IL-Vitamins-Leah- Tag Team: COMPLETE! Flashcards
Primary v Secondary malnutrition:
whats the difference?
- primary: essential component of diet is MISSING
- secondary: essential component of diet is not properly utilized in the body (i.e. poor absorption)
Infants on artificial milk need ___ supplement.
Mountainous regions need ___ supplements?
- iron
- iodine –> goiter
How does alcoholism lead to malnurition?
4 common vitamin deficiencies in alcoholics?
- poor diet (primary)
- poor absorption (secondary)
- poor use/storage (secondary)
-lack B1 (thiamine), B9 (folate), B12 (pyridoxine), and vitamin A.
How does illness effect BMR?
^^ BMR –> ^^ daily requirements for all nutrients
Definition of Protein Energy Malnutrition and three additional way to evaluate for PEM:
- 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
What are the two ends of the PEM spectrum?
- marasmus (overall calorie deficit, wasting)
- kwashiorkor (protein deficit, swollen belly)
Skeletal muscle/somatic compartments are effected by which end of the PEM spectrum? Organs are effected by which end?
- visceral compartments/ organs: kwashiorkor
- somatic/SKM: marasmus
Labs assc with marasmus
normal electrolytes and protein
anemia, vitamin deficiencies
How is the immune system effected by marasmus? Bone marrow?
- immune system: ^^ infections
- bone marrow: hypoplasia = anemia
Kwashiorkor:
common geographic locations
cause of the assc edema?
- Africa, Asia
- low albumin –> low oncotic pressure –> edema and ascites
Kwashiorkor:
assc changes in the skin & hair?
- skin: “flakey paint”, alternating zones of hyper/hypopigmentation and desquamation
- hair: loss of color or “flag sign” (alternation); fine
How is the intestine effected by kwashiorkor?
Liver? Marrow?
- loss of villi/microvilli = loss of absorption & diarrhea
- fatty liver
- hypoplastic marrow
Populations with secondary PEM?
- elderly
- chronically ill
- bedridden patients
PEM in a cancer patient is aka?
What causes it?
cachexia
tumors produce TNF, IL1, IL6
Signs of secondary PEM?
-subQ fat depletion
-quads/deltoids waste
-ankle/sacral edema
~^^ infections/sepsis and poor wound healing
Define:
anorexia
bulimia
AN: self inflicted starvation
BN: binging –> purging
Clinical findings assc with AN
- amenorrhea (low GnRH –> low LH/FSH)
- hypokalemia –> arrhythmia
- hypothyroid sx including lanugo
- low estrogen –> low bone density
- other findings similar to PEM
Major medical complications of BN:
- arrhythmias
- pulmonary aspiration
- esophageal/ gastric rupture
**also may see amenorrhea for same reason as AN
Sudden death in AN/BN is caused by?
- hypokalemia –> arrhythmia
* *NOTE: these patients otherwise have BRADYcardia due to hypothyroid.
How many vitamins are necessary for health? Which MUST come from diet?
- 13
- C must come from diet
Fat soluble vitamins?
Water soluble?
- Fat: KADE
- Water: B,C
Examples of endogenously synthesized vitamins?
- bioton
- tryptophan –> niacin
- D/K
Causes of fat malabsorption?
- diarrhea
- bypass surgery
- mineral oil use
Where is vitamin A stored?
How is it transported?
Normal levels?
- stored in perisinusoidal cells of liver
- trasported by retinol binding protein
- 30-50 ug/ml normal; sx at 20 `
How is vitamin A depleted in kids?
What pediatric population is always low in vitamin A?
- infection lows A in kids
- newborn infants always low in A
Four causes of A def. in adults?
- celiac
- mineral oil
- bypass
- IBS
Anything else causing poor fat absorption
Four forms of vitamin A
retinol: transport
retinol ester: storage in liver
retinal: visual pigment
retinoic acid: growth
What carries retinol from intestine to liver?
Binds retinol in the blood?
Takes up retinol at liver?
- chylomicrons to liver
- retinol binding protein in blood
- apolipoprotein E receptor
What is a vitamin A provitamin?
B-carotene (carrots)
Functions of Vitamin A (6)
- vision
- maintains epi
- antioxidant
- immunity
- FA metabolism
- treatment of skin disorders/
Manifestations of A deficiencies in the eyes: (7)
- night blindness
- conjunctival xerosis (dry)
- bitots spots (keratin buildup, white circle)
- corneal xerosis
- xeropthalmia
- keratomalacia
- corneal ulcers (iris prolpase, fever/ eye loss/death)
How does low vitamin A effect:
- lungs
- pancreas
- kidneys
- skin
SQUAMOUS METAPLASIA OF ALL=
- bronchopneumonia
- stones –> hematuria, nephrolithiasis
- follicular hyperkeratosis of skin
Symptoms of vitamin A tox (acute)
blurred vision, H/A, N/V, stupor
Symptoms of vitamin A tox (chronic)
anorexia, N/V, bone joint pain/ fractures
Effects of ^^ vit A in pregnancy?
- cardiotoxic to fetus
- cleft lip and palate
Vitamin C is aka?
Disease assc with deficiency? Who gets it?
- ascorbic acid
- deficiency = scurvy (alcoholics, elderly)
C functions:
collagen formation
iron absorption
antioxidant, reduces LDL and atherosclerosis
Scurvy/ C def. symptoms (4)
- poor wound healing
- hemorrhage (fragile vessels)
- bone disease
- swelling of joints = pseudparalysis & frog leg postn.
What are the body’s two sources of vitamin D?
- dietary (fortified milk, eggs, liver, etc)
- 90% endogenously produced via photosynthesis from 7-dehydrocholesterol in skin
What are the two forms of vitamin D?
- vitamin D3 (cholecalciferol, made in skin via photoE)
- vitamin D2 (ergocalciferol, ingested from plants)
Describe the most common pathway of vitamin D metabolism from start to finish; which enzymes are implicated in the liver and kidney?
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)
a1-Hydroxylase (1-OHase) activity is influenced by plasma phosphate, PTH, and Ca++ how?
- ^ activity with HYPOphosphatemia
- ^ activity with ^ PTH
- Indirectly responds to Ca++ levels as a result of PTH
What is the major function of 1, 25 Dihydroxyvitamin D?
How does it affect the intestine, kidney, and bone?
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)
How might one become deficient in vitamin D?
What do we call this in children vs. adults?
How does it primarily present?
- 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
How does vitamin D affect the body in hypocalcemia state (PTH, Bone, Kidney)?
- ^ PTH secretion
- ^ osteoclast activity
- ^ renal PO4 excretion
- DECREASE renal Ca excretion
At what age does Rickets most commonly occur?
Hod does it affect the appearance of the head, ribs, sternum, spine and limbs?
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
Describe how osteomalacia presents in the adult; which bones does it most commonly affect?
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)
Name two factors that will directly increase activity of 1-OHase:
- HYPO-PO4
- HYPER-PTH
1, 25 vit D stimulates osteoblasts to do two things:
- ^ RANK L expression (^NFKB pathway)
- ^ Osteocalcin production (Ca binding protein)
What are some negative outcomes from megadoses of vitamin D? (3)
- calcification of soft tissue
- bone pain
- HYPERcalcemia
**Prolonged sun exposure will NOT cause toxicity; only ingestion
Define obesity.
What are three alternative ways to measure this?
BMI GREATER than 30 kg/m^2
Can also measure tricep skin folds, mid-arm circumference, waste hip ratio
What is central or visceral obesity?
When fat accumulates in trunk BEYOND SQ tissue; engulfs organs and mesentery
Which gene is responsible for the production of leptin?
What does leptin do?
What happens if patients are leptin deficient?
“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
What is the role of the db gene in leptin regulation?
db gene is the gene for the leptin receptor; if it is mutated, dysfunctional or absent this can lead to obesity early in life
What is adiponectin?
Who has a high concentration?
What are its three effects on FA metabolism?
How does it affect insulin sensitivity?
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
What is Ghrelin? Where is it produced and when?
I which patients is it deregulated?
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
What is PPY? Where is it produced?
Produced in ilium and colon; increases in response to food intake to curb energy intake (satiety hormone) and remains low while fasting
What is metabolic syndrome and of what disease is it a consequence?
Metabolic syndrome: visceral adiposity + DM2 + HTN + Dyslipidemia (^ TG, LOW HDL)
This is a consequence of obesity
What is Pickwickian Syndrome? With what disease state is it associated?
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.
How does obesity influence steroid hormone metabolism?
How does this affect risk of malignancy?
- changes estrogen (^^^) and androgen balance
- ^^^ estrogen increases risk of malignancy and coagulopathy
How does obesity affect the liver?
Can cause nonalcoholic fatty liver disease; will be yellow and less dense
Which arthritis is associated with obesity?
osteoarthritis
Which type of DM is associated with obesity?
DM2
How does obesity affect the gallbladder?
HDL levels?
Causes cholelithiasis with ^ cholesterol stones;
Obesity will DECREASE HDL levels and ^ TGs
