Easy Points: Pathology - Nutritional Diseases

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Easy Points: Pathology - Nutritional Diseases
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2013-11-27 09:11:28
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Pathology: Nutritional Diseases, OLFU2106
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  1. Secondary malnutrition results from:
    linsufficient intake

    l malabsorption

    l impaired utilization or storage

    l excess loss

    lincreased need for nutrients.
  2. Etiology of malnutrition
    lPoverty

    lInfections

    lAcute and chronic illnesses

    lChronic alcoholism

    lIgnorance and failure of diet supplementation

    lSelf-imposed dietary restriction

    lOther causes:

    lgastrointestinal diseases

    lmalabsorption syndromes

    lgenetic diseases

    l specific drug therapies

    ltotal parenteral nutrition
  3. When do you consider a child is malnourished?
    • A child is considered
    • malnourished, when weight falls to less than 80% of normal.
  4. Marasmus
    lSevere reduction in caloric intake

    • lsomatic compartment (proteins in skeletal
    • muscle)
  5. lprotein deprivation is relatively greater than
    the reduction in total calories

    lvisceral compartment (protein stores in the
    visceral organs, primarily the liver)
    Kwashiorkor
  6. Clinical findings of which disorder?
    lgrowth retardation

    lloss of muscle mass: catabolism
    and depletion of the somatic        protein compartment

    lserum albumin levels: either
    N or only slightly ↓

    l loss subcutaneous fat:
    mobilized
    and used as fuel

    lextremities are emaciated

    lAnemia  & multiple vitamin deficiencies

    lT cell–mediated immune
    deficiency → concurrent infections
    Marasmus
  7. Clinical manifestations of which disorder:
    lGeneralized or dependent edema

    lRelative sparing of subcutaneous fat and muscle mass

    l“flaky paint”dermatitis -alternating zones of hyperpigmentation, areas of
    desquamation, and hypopigmentation

    lHair changes

    lFatty liver

    lVitamin deficiencies

    lDefects in immunity and secondary infections
    Kwashiorkor
  8. Populations at risk for secondary PEM
    • lchronically
    • ill

    l elderly

    • lbedridden
    • patients

    • l> 50% of
    • elderly residents (U.S)-malnourished

    • weight
    • loss  of > 5% ↑risk of mortality (5x
  9. Signs of secondary PEM
    • lDepletion
    • of subcutaneous fat

    • larms, chest wall, shoulders, or metacarpal
    • regions

    lWasting

    lquadriceps femoris and deltoid muscles & ankle or sacral edema.
  10. Central anatomic change in PEM
    • lgrowth
    • failure

    • lperipheral edema
    • (kwashiorkor)

    • lEnlarged
    • fatty liver (kwashiorkor)

    • lloss of
    • body fat and atrophy of muscle

    • l↓mitotic
    • index in the  crypts of the glands (small
    • bowel)

    • lhypoplastic
    • bone marrow (kwashiorkor and marasmus)

    • lcerebral
    • atrophy -  during 1 or 2 years of life

    • lthymic and
    • lymphoid atrophy (kwashiorkor > marasmus)
  11. lA form of PEM in patients with AIDS or advanced cancers

    lOccurs 50%
    of cancer patients
    Cachexia
  12. lcharacterized
    by:

    l extreme weight loss, fatigue, muscle atrophy,
    anemia,
    anorexia, and edema
    cachexia
  13. Cachetic agents:
    • lPIF (proteolysis-inducing
    • factor)

    • lglycosylated polypeptide excreted in the
    • urine of weight-losing patients with pancreatic, breast, colon, and other
    • cancers

    lLMF (lipid-mobilizing factor)

    lincreases fatty acid oxidation 

    • lpro-inflammatory cytokines such as TNF, IL-2
    • & IL-6
  14. lPIF (proteolysis-inducing
    factor)

    lglycosylated polypeptide excreted in the
    urine of weight-losing patients with pancreatic, breast, colon, and other
    cancers

    lLMF (lipid-mobilizing factor)

    lincreases fatty acid oxidation 

    lpro-inflammatory cytokines such as TNF, IL-2
    & IL-6
    Anorexia nervosa
  15. Clinical findings in anorexia nervosa
    • lSecondary
    • amenorrhea

    • l↓thyroid
    • hormone release

    • lcold intolerance, bradycardia,
    • constipation, and changes in the skin and hair

    • ldry and
    • scaly skin

    • l↓ Bone
    • density

    lAnemia, lymphopenia, & hypoalbuminemia

    • lcardiac
    • arrhythmia and sudden death

    lHypokalemia
  16. lmore common
    than anorexia nervosa

    lbetter
    prognosis

    lOccurs 1%
    to 2% of women and 0.1% of men, (average onset at 20 years of age)

    lBinge
    eating followed by induced vomiting

    lprincipally carbohydrates
    Bulimia
  17. Clinical findings in bulimia
    • lAmenorrhea
    • < 50%

    • lbec.
    • weight and gonadotropin levels are maintained near normal

    • lmajor
    • medical complications:

    • lelectrolyte imbalances (hypokalemia)
    • → cardiac arrhythmias

    lpulmonary aspiration of gastric contents

    l esophageal and gastric cardiac rupture.
  18. lgroup of
    related compounds that include

    lRetinol

    lRetinal (11-cis) – required
    for normal vision

    l retinoic acid – normal
    morphogenesis, growth, & cell differentiation

    l Retinoids → synthetic molecules that are chemically
    related to retinol. NO vitamin A–like biologic activity
    Vitamin A
  19. Dietary sources of Vitamin A
    lAnimal-derived foods

    • lYellow and leafy green vegetables →
    • carotenoids →  contribute approx. 30% Vit.A
  20. Which vitamin?
    lMaintenance of normal vision

    lCell growth and differentiation

    lHost resistance to infections

    lHumoral immunity, T-cell mediated
    immunity, natural killer cell activity, and phagocytosis

    lPhotoprotective and
    antioxidant agents
    Vitamin A
  21. Vitamin used for skin disorders (severe acne
    and certain forms of psoriasis)
    Retinoids
  22. Vitamin used for acute promyelocytic leukemia (15 : 17) translocation
    all-trans retinoic acid 
  23. Vitamin used for Neuroblastoma
    13-cis retinoic acid
  24. Pathologic effects of Vitamin A
    lHyperkeratotic skin lesions

    • lXerophthalmia (e.g. Bitot spots _ white patches of keratinized
    • epithelium appearing on the sclera)

    lCorneal ulceration

    lBlindness
  25. Symptoms for which vitamin toxicity?
    lheadache, dizziness, vomiting, stupor, and blurred vision,
    seizures & exfoliative dermatitis
    Acute toxic Vitamin A
  26. Symptoms for which type of toxicity?
    lweight loss, anorexia, nausea, vomiting, and bone and joint
    pain

    lPredisposition
    to bone fractures (due to stimulation of osteoclasts)
    Chronic toxicity of Vitamin A
  27. Which vitamin?

    labsorbed in the jejunum along with fats

    ltransported in the blood bound to a protein

    lTo achieve biological potency, must be hydroxylated to active metabolites in
    the liver and kidney

    lpromotes calcium and phosphate absorption from the small
    intestine and may directly influence mineralization of bone
    Vitamin D
  28. Vitamin that prevents the following:
    lrickets (in children whose epiphyses have not already
    closed)

    losteomalacia (in adults)

    lhypocalcemic
    tetany.
    Vitamin D
  29. lStimulation of intestinal calcium absorption

    lStimulation of calcium reabsorption in the kidney

    lInteraction with parathyroid hormone (PTH) in the regulation of blood
    calcium

    lMineralization of bone
    Vitamin D
  30. Causes of Vitamin D deficiency
    • lChronic renal failure (MCC)
    • – lack α 1 hydroxylase

    lPoor diet  - elderly & alcoholism

    lMalabsorption – celiac dse.

    lLiver disease – cirrhosis

    l↓ first hydroxylation

    lDrugs enhancing cytochrome P-450 system

    le.g phenytoin, alcohol, barbiturates → ↑ metabolism of 25-(OH)-D3

    lHypothyroidism/hyperphosphatemia - ↓ α 1 hydroxylase synthesis

    lGenetic dses.

    lType I Vit. D – dependent ricket

    lType II Vit. D – dependent ricket
  31. Clinical findings in which disorder?
    lGrowth failure

    lSkeletal abnormalities

    lRachitic rosary

    lCraniotabes
    Rickets
  32. Most common cause of Vitamin D toxicity
    • inordinate
    • consumption of vitamin preparations
  33. Conditions of hypervitaminosis D
    • lHypercalcemia - initial
    • response to excess vitamin D

    lweakness and headaches

    lnephrolithiasis or nephrocalcinosis

    • lEctopic
    • calcification

    lblood vessels, heart, and lungs



    • lIn children
    • - metastatic calcifications of soft tissues (kidney)



    • lIn adults -
    • bone pain and hypercalcemia
  34. Most active form of Vitamin E
    α –tocopherol
  35. Functions of vitamin E
    lAntioxidant

    • lPrevents free radical generated-lipid peroxidation of polyunsaturated fatty
    • acids in the cell membrane
  36. Causes of Vitamin E deficiency
    lChronic fat malabsorption

    labelalipoproteinemia
  37. lbone disease in growing children

    l hemorrhages and healing defects (children and adults)
    Scurvy
  38. Function of which vitamin?
    • lactivation of prolyl and lysyl hydroxylases providing for hydroxylation
    • of procollagen

    lReducing agent

    • lReduction of iron from
    • ferric to ferrous state

    lKeeps tetrahydrofolate  in the reduced form

    • lAnti-oxidants (traps oxygen
    • radical and regenerating the antioxidant form of
    • vitamin E)

    lSynthesis of cathecolamines

    lPrevents nitrosoamine
  39. Symptoms of which vitamin deficiency?
    lPoor wound healing

    lBone pain

    lHemostasis abnormalities

    lScorbutic rosary

    lBleeding of gums

    lPeriodontitis/loss of teeth

    lAnemia

    lIncrease bleeding time
    Vitamin C
  40. lCoenzyme
    for Carboxylation of
    Glutamate in the Postsynthetic Modification of Calcium-Binding Proteins
    Vitamin K
  41. lREQUIRED
    FOR SYNTHESIS OF BLOOD-CLOTTING PROTEINS: Factor II, VII, IX, X, protein C and S
    Vitamin K
  42. Causes of Vitamin K deficiency
    lBroad spectrum antibiotics

    lMalabsorption syndromes

    lNewborn 

    lDrugs e.g. coumarin and warfarin

    linhibit formation of the Gla residues of prothrombin and Factors VII, IX and X.
  43. Clinical manifestations of Vitamin K deficiency
    lEcchymoses

    lGI bleeding
  44. Lab tests for vitamin K deficiency
    lProlonged prothrombin time (PT) – best test

    lProlonged PTT
  45. Functions of Thiamine
    • lregulates oxidative decarboxylation of α-keto acids, leading
    • to the synthesis of adenosine triphosphate

    lacts as a cofactor for transketolase in the pentose phosphate pathway

    • lit maintains neural membranes and normal nerve conduction
    • (chiefly of peripheral nerves)
  46. Which vitamin deficiency?
    lChronic alcoholics

    lpernicious vomiting of pregnancy
    Thiamine
  47. Major targets for thiamine deficiency
    • A, The flabby,
    • four-chambered, dilated heart of wet beriberi.
    • B, The peripheral neuropathy with myelin degeneration leading to footdrop, wristdrop, and sensory changes
    • in dry beriberi.
    • C, Hemorrhages into the mamillary bodies in the Wernicke-Korsakoff syndrome
  48. Dietary sources of Riboflavin
    lmeat, dairy products, and vegetables 
  49. Functions of which vitamin:
    lcoenzymes flavin mononucleotide and flavin adenine dinucleotide, which
    participate in a wide range of oxidation-reduction reactions
    Riboflavin
  50. Causes deficiency of which vitamin?
    lAlcoholics

    lChronic infection

    lAdvanced cancer

    lAnorexia nervosa

    lIndividuals who avoid dairy products
    Riboflavin
  51. Functions of niacin
    • lEssential component  of
    • Coenzymes

    lNAD - metabolism of fat, carbohydrates, and amino acids

    lNADP – Pentose phosphate shunt (synthesis of glutathione) 
  52. Sources for which vitamin?
    grains,
    legumes, and seed oils and in much smaller quantities in meats
    Niacin
  53. The following causes which vitamin deficiency?
    lTryptophan deficiency

    lAlcoholics

    lchronic debilitating illnesses, including HIV
    infection

    l Long term use of isoniazid and 6-mercaptopurine.
    Niacin
  54. Which disorder and vitamin deficiency?
    l“ rough skin”

    lThree Ds“

    lDermatitis – redness, thickening  & roughening of the skin → scaling and
    desquamation

    lDiarrhea – caused
    by atrophy of GIT mucosa → submucosal inflammation → ulceration

    lDementia – neuron degeneration in the brain, accompanied by degeneration
    of spinal cord
    Pellagra
  55. Vitamin?
    lFunction:

    lcofactor for enzymes involved in lipids and amino acid
    metabolism
    Pyridoxine
  56. Vitamin?
    lCauses of deficiency:

    lProcessed food

    lAlcoholics – due to acetaladehyde

    lIsoniazid – pyridoxine antagonist

    lPregnancy - ↑ demand
    Pyridoxine
  57. Which vitamin deficiency?
    lseborrhoea dermatitis,

    lcheilosis,

    lglossitis,

    lperipheral neuropathy

    lsometimes convulsions.
    Pyridoxine
  58. Functions of which vitamin?
    essential
    cofactors in nucleic acid synthesis
    Folate
  59. Causes of folate deficiency?
    lPregnancy

    • loral contraceptives, anticonvulsants, ethanol, and cigarette
    • smoking interfere with folate absorption and
    • metabolism

    lintestinal malabsorption

    lmetastatic cancer
  60. Which vitamin deficiency?
    lMegaloblastic anemia

    lNeural tube defects

    lContribute to development of
    colon cancer
    Folate
  61. an accumulation of adipose tissue that is of sufficient magnitude to impair health
    Obesity
  62. BMI parameters
    lBMI bet. 25 kg/m2 and 30 kg/m2- - overweight

    lBMI above 30 kg/m2 - obese

    • lBMI > 40 kg/m2
    •  -
    • morbid obesity
  63. lprotein product of the ob
    gene and is mainly produced in adipocytes

    linsulin-stimulated glucose
    metabolism

    limportant factor in the regulation of leptin levels

    lIn
    Hypothalamus it stimulates POMC/CART neurons that produce anorexigenic neuropeptides (MSH) and
    inhibits NPY/AgRP neurons
    that produce  (orexigenic) neuropeptides
    Leptin
  64. Functions of leptin
    • lRegulates
    • not only food intake but also energy expenditure

    • lstimulates physical activity, heat production,
    • and energy expenditure

    • lcan
    • function as a pro-inflammatory cytokine

    • l
    • participates in the regulation of hematopoiesis and lymphopoiesis
  65. lstimulate fatty acid oxidation in muscle, causing a decrease in fat
    mass

    lfat-burning
    molecule” and the “guardian angel against obesity,”

    l↓ the
    influx of fatty acids to the liver and the total hepatic triglyceride content

    l↓ glucose
    production in the liver
    Adiponectin

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