of glucose to muscle/adipose

174
Q

Chromium deficiency is most often due to what?

A

Deficiency most often due to TPN

175
Q

What is the function of selenium?

A

Selenium is an antioxidant

176
Q

Selenium deficiency is most often due to what?

A

Deficiency usually due to TPN

177
Q

What are the functions of fluoride?

A

Functions: part of calcium hydroxyapatite in bone/teeth; prevent dental caries

178
Q

What is the cause of fluoride deficiency?

A

Deficiency: inadequate intake fluoridated water

179
Q

What are the clinical findings of fluoride excess?

A

Excess: chalky tooth deposits, calcification of ligaments, risk for bone fracture

180
Q

What are the types of dietary fiber?

A

Fiber types: insoluble, soluble

181
Q

What are the features of insoluble fiber?

A

Insoluble fiber: nonfermentable, ↑stool bulk, softens stool

182
Q

What are the features of soluble fiber?

A

Soluble fiber: fermentable, softens stool, ↑fecal bacterial mass

183
Q

An increase in fiber may reduce the risk of what?

A

↑Fiber may reduce risk for endometrial, breast, colon cancer

↑Fiber: ↓risk for sigmoid diverticulosis by preventing constipation

184
Q

How does soluble fiber decrease the risk of heart disease?

A

Soluble fiber lowers serum cholesterol

185
Q

What can be treated by sodium-restriction?

A

Sodium restriction: hypertension, heart failure, chronic liver/kidney disease

186
Q

What can be treated by protein-restriction?

A

Protein-restriction: Rx chronic renal failure, cirrhosis

Rapid Review Pathology (14 decks)

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