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Clin Med > GI: vitamin deficiencies & ODs > Flashcards

GI: vitamin deficiencies & ODs Flashcards

1
Q

Vitamin A also called?

A

retinol

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2
Q

retinol

A

vit a

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3
Q

thiamine also called

A

Vit B1

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4
Q

Vit B1

A

thiamine

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5
Q

Vit B2 also called

A

riboflavin

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6
Q

Riboflavin

A

Vit B2

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7
Q

Vit B3 also called

A

Niacin

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8
Q

Niacin

A

Vit B3

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9
Q

Vit B6 also called

A

pyridoxine

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10
Q

pyridoxine

A

vit B6

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11
Q

Vitamin B12 also called

A

Cobalamin

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12
Q

Cobalamin

A

Vit B12

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13
Q

Vit C also called

A

Ascorbic acid

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14
Q

Ascorbic Acid

A

Vit C

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15
Q

list the fat sol vitamins

A

A
D
K
E

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16
Q

list the water sol vitamins

A 
B1
B2
B3
B5
B6
B7
B9
B12 
C
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17
Q

vit B5 also called

A

pantothenic acid

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18
Q

pantothenic acid

A

vit B5

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19
Q

vit B7 also called

A

biotin

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20
Q

Biotin

A

Vit B7

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21
Q

Vit B9 also called

A

folate

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22
Q

folate

A

Vit B9

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23
Q

follicular hyperkeratosis assoc with which vit deficiency

A

A and C

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24
Q

Pallor assoc with which vitamin deficiency

A

iron
folate
B12

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25
Q

Subcutaneous fat loss and temporal wasting assoc with which vitamin deficiency

A

Calories

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26
Q

Spooning of nails assoc with which vitamin deficiency

A

Iron

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27
Q

Night blindness assoc with which vitamin deficiency

A

Vit A

28
Q

Glossitis of the tongue assoc with which vitamin deficiency

A

B6
B12
Folate

29
Q

bleeding gums assoc with which vitamin deficiency

A

Vit C

30
Q

Goiter assoc with which vitamin deficiency

A

Iodine

31
Q

decr position and vibratory sense assoc with which vitamin deficiency

A

B12

32
Q

Disorientation/AMS assoc with which vitamin deficiency

A

Thiamine

33
Q

s/s of acute vit A toxicity

A 
blurry vision 
nausea 
vomiting 
vertigo 
idiopathic intracranial HTN
34
Q

s/s of chronic Vit a toxicity

A

teratogenicity, alopecia, ataxia, visual changes, skin disorders

35
Q

three reasons why vitamin def are not as common in Western countries

A

food fortification
plentiful and varied and inexpensive food supply
supplements

36
Q

which patients are generally at risk for vitamin deficiencies

A 
chronically ill 
ETOH 
post gastric bypass surgery 
geriatrics 
dialysis PT 
use of diuretics
37
Q

body has large stores of which vits

A

A and B12

38
Q

Triad of s/s for wernicke Encephalopathy

A

Ataxia
global confusion
ophthalmopleiga (paralysis of ocular muscles)

39
Q

which vitamin deficiencies can be caused by Isoniazid treatment

A

Niacin– B3

Pyridoxine–B6

40
Q

long-term vegan PT…. what vitamin deficiency are we concerned about?

A

Vit B12–Cobalamin

41
Q

Difference b/w Calcifreol and Ergocalciferol

A

Calciferol– active form

Ergo– not active form

42
Q

Hemodialysis patients require calciferol or ergocalciferol and WHY?

A

Calciferol (active form)

because the body does not need to take extra step to convert calciferol as it is the active form

43
Q

Vit D is _____ in the skin in response to UV radiation

Vit D is ____ from diet

A

synthesized on skin

absorbed from diet

44
Q

where is the final step of Vit D activation take place? aka the second hydroxylation

A

Kidneys

why hemodialysis PTs need to take califerol supplements and not the ergocalciferol **

45
Q

name the Three layers of chondrocytes are present in the normal growth plate:

A

reserve zone
proliferating zone
hypertrophic zone

46
Q

rickets affects which layer of chondrocytes

A

hypertropic zone… characterized by expansion of this layer

47
Q

Vitamin B1

  • also called?
  • sources
  • MC etiology
A

THIAMINE

Sources
*breads and cereal

Etiologies:
*ETOH MC

CM:

  1. Dry Beriberi–CNS changes
    * neuropathy
    * impaired coordination and reflexes
  2. Wet Beriberi–high output HF+ dilated cardiomyopathy
  3. Wernicke Ecephalopathy–EMERGENCY
    * triad of: ataxia, global confusion, and opthalmoplegia (paralysis of ocular muscle)
    * **this is MC in ETOH abuse
  4. Korsakoff Dementia
    * irreversible*
    * memory loss, confabulation and psychosis

TX:

  1. IV thiamine
  2. PO thiamine
48
Q

COAT RACK

*seen with which vit def

A 
C: confusion 
O: Opthalmoplegia 
A: ataxia 
T: Thiamine deficiency 
^^^wernicke

R: retrograte amnesia
A: anterograde amnesia
C: confabublation
K: korsakoff’s psychosis

VIT b1!!

49
Q

Vit B2

  • also called
  • soures
  • RF
  • CM
A

Riboflavin

sources: milk, eggs, meat, quinoa, avocado

CM:
*ORAL: magenta color tongue, glossitis, angular chelitits (fissuring corner of mouth), stomatitis, pharyngitis

  • OCCULAR: photophobia, corneal lesions
  • GENITAL: scrotal dermatitis

**VEGANS are at risk-

50
Q

Vit B3

*also called

A

NIACIN

Sources: meats, grains, legumes
*this was eliminated in US bc of food fortification

Etiologies:

  • diets that lack in tryptophan
  • diets high in untreated corn
  • dz that decrease tryptophan

CM: PELLAGRA

  1. Dermatitis
  2. Diarrhea
  3. Dementia
  4. Death
51
Q

Vit B6

  • also aclled
  • sources
  • RF
  • CM
A

PYRIDOXINE

sources: meats, fruits

Etiologies:

  • ETOH
  • Isoniazid
  • Levodopa

CM:

  1. Neurologic: peripheral neuropathy, seizures, HA, Odd changes
  2. OThers: glossitis, flaky skin

RF:

  • TB treatment with isoniazid
  • Parkinsons
52
Q

what vit supplement do we reccomend to

  1. vegans
  2. PT being treated for TB
A
  1. B6 and B12*****

2. B6

53
Q 
Vit B12 
*also called 
RF 
Etiologies--MCC? 
CM--MC initial s/s ? 
-diagnosis--lab findings
A

COBALAMIN–released by the acidity of the stomach and combines with IF where it is absorbed mainly by distal lumen

sources: mainly animal products

RF:
*vegan PT

Etiologies 
MCC: pernicious anemia****** causes gastric atrophy 
-CD 
-zollinger-ellison syndrome
-ETOH 
-gastric bypass surgery 
-Meds: metformin, PPis, hydroxyurea 
-vegan diet

CM:

  • anyone with anemia s/s: fatigue, exercise intolerance, pallor
  • glossitis
  • diarrhea
  • malabsoprtion

*NEURO: symmetric parathesias MC inital symptom
-lateral and posterior spinal cord demyelination/degeneration
-ataxia
-weakness
-vibratory, sensory and proprioception deficits
-decrease DTR
+Babinski
-seizures
-psychosis

Diagnosis:
*lab work

TX:

  • B12 replacement: PO, SL, Nasal, IM, deep SQ
    1. mild-moderate: PO B12
    2. Symptomatic anemia and/or neuro findings
    a) IM dose weekly until def is corrected.. then monthly
    b) PT can switch to a monthly PO dose after s/s resolve

PERNICIOUS ANEMIA PT:
**LIFE LONG IM TX

54
Q

liver can store how much B12?

A

2 mg

*why s/s of defiiency might not show for a little

55
Q

why are the s/s widespread for B12 def

A

B12 is needed for DNA synthesis and cell devision… so the neuro s/s are caused by inability to maintian mylen sheath

56
Q 
Vit C 
*also called 
*sources 
CM 
TX 
Diagnosis
A

Ascorbid ACid

soures: citrus and greeen veg

CM: SCURVY
1. Hyperkeratosis: hyperkeratotic follicular papules

  1. Hemorrhage: vascular fragility w/ recurrent bleeding in bums, skin and joints + imparied wound healing
  2. Hematologic: glossitis, malaise, weeakness

Diagnosis:
-lab work

TX:

  • replacment
  • general s/s improve in days
  • hematologic s/s take weeks
57
Q

Vit D

  • sources
  • CM
  • TX
A

sources: fatty fish, egg yolks, beef, mushrooms, sun

CM:
1. low bone turnover and decr osteoid mineralization (osteromalacia) ADULTS
and/or
2. decr cartilage at the epiphyseal plates (rickets) KIDS

TX

  • PO ergocalciferol
  • supplementation for dialysis PT is calciferol (active form)
58
Q

Vit D helps with?

A

absorption of CA2+ and phosphate

59
Q 
Osteomalacia 
-define 
CM 
Diangosis 
tx
A

demineralization of the bone osteoid only (soft bones)

CM:

  • diffuse bone pain and tenderness
  • Muscular weakness
  • Hip pain
  • bowing long bones

diagnosis:
- lab work: decr CA, phosphate, 25-hydroxyvitamin D levels

TX:
PO ergocalciferol

60
Q

Rickets

  • define
  • etologies
  • CM
  • diagnoss
  • tx
A

Vit D def MC b/w 3MO and y years–bc calcium needs are high and there is usualyl decrease sunlight exposure

Etiologies:

  • dietary def–prolonged BF w.o vit D supp
  • celiac
  • CF

CM:

  • delyaed fontanel closure
  • growth delays
  • delayed dentition
  • genu vargum (lateral bowing of the femur and tibia)

Diag:
-lab work

Tx:
-supplementation via oral drops

61
Q

PKU

  • define/patho
  • CM
  • diagnosis
A

autosomal recessive disorder of amino acid metabolism associated with phenylketone neurotoxicity
*due to build up of phenylalanine in urine and blood

PATHO: decrease in the hepatic enzyme Phenylalanine Hydroxase– b/d PHE into tyrosine
*toxciity is irreversible if not detected by 3 YO

CM
*after birth: vomitnig, mental delays, irritability, convulsions, eczema, incr DTR, intellectual disability

Diagnosis:
-increased srum PHE
-urine is musty odor
-newborn screening is routinely done in the US**
MC affects kids who are blone, blue eye with fair skin*
—susspect this in kids who are born outside US**

TX:

  • lifetime dietary restriction of PHE
  • tyrosine supp
  • avoid food high in PHE: milk cheese nuts fish chicken meats eggs legumes aspartame
62
Q 
Celiac Spruce 
*patho 
*inr incidence with? 
CM
diagnosis--initial TOC and confirmatory/definitive?
A

PATHO: TWO 2 HYPERSENSITIVITY RXN

  • auto immune mediated inflammation
  • Sm bowel
  • rx with alpha-gliadin in gluten food –wheat barley rye

*auto immune damage–>loss of villi–>malabsorption

MC in females, european descent–irish and finnish
*certain HLA types too

CM:

  • malabsoprtion: diarrrhea, abdominal pain, distention, bloating, steatorrhea, growth delays in kids
  • dermatitis herpetiformis: pruritic, papulovesicular rash MC on extensor surfaces, neck trunk and scalp

Diagnosis:

  1. screening: tissue transglutaminase (tTG IgA) antibodies– INITIAL TOC
    * endomysial IgA (EMA) done too
  2. Definitive and confirmatory: small bowel biopsy–atrophy of villi

TX:

  • GF diet
  • limit oats
  • vit supp
63
Q

Lactose Intolerance
*CM
Diagnosis-TOC?

A 
CM: 
-loose stools 
-abdominal pain 
-Flatulence 
-Borborygmi (stomach growls) 
after ingestion of milk

Diagnosis:
TOC: hydrogen breath test (H+ is produced when colonic bacteria ferment the undigested lactose)
*usually a clinical diagnosis

64
Q

Peanut and tree nut allergy
-type of rxn
RF

A

Type 1 Mediated hypersensitivity rxn–IgE mediated

RF:

  • genetics
  • timing of exposure: if parents delay exposure to nuts until >3=increases risk

CM
-anaphylaxis

TX:

  • pt education
  • avoidane of the food
  • epi autoinjector
65
Q

Acetaminophen OD:

-what is a toxic dose

A

toxic dose: 150-200 mg/kg

CM:

  • n/v shortly after ingstion
  • hepatic aminotransferase begins to incr 24-48 hours after ingestions–usually no other signs of toxicity

SEVERE:
*fulminant hepatic necrosis–>jaundice, hepatic encephalopathy, AKI, death

Rarely, a massive ingestion (>500mg/L) can cause:

  • seizures
  • coma
  • hypotension
  • metabolic acidosis

WORSE WHEN combined with ETOH or other drugs cytochrome P450

Diagnosis:
-Nomogram–tells us PT risk for hepatoxicity

TX:

  • gastric lavage
  • oral ativ charc
  • NAC–most effective if taken 8-10 hrs post ingestion
  • contact local poison control
  • dialysis rare needed
66
Q 
Salicylates 
-list sources 
-chemical composition 
-what can cause intoxication 
T1/2?

CM

  • acute
  • moderate
  • serious
A

ASA, methyl salicylate, pepto

chemical comp:
*uncoupled cellular oxidative phosphorylation–>resulting in anaerobic metabolism–excessive production of lactic acid + heat–>interfere w/ Kreb Cycle enzymes

*single ingestion of more than 200 mg/kg can cause intoxication

t1/2= 2-3 in SMALL doses
can incr to 20 hours with OD

CM:

  1. acute: n/v, gastritis
  2. moderate: hyperpnea–deep and rapid breathing), tachycardia, tinnitus
  3. Serius: agitation, confusion, seizures, cardivoasc collpase, pulmonary edema, hyperthermia, DEATH

Diagnosis:
lab work will show anion gap metabolic acidosis–confirmed by measuring serum salicylate level
>100**
*respiratory alkalosis seen with ABGs

TX:

  • gastric lavage
  • activ charcoal: 60-100 g PO
  • glucose
  • IV sodium bicarb
  • potassium chloride
  • hemodilysis for severe metabolic acidosis

Clin Med (52 decks)

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