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General Pathology > Nutritional Disorders > Flashcards

Nutritional Disorders Flashcards

1
Q

Micronutrients - act as _____, ______or ______ components

A
  1. coenzymes
  2. hormones
  3. structural
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2
Q

What are trace minerals?

A

Elements present in living tissues in small amounts. Includes both essential and nonessential

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3
Q

What are common causes of malnutrition? (4)

A
  • Poverty: homeless, elderly, children of the poor
  • Ignorance
  • Chronic alcoholism
  • Self-imposed dietary restrictions
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4
Q

Deficiencies and over-indulgance/consumption of what 3 things can result in nutritional disease?

A

-Macros (CHO, Pro, Fats, Cals)
-Vitamins and Minerals
-Water (dehydration and water intoxication)

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5
Q

Emaciation resulting from inadequate intake of calories (i.e. starvation)

A

marasmus

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6
Q

Intake of what macros are deficient in marasmus?

A

all of them (CHO, Pro, fats)

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7
Q

what occurs to the body during marasmus/starvation? (i.e. how does the body make energy?)

A
  1. uses stores of liver and muscle glycogen
  2. uses subcutaneous fat
  3. uses muscle protein (organ and blood protein conserved)
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8
Q

selective protein malnourishment while maintaining calories from carbs

A

Kwashiorkor

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9
Q

what CHO-rich and Pro-poor foods are often the cause of Kwashiorkor

A

maize (corn) and rice milk

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10
Q

how is protein depletion manifested in the body in Kwashiorkor

A

loss of organ protein (albumin) –>
-generalized edema (anasarca)
-fatty liver
-hair and skin changes (loss of pigment and flaky skin)
-parotid enlargement

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11
Q

why is body fat relatively spared in Kwashiorkor?

A

CHO supplies energy

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12
Q

during Kwashiorkor, does the child appear emaciated? why/why not?

A

no –> edema = bloating

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13
Q

what symptom of Kwashiorkor causes the protuberant abdomen?

A

fatty liver

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14
Q

what hair and skin changes (due to protein deficiency) can be seen in Kwashiorkor?

A

-depigmented hair and alopecia “hair loss”
-flaky paint skin

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15
Q

In marasmus visceral protein (organ and blood protein) is _______, while in Kwashiorkor it is _______.

A
  1. conserved (so near normal levels)
  2. lost
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16
Q

self-induced starvation

A

anorexia nervosa

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17
Q

what is the major population that anorexia nervosa is seen in?

A

young adult females

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18
Q

what are the 2 major clinical symptoms of anorexia nervosa?

A

marasmus and amenorrhea (menstruation ceases)

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19
Q

what causes the death of most anorexia nervosa patients?

A

starvation, infection, arrhythmia from hypokalemia

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20
Q

what has the highest death rate of any psychiatric disorder?

A

anorexia nervosa

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21
Q

purge eating followed by induced vomiting

A

bulimia

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22
Q

what is the major population that bulimia is seen in?

A

young adult females

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23
Q

what nutritional disorders result in parotid/salivary gland enlargement?

A

-marasmus
-Kwashiorkor
-anorexia nervosa
-bulimia
-obesity

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24
Q

what does bulimia result in physiologically? (3)

A

-electrolyte imbalance (hypokalemia) –> arrhythmia
-acid erosion of lingual upper teeth surfaces (perimolysis)
-parotid enlargement

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25
Q

Both Anorexia nervosa and bulimia can feature a deficiency of what 3 vitamins/minerals?

A

-vitamin C
-niacin
-zinc

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26
Q

this occurs when caloric intake exceeds expenditure with excess being stored as triglycerides in adipose

A

obesity

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27
Q

T/F overeating is multifactorial due to both genetic and voluntary components

A

true

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28
Q

what 2 things regulate overeating?

A

-number of fat cells
-hypothalamus (hormones)

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29
Q

T/F childhood overeating increases the total number of fat cells, which will then become fixed by adolescence

A

true

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30
Q

What percent overweight is associated with health risks?

A

20% (BMI >30)

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31
Q

what type of fat is more dangerous/more associated with health risks: visceral or subcuntaneous?

A

visceral

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32
Q

in an obese state, what do fat cells produce? (3)

A

-leptin
-adiponectin
-cytokines

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33
Q

what does leptin do? is the net result good or bad? (2)

A

-decreases appetite in hypothalamus
-causes secretion of Norepinephrine –> burns fat
-GOOD

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34
Q

what does adiponectin do? is the net result good or bad? (2)

A

-directs fatty acids to muscle for oxidation
-makes liver sensitive to insulin
-GOOD

anti- inflammatory, diabetic, atherogenic, proliferative
fat burning molecule

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35
Q

T/F obese people have more fat cells at birth and defects in regulatory hormones or their receptors

A

true

(This is bad)

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35
Q

during a state of obesity, what hormone is produced in more excess by the stomach? what does it do?

A

-ghrelin
-increases appetite

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35
Q

what hormone is secreted after a meal? what organs make and secrete it? what part of the brain does it act on and what does it do?

A

-Peptide YY
-made in ileum and colon
-acts on hypothalamus to curb appetite

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35
Q

what do the cytokines that are made by fat cells cause? is the net result good or bad? (2)

A

-subclinical inflammation
-high C-reactive protein
-BAD

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35
Q

what is the proposed pathogenesis on how the gut microbiome affects obesity? (3)

A

-bacteria break down ingested indigestible polysaccharides –> simple carbs that can be digested –> increases caloric intake
-bacterial products increase ghrelin secretion = increases appetite
-bacterial products –> gut inflammation –> mucosa permeable to cytokines –> increased insulin resistance

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35
Q

T/F variations in gut bacteria/the gut microbiome can affect what and how much you eat

A

true

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35
Q

where in the brain is the appetite control center?

A

hypothalamus

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35
Q

in regards to preventing/treating obesity what bacteria should be introduced to the gut microbiome?

A

bacteria that produce butyrate

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36
Q

what are systemic health risks associated with obesity? (10)

A

-Type II Diabetes
-Hypertriglyceridemia
-hypercholesterolemia
-low HDL
-Fatty liver disease and cirrhosis
-gallstones
-hyperestrogemia
-cancer (esophagus, thyroid, colon, kidney, prostate, gallbladder)
-parotid enlargement
-Pickwickian (hypoventilation) syndrome

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36
Q

how does obesity correlate with T2DM comordibity?

A

obesity –> adipose produces cytokines –> inflammation –> activates IL-1 –> insulin resistance, elevated BG and compensatory hyperinsulinemia

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36
Q

what are gallstones composed of?

A

cholesterol

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36
Q

Hypertriglyceridemia, hypercholesterolemia, and low HDL, all of which can be caused by obesity, lead to what disease states? (3)

A

Atherosclerosis, heart attack, stroke

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37
Q

the hyperestrogenemia caused by obesity contributes to what disease states? (2)

A

endometrial and breast cancer

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38
Q

what is Pickwickian (hypoventilation) syndrome?

A

enormous abdominal obesity –> compresses diaphragm –> restricts ventilation, sleep apnea, hypoxia

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39
Q

what foods are a source of vitamin A? (3)

A

vegetables, dairy, liver

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40
Q

where is vitamin A stored in the body and for how long?

A

Ito (stellate) cells in the liver for 6 months

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41
Q

what are the functions of Vitamin A? (4)

A

-rhodopsin for night vision
-differentiation of mucous
-antioxidant
-enhances immune system

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42
Q

what disease states is vitamin A used in treatment for? (2)

A

psoriasis and a type of leukemia

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43
Q

what can cause a vitamin A deficiency? (2)

A

-diet
-fat malabsorption or bile disease

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44
Q

what are symptoms of a vitamin A deficiency? (3)

A

-night blindness
-squamous metaplasia
-increase mortality from infection (esp measles and diarrhea)

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45
Q

describe the symptoms of squamous metaplasia, which is caused by a vitamin A deficiency (7)

A

-dry eyes
-corneal blindness
-dry mouth
-skin lesions
-premalignant oral lesions
-pneumonia
-kidney stones

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46
Q

what are symptoms of a vitamin A overdose/excess? (3)

A

-carotemia (non-toxic)
-headaches & vomiting
-birth defects

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47
Q

in regards to vitamin A, what are pregnant women told not to take/use due to the correlation with birth defects?

A

retinoids

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48
Q

what is carotemia?

A

a yellow color in the skin and fat from stored beta carotene (from Vit A)

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49
Q

what are good sources of vitamin D?

A

-suntan (UVB for 15 min; 90%)
-dairy, fish oil, grains (10%)

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50
Q

what are the functions of vitamin D? (2)

A

-mineralizes osteoid
-maintain serum Ca2+

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51
Q

how does vitamin D maintain serum Ca2+? (3)

A

-increases intestinal absorption
-mobilizes Ca2+ from bone (with PTH)
-reabsorbs calcium from distal renal tubules

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52
Q

what does a vitamin D deficiency result in? (3)

A

-Kids = rickets
-adults = osteomalacia
-increased risk of cancer (colon, breast, prostate)

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53
Q

what can cause a vitamin D deficiency? (6)

A

-diet
-no sun
-genetic dz
-kidney dz
-malabsorption
-drugs

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54
Q

describe what happens during rickets? what does this result in, symptom-wise?

A

osteoid produced but is not mineralized =

-soft, deformed bones, bow legs, hypoplastic teeth, deformed skull

-persistence of distorted cartilage masses (Rachitic rosary and pigeon breast deformity)

(children)

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55
Q

describe what happens during osteomalacia?

A

bone fractures

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56
Q

can a vitamin D deficiency cause hypocalcemia?

A

yes but rare –> only if severely deficient bc PTH will mobilize Ca2+ from the bones

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57
Q

what can cause someone to have an excess of vitamin D?

A

dietary supplementation

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58
Q

what does vitamin D excess cause? (2)

A

-hypercalcemia
-kidney stones

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59
Q

people do not get enough vitamin D today because of _____

A

protection from sunlight

60
Q

what disease states have a decreased risk when someone is taking a vitamin D Rx? (3)

A

-DM
-cancer
-alzheimers
-sepsis (possibly)

61
Q

what are good sources of vitamin E?

A

widely available

62
Q

where is vitamin E stored in the body?

A

fat deposits

63
Q

what is the function of vitamin E?

A

antioxidant –> scavenges free radicals along with selenium

64
Q

is a vitamin E deficiency caused by diet?

A

no

65
Q

when can a vitamin E deficiency be seen?

A

with fat malabsorption diseases

66
Q

what are 4 symptoms caused by a vitamin E deficiency?

A

-loss of nerve cells in spinal cord and nerve myelin –> loss of reflexes, proprioception, pain sensation
-shortened RBC life
-increase cancer?
-increased atherosclerosis?

67
Q

what can excess vitamin E cause?

A

bleeding diathesis

68
Q

what are good sources of vitamin K? (2)

A

leafy green vegetables and gut bacteria

69
Q

what are the functions of vitamin K? (2)

A

-cofactor to carboxylate glutmate
-gets oxidizes as it carboxylates and is recycled when reduced by liver

70
Q

as a cofactor to carboxylate glutmate, vitamin K allows calcium binding sites on what?

A

-clotting factors VII, IX, X, and prothrombin
-osteocalcin

71
Q

what does osteocalcin do?

A

involved in calcium binding in the bone matrix

72
Q

what can cause a vitamin K deficiency? (3)

A

-fat malabsorption diseases

-patients of coumadin

-no gut bacteria (antibiotics, neonatal period)

73
Q

what symptoms occur due to a vitamin K deficiency? (2)

A

-bleeding (esp in neonates)
-poor calcification of bone matrix

74
Q

what is B1?

A

thiamine

75
Q

many foods are a good source of thiamine (B1), except what?

A

processed rice, sugar and flour

76
Q

T/F cooking lowers thiamine/B1 levels?

A

true

77
Q

what are the functions of thiamine (B1)? (3)

A

-synthesis of ATP
-pentose phosphate pathway
-maintains membranes of peripheral nerves

78
Q

what can cause a thiamine (B1) deficiency? (3)

A

-diet of processed carbs
-alcoholism
-excess vomiting

79
Q

what are the 2 thiamine (B1) deficiency diseases?

A

-Dry beri beri
-Wet beri beri
-Wernicke-Korsakoff sx

80
Q

describe the symptoms of Dry beri beri (thiamine/B1 deficiency)

A

symmetric demyelinization of peripheral nerves –> wrist and ankle drop, loss of reflexes and muscle weakness

81
Q

describe the symptoms of wet beri beri (thiamine/B1 deficiency)

A

-peripheral vasodilation
-flabby heart
-AV shunting of blood
-all result in: high output cardiac failure and edema

82
Q

describe the symptoms of Wernicke-Korsakoff sx (thiamine/B1 deficiency)

A

-unsteady gait
-mental confusion

83
Q

what is a good source of riboflavin/B2?

A

widely distributed

84
Q

what is B2?

A

Riboflavin

85
Q

what are the functions of riboflavin/B2? (2)

A

-FAD –> involved in REDOX rxns in intermediary metabolism
-mitochondrial enzymes

86
Q

what can lead to a riboflavin/B2 deficiency? (4)

A

-impoverished countries
-malabsorption diseases
-alcoholism
-debilitation

87
Q

what symptoms result from a riboflavin/B2 deficiency? (6)

A

-anemia
-angular cheilitis
-magenta tongue
-corneal vascularization and ulceration
-dermatitis of nasolabial folds (rare)
-genital lesions

88
Q

what is a good source of niacin?

A

-grains, legumes (NOT corn)
-can be converted from tryptophan, which is in: fish, turkey, meat, nuts, grains

89
Q

what are the functions of niacin? (2)

A

-NAD and NADP –> needed in intermediary metabolism of fat, CHO, amino acids
-large doses –> lowers LDLs

90
Q

what can a niacin (or tryptophan) deficiency result from?

A

-corn diets (south)
-alcoholics
-eating disorders
-debilitating dz
-seizures meds
-carcinoid syndrome

91
Q

what is carcinoid syndrome?

A

when tryptophan is converted to 5-HT can’t be converted to niacin

92
Q

what is the disease caused by a niacin deficiency?

A

Pellagra

93
Q

what are the symptoms of pellagra (niacin deficiency)?

A

-thick, red, dry scaly skin patches around the neck
-oral lesions
-diarrhea caused by atrophy of columnar intestinal lining
-dementia caused by neuronal degeneration

(3Ds: dermatitis, diarrhea, dementia)

94
Q

what can excess niacin result in?

A

-flushing of skin
-liver damage
-increases fasting blood sugar

(seen in high cholesterol tx)

95
Q

what is B6?

A

Pyridoxine

96
Q

what is a source of pyridoxine/B6?

A

widely distributed

97
Q

what are the functions of pyridoxine/B6? (2)

A

-involved in metabolism of lipids and AAs
-required for heme synthesis

98
Q

what can lead to a pyridoxine/B6 deficiency?

A

-destroyed in food processing
-antagonized by drugs (isoniazid, estrogens, alcohol)
-increased demand in pregnancy

99
Q

what are the symptoms of a pyridoxine/B6 deficiency?

A

-elevated homocysteine –> atherosclerosis, thrombosis
-resembles riboflavin deficiency (angular cheilitis, glossitis, dermatitis, peripheral neruopathy)
-mild anemia

100
Q

what are therapeutic doses of pyridoxine/B6 used for?

A

-carpal tunnel sx
-to counteract deficiency caused by isoniazid

101
Q

what are good sources of Cobalamin/B12?

A

meat, gut bacteria

102
Q

what is B12?

A

Cobalamin

103
Q

what is required in order for Cobalamin/B12 to be absorbed? where is it absorbed?

A

-intrinsic factor (in stomach)
-absorbed in distal ileum

104
Q

where is Cobalamin/B12 stored in the body and for how long?

A

liver; 5-20 years

105
Q

what are the functions of Cobalamin/B12? (4)

A

-Converts homocysteine to methionine
- Converts methylmalonyl CoA to succinyl CoA
-Needed for folate metabolism and DNA synthesis
-maintenance of myelin in spinal cord

106
Q

what can lead to a Cobalamin/B12 deficiency? (5)

A

-vegan (no other diet issue)
-chronic atrophic gastritis with loss of parietal cells (intrinsic factor)
-malabsorption in ileum (Crohn dz)
-lymphoid malignancies that steal B12
-chronic Nitric Oxide inhalation

107
Q

why can chronic Nitric Oxide inhalation lead to a state of Cobalamin/B12 deficency?

A

NO = B12 antagonist = causes demyelination

108
Q

what are symptoms of a Cobalamin/B12 deficency?

A

-megaloblastic anemia
-loss of other rapidly dividing cells (neutrophils, germ cells, intestinal epithelium, chronic atrophic glossitis)
-raises serum homocysteine levels
-raises methylmalonic acid levels
-demyelination

109
Q

why does megaloblastic anemia occur during a Cobalamin/B12 deficency?

A

due to impaired folate utilization = RBCs get big but cannot divide

110
Q

what do raised serum homocysteine levels (due to a Cobalamin/B12 deficency) lead to?

A

makes blood hypercoagulable –> accelerates atherosclerosis

111
Q

what do raised methylmalonic acid levels (due to a Cobalamin/B12 deficency) lead to?

A

demyelination of spinal tracts –> numbness and tingling of extremities then irreversible paraplegia

112
Q

what are good sources of folate?

A

Vegetables

113
Q

T/F cooking can destroy folate

A

true

114
Q

where is folate absorbed in the body?

A

proximal ileum

115
Q

where is folate stored in the body and for how long?

A

liver; 6 mo

116
Q

what is the function of folate?

A

required for DNA replication and cell division

117
Q

what can lead to a folate deficiency? (6)

A

-diet
-pregnancy (6-fold increase in need)
-malignancies and chemo Rx
-alcohol (folate antagonist)
-BCP
-cigs

118
Q

what symptoms can result from folate deficiency? (6)

A

-megaloblastic anemia (B12 anemia w/o neural defects)
-neutropenia, loss of germ cells and GI epithelium
-chronic atrophic glossitis
-colon cancer (contributes)
-increased serum homocysteine
-fetal neural tube defects (spina bifida)

119
Q

what is ascorbic acid?

A

Vitamin C

120
Q

what are goods sources of vitamin C?

A

fruits, vegetables, fish, milk

121
Q

why are humans are one of the few animals that CANNOT make vitamin C?

A

missing enzyme L-gluconolactone oxidase

122
Q

can vitamin C be stored?

A

no

123
Q

what are the functions of vitamin C? (3)

A

-hydroxylation of procollagen

-antioxidant (with Vit W)

-synthesis of norepinephrine

124
Q

what can lead to a vitamin C deficiency?

A

-weird diets –> only beef/dairy
-alcoholics
-elderly
-infants on formula
-faddists
-autism
-bulimia

125
Q

when can a vitamin c deficiency occur?

A

2-3 months after 0 intake

126
Q

what is a vitamin C deficiency?

A

Scurvy

127
Q

what are symptoms of scurvy?

A

puerpera and hematomas in gingiva, skin, joints, and perisosteum

(swollen, bleeding gums and perifolicular hemorrhage with corkscrew hairs)

128
Q

what is the pathogenesis behind the puerpera and hematomas in scurvy?

A

-collagen without hydroxyproline = weak (esp in caps and venules)
-deformed bones due to lack of osteoid matrix

129
Q

how might vitamin C deficiency may contribute to GI cancers and atherosclerosis?

A

via reduced antioxidant effect

130
Q

what can an excess in vitamin C result in?

A

kidney stones and Fe overload (only seen in high doses)

131
Q

what vitamins and minerals have neurologic manifestations? (5)

A

-thiamine
-vitamin B12
-pyridoxine
-folate (embryonic neural tube defects)
-vitamin E

132
Q

what vitamins and minerals have bone manifestations? (4)

A

-vitamin C (matrix)
-vitamin D (calcification)
-vitamin K (calcification)
-calcium

133
Q

what vitamins and minerals are antioxidants? (4)

A

-Vit A, C, E
-Selenium

134
Q

what vitamins and minerals have bleeding manifestations? (3)

A

Vit C, K and excess E

135
Q

what vitamins and minerals have skin manifestations? (6)

A

-Vit A, C
-niacin
-riboflavin
-pyridoxine
-zinc

136
Q

what vitamins and minerals have oral manifestations? (9)

A

-vitamin A

-vitamin B12

-folate

-riboflavin

-pyridoxine

-niacin

-iron

-vitamin C

-zinc

137
Q

of the vitamins and minerals that have oral manifestations, which cause angular cheilitis and atrophic glossitis? (4)

A

-riboflavin

-pyridoxine

-niacin

-iron

138
Q

of the vitamins and minerals that have oral manifestations, which cause bleeding gums and periodontal dz? (1)

A

Vitamin C

139
Q

of the vitamins and minerals that have oral manifestations, which cause perioral rash?

A

zinc

140
Q

which vitamins and minerals can be used for vitamin therapy?

A

-C, E (antioxidants)
-niacin (lowers LDL)
-folate and B12 (prevent neural defects, lower homocysteine, colon cancer)
-B complex (pregnancy)
-K (calcification)
-pyridoxine (carpal tunnel sx)

141
Q

what is the function of calcium? (3)

A

-bone mineralization
-clotting factor
-regulated by PTH and Vit D

142
Q

what causes hypocalcemia? (3)

A

-renal failure
-rickets
-no parathyroid (DiGeorge sx)

143
Q

what causes hypercalcemia? (5)

A

-parathyroid tumor
-end stage renal dz with phosphate retention
-bone destroying tumors
-excess dietary Ca (antacids) or Vit D
-granulomatous dz (sarcoid)

144
Q

what are signs of hypocalcemia? (3)

A

-hypocalcified teeth
-tetany
-no clotting disorder

145
Q

what are signs of hypercalcemia?

A

metastatic calcification in alkaline tissue (stomach, lungs, kidney) –> causes nephrocalcinosis and nephrolithiasis with kidney damage

146
Q

what are good sources of iron?

A

meat, green vegetables

147
Q

how is iron stored?

A

conserved in the body from worn out RBC by macrophages as hemosiderin

148
Q

what is the function of iron?

A

required for Hb, Mb, cytochromes and catalase

149
Q

what can lead to an iron deficiency? (2)

A

-diet (rare – formula fed infants, Scandinavians)
-Chronic blood loss (menstruation, GI ulcers, cancers)

150
Q

what can an iron deficiency lead to? (3)

A

-anemia
-oral mucosal atrophy
-Plummer Vinson Sx

151
Q

what is Plummer Vinson Sx?

A

severe iron deficiency in Scandinavian women –> leads to oral and esophageal atrophy with cancers

152
Q

what can excess iron lead to? (2)

A

-hemosiderosis
-hemochromatosis

153
Q

what is hemosiderosis?

A

iron stored in macrophages of bone marrow, LNs, and spleen –> no symptoms

154
Q

what is hemochromatosis?

A

massive iron overload in many organs –> systemic dz

155
Q

what can lead to a water deficiency?

A

-reduced intake
-excessive excretion

156
Q

what can water intoxication lead to?

A

death by arrhythmia due to electrolyte imbalance (hypokalemia and hyponatremia) and pulmonary edema

157
Q

what malabsorptive diseases are associated with vitamin/mineral deficiencies and which vitamins/minerals are involved? (5)

A

-Chron Dz: vit A, C, thiamine, folate, B12, D, Fe

-Celiac Dz: Zn, vit ADEK

-autoimmune chronic gastritis: B12

-total parenteral nutrition: given to pat with chronic Gi dz due to low thiamine, vit C, and Zn

-gastric bypass and banding

158
Q

______ is the most common autosomal recessive disease in caucasians and leads to a deficiency in what vitamins/minerals?

A

-cystic fibrosis
-vit ADEK, Zn, fats

159
Q

Autism usually correlates to Vit A and C deficiencies. why?

A

fresh fruits and vegetables cause taste and texture aversions = avoided

160
Q

alcoholism can lead to a deficiency in what?

A

all B vitamins (antagonist)

General Pathology (32 decks)

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