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DT4- Exam 2 > IL-Vitamins-Leah- Tag Team: COMPLETE! > Flashcards

IL-Vitamins-Leah- Tag Team: COMPLETE! Flashcards

1
Q

Primary v Secondary malnutrition:

whats the difference?

A
  • primary: essential component of diet is MISSING

- secondary: essential component of diet is not properly utilized in the body (i.e. poor absorption)

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2
Q

Infants on artificial milk need ___ supplement.

Mountainous regions need ___ supplements?

A
  • iron

- iodine –> goiter

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3
Q

How does alcoholism lead to malnurition?

4 common vitamin deficiencies in alcoholics?

A
  • poor diet (primary)
  • poor absorption (secondary)
  • poor use/storage (secondary)

-lack B1 (thiamine), B9 (folate), B12 (pyridoxine), and vitamin A.

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4
Q

How does illness effect BMR?

A

^^ BMR –> ^^ daily requirements for all nutrients

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5
Q

Definition of Protein Energy Malnutrition and three additional way to evaluate for PEM:

A
  • body weight less than 80% of normal in a child or BMI below 16.
  • can also measure skin folds (fat), arm circumference (muscle), or serum protein
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6
Q

What are the two ends of the PEM spectrum?

A
  • marasmus (overall calorie deficit, wasting)

- kwashiorkor (protein deficit, swollen belly)

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7
Q

Skeletal muscle/somatic compartments are effected by which end of the PEM spectrum? Organs are effected by which end?

A
  • visceral compartments/ organs: kwashiorkor

- somatic/SKM: marasmus

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8
Q

Labs assc with marasmus

A

normal electrolytes and protein

anemia, vitamin deficiencies

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9
Q

How is the immune system effected by marasmus? Bone marrow?

A
  • immune system: ^^ infections

- bone marrow: hypoplasia = anemia

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10
Q

Kwashiorkor:
common geographic locations
cause of the assc edema?

A
  • Africa, Asia

- low albumin –> low oncotic pressure –> edema and ascites

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11
Q

Kwashiorkor:

assc changes in the skin & hair?

A
  • skin: “flakey paint”, alternating zones of hyper/hypopigmentation and desquamation
  • hair: loss of color or “flag sign” (alternation); fine
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12
Q

How is the intestine effected by kwashiorkor?

Liver? Marrow?

A
  • loss of villi/microvilli = loss of absorption & diarrhea
  • fatty liver
  • hypoplastic marrow
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13
Q

Populations with secondary PEM?

A
  • elderly
  • chronically ill
  • bedridden patients
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14
Q

PEM in a cancer patient is aka?

What causes it?

A

cachexia

tumors produce TNF, IL1, IL6

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15
Q

Signs of secondary PEM?

A

-subQ fat depletion
-quads/deltoids waste
-ankle/sacral edema
~^^ infections/sepsis and poor wound healing

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16
Q

Define:
anorexia
bulimia

A

AN: self inflicted starvation
BN: binging –> purging

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17
Q

Clinical findings assc with AN

A
  • amenorrhea (low GnRH –> low LH/FSH)
  • hypokalemia –> arrhythmia
  • hypothyroid sx including lanugo
  • low estrogen –> low bone density
  • other findings similar to PEM
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18
Q

Major medical complications of BN:

A
  • arrhythmias
  • pulmonary aspiration
  • esophageal/ gastric rupture

**also may see amenorrhea for same reason as AN

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19
Q

Sudden death in AN/BN is caused by?

A
  • hypokalemia –> arrhythmia

* *NOTE: these patients otherwise have BRADYcardia due to hypothyroid.

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20
Q

How many vitamins are necessary for health? Which MUST come from diet?

A
  • 13

- C must come from diet

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21
Q

Fat soluble vitamins?

Water soluble?

A
  • Fat: KADE

- Water: B,C

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22
Q

Examples of endogenously synthesized vitamins?

A
  • bioton
  • tryptophan –> niacin
  • D/K
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23
Q

Causes of fat malabsorption?

A
  • diarrhea
  • bypass surgery
  • mineral oil use
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24
Q

Where is vitamin A stored?
How is it transported?
Normal levels?

A
  • stored in perisinusoidal cells of liver
  • trasported by retinol binding protein
  • 30-50 ug/ml normal; sx at 20 `
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25
Q

How is vitamin A depleted in kids?

What pediatric population is always low in vitamin A?

A
  • infection lows A in kids

- newborn infants always low in A

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26
Q

Four causes of A def. in adults?

A
  • celiac
  • mineral oil
  • bypass
  • IBS

Anything else causing poor fat absorption

27
Q

Four forms of vitamin A

A

retinol: transport
retinol ester: storage in liver
retinal: visual pigment
retinoic acid: growth

28
Q

What carries retinol from intestine to liver?
Binds retinol in the blood?
Takes up retinol at liver?

A
  • chylomicrons to liver
  • retinol binding protein in blood
  • apolipoprotein E receptor
29
Q

What is a vitamin A provitamin?

A

B-carotene (carrots)

30
Q

Functions of Vitamin A (6)

A
  • vision
  • maintains epi
  • antioxidant
  • immunity
  • FA metabolism
  • treatment of skin disorders/
31
Q

Manifestations of A deficiencies in the eyes: (7)

A
  • night blindness
  • conjunctival xerosis (dry)
  • bitots spots (keratin buildup, white circle)
  • corneal xerosis
  • xeropthalmia
  • keratomalacia
  • corneal ulcers (iris prolpase, fever/ eye loss/death)
32
Q

How does low vitamin A effect:

  • lungs
  • pancreas
  • kidneys
  • skin
A

SQUAMOUS METAPLASIA OF ALL=

  • bronchopneumonia
  • stones –> hematuria, nephrolithiasis
  • follicular hyperkeratosis of skin
33
Q

Symptoms of vitamin A tox (acute)

A

blurred vision, H/A, N/V, stupor

34
Q

Symptoms of vitamin A tox (chronic)

A

anorexia, N/V, bone joint pain/ fractures

35
Q

Effects of ^^ vit A in pregnancy?

A
  • cardiotoxic to fetus

- cleft lip and palate

36
Q

Vitamin C is aka?

Disease assc with deficiency? Who gets it?

A
  • ascorbic acid

- deficiency = scurvy (alcoholics, elderly)

37
Q

C functions:

A

collagen formation
iron absorption
antioxidant, reduces LDL and atherosclerosis

38
Q

Scurvy/ C def. symptoms (4)

A
  • poor wound healing
  • hemorrhage (fragile vessels)
  • bone disease
  • swelling of joints = pseudparalysis & frog leg postn.
39
Q

What are the body’s two sources of vitamin D?

A
  • dietary (fortified milk, eggs, liver, etc)

- 90% endogenously produced via photosynthesis from 7-dehydrocholesterol in skin

40
Q

What are the two forms of vitamin D?

A
  • vitamin D3 (cholecalciferol, made in skin via photoE)

- vitamin D2 (ergocalciferol, ingested from plants)

41
Q

Describe the most common pathway of vitamin D metabolism from start to finish; which enzymes are implicated in the liver and kidney?

A

Think: SKIN–> LIVER–> KIDNEY

SKIN: 7-dehydrocholesterol–> Pre-D3 + Heat–> D3–>
D3 binds plasma a1-globulin (DBP)–> Transport to LIVER

LIVER 25-Ohases: D3–> 25(OH)D–>

KIDNEY a1-Hydroxylase: 25(OH)D–> 1, 25(OH)2D
(MOST ACTIVE FORM)

42
Q

a1-Hydroxylase (1-OHase) activity is influenced by plasma phosphate, PTH, and Ca++ how?

A
  • ^ activity with HYPOphosphatemia
  • ^ activity with ^ PTH
  • Indirectly responds to Ca++ levels as a result of PTH
43
Q

What is the major function of 1, 25 Dihydroxyvitamin D?

How does it affect the intestine, kidney, and bone?

A

Maintains normal plasma Ca++ and PO4:

  • ^ intestinal Ca++ absorption
  • ^ renal Ca++ reabsorption in PT
  • ^ (w/ PTH) RANKL on OSTEOBLASTS–> Binds RANK on preosteoclasts–> ^ # mature OSTEOCLASTS
  • ^ mineralization of bone and epiphyseal cartilage
  • ^ osteoblast synthesis of OSTEOCALCIN (Ca++ BP)
44
Q

How might one become deficient in vitamin D?
What do we call this in children vs. adults?
How does it primarily present?

A
  • Insufficient dietary intake/ limited light exposure
  • Fat malabsorption syndromes (IBD)
  • Liver or renal disease

This is Rickets in kids and Osteomalacia in adults; disease results in unmineralized bone matrix w soft bones

45
Q

How does vitamin D affect the body in hypocalcemia state (PTH, Bone, Kidney)?

A
  • ^ PTH secretion
  • ^ osteoclast activity
  • ^ renal PO4 excretion
  • DECREASE renal Ca excretion
46
Q

At what age does Rickets most commonly occur?

Hod does it affect the appearance of the head, ribs, sternum, spine and limbs?

A

Most common before 1 yoa

  • ^ frontal bossing + squareness of head
  • “rachitic rosary” @ costochondral jxns
  • “pigeon breast deformity” @ sternum (resp muscles pulling weak ribs in)
  • lumbar lordosis + bowing of legs
47
Q

Describe how osteomalacia presents in the adult; which bones does it most commonly affect?

A

Most commonly causes softening (low osteoid matrix) in vertebral bodies and femoral neck; will ultimately lead to muscle wasting as well as bone softening (osteopenia)

48
Q

Name two factors that will directly increase activity of 1-OHase:

A
  • HYPO-PO4

- HYPER-PTH

49
Q

1, 25 vit D stimulates osteoblasts to do two things:

A
  • ^ RANK L expression (^NFKB pathway)

- ^ Osteocalcin production (Ca binding protein)

50
Q

What are some negative outcomes from megadoses of vitamin D? (3)

A
  • calcification of soft tissue
  • bone pain
  • HYPERcalcemia

**Prolonged sun exposure will NOT cause toxicity; only ingestion

51
Q

Define obesity.

What are three alternative ways to measure this?

A

BMI GREATER than 30 kg/m^2

Can also measure tricep skin folds, mid-arm circumference, waste hip ratio

52
Q

What is central or visceral obesity?

A

When fat accumulates in trunk BEYOND SQ tissue; engulfs organs and mesentery

53
Q

Which gene is responsible for the production of leptin?
What does leptin do?
What happens if patients are leptin deficient?

A

“ob gene” stimulates production of leptin by adipocytes in response to abundant fat stores

Leptin ^ E expenditure, ^ heat generation, ^ physical activity, and DECREASES food intake

Absence of ob gene = NO LEPTIN= early obesity

54
Q

What is the role of the db gene in leptin regulation?

A

db gene is the gene for the leptin receptor; if it is mutated, dysfunctional or absent this can lead to obesity early in life

55
Q

What is adiponectin?
Who has a high concentration?
What are its three effects on FA metabolism?
How does it affect insulin sensitivity?

A

Concentration of adiponectin is INVERSE to fat stores (^ in LEAN FOLKS)

Adiponectin directs FA for muscle use, decreases FA uptake in liver, and decreases glucose production by liver

Adiponectin ^ insulin sensitivity

56
Q

What is Ghrelin? Where is it produced and when?

I which patients is it deregulated?

A

Produced in stomach and hypothalamus; it increases before meals to stimulate food intake and drops 1-2 hours after meals

Postpriandal decrease is attenuated in obese folks, so they keep eating longer than other people

57
Q

What is PPY? Where is it produced?

A

Produced in ilium and colon; increases in response to food intake to curb energy intake (satiety hormone) and remains low while fasting

58
Q

What is metabolic syndrome and of what disease is it a consequence?

A

Metabolic syndrome: visceral adiposity + DM2 + HTN + Dyslipidemia (^ TG, LOW HDL)

This is a consequence of obesity

59
Q

What is Pickwickian Syndrome? With what disease state is it associated?

A

Pickwickian syndrome is hyper somnolence with hypoventilation syndrome; which is associated with sleep apnea and polycythemia (response to hypoventilation)

This syndrome is associated with obesity.

60
Q

How does obesity influence steroid hormone metabolism?

How does this affect risk of malignancy?

A
  • changes estrogen (^^^) and androgen balance

- ^^^ estrogen increases risk of malignancy and coagulopathy

61
Q

How does obesity affect the liver?

A

Can cause nonalcoholic fatty liver disease; will be yellow and less dense

62
Q

Which arthritis is associated with obesity?

A

osteoarthritis

63
Q

Which type of DM is associated with obesity?

A

DM2

64
Q

How does obesity affect the gallbladder?

HDL levels?

A

Causes cholelithiasis with ^ cholesterol stones;

Obesity will DECREASE HDL levels and ^ TGs

DT4- Exam 2 (12 decks)

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