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MOD II Exam 1 > Robbins - Chp 9 & 10 > Flashcards

Robbins - Chp 9 & 10 Flashcards

1
Q

Vitamin A Functions

A

Vision - used in synthesis of rhodopsin
Cell proliferation -> activation of retinoic acid receptors (RARs) by their ligands (squamous metaplasia of epithelium if deficient)
Lipid Metabolism - fatty acid oxidation (RXR activated by 9-cis-retinoic acid)
Immunity - gut epithelium, stimulates immune system

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2
Q

Vitamin A deficiency

A 
Celiac, Chrohn’s
Caused by bariatric surgery
Xeropthalmia
Night blindness
Dry, scaly skin
Corneal degeneration
Immunosuppression
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3
Q

Vitamin A Excess

A

Acute toxicity - nausea, vomiting, vertigo, blurred vision
Chronic toxicity - alopecia, dry skin, hepatic toxicity and enlargement, arthalgias, and pseudotumor cerebri
Teratogenic (cleft palate, cardiac abnormalities)

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4
Q

Vitamin D functions

A

Increases Ca absorption with TRPV6
Interaction with PTH (enhance RANKL on osteoblasts -> binds RANK on osteoclasts and activates them -> breakdown bone for resorption)

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5
Q

Vitamin D deficiency

A

Rickets
- frontal bossing, square head, rachitic rosary, pigeon breast deformity, lumbar lordosis, leg bowing
Osteomalacia
- persistent osteoid bone is weak and vulnerable to fractures of vertebral body and femoral neck

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6
Q

Vitamin C function

A

(Ascorbic acid)

  • antioxidant - facilitate iron absorption by reducing it to the Fe2+ state
  • necessary for hydroxylation of proline and lysis in collagen synthesis
  • necessary for dopamine beta-hydroxylase, which converters dopamine to NE
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7
Q

Vitamin C deficiency

A

Scurvy - swollen gums, bruising, petechiae, hemarthrosis, anemia, poor wound healing, corkscrew hair

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8
Q

Vitamin C excess

A

Nausea, vomiting, diarrhea, fatigue

Can increase iron toxicity in predisposed individuals by increasing dietary iron absorption

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9
Q

Zinc deficiency

A
  • rash around eyes, mouth, nose, and anus called acrodermatitis enteropathica
  • anorexia and diarrhea
  • growth retardation in children
  • depressed mental function
  • depressed wound healing and immune response
  • impaired night vision
  • infertility
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10
Q

Iron deficiency

A

Hypochromic microcytic anemia

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11
Q

B12 deficiency (cobalamin)

A

Megaloblastic pernicious anemia and degeneration of posterolateral spinal cord tracts

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12
Q

B3 Deficiency (niacin)

A

Pellagra - the three Ds: dementia, dermatitis, diarrhea

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13
Q

B1 Deficiency (thiamine)

A

Dry and wet beriberi, Wernicke syndrome, Korsakoff syndrome

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14
Q

Folate deficiency (B9)

A

Megaloblastic anemia, neural tube defects

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15
Q

BMI categories

A

18-25 -> good
25-30 -> overweight
>30 -> obese

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16
Q

POMC and CART

A
  • increase MSH and MC3/4R -> increased TSH and CRH -> increased energy expenditure (increase BMR)
17
Q

NPY and AgRP

A

Increase Y1/5R -> increase MCH and orexin -> increases appetite (orexigenic)

18
Q

Leptin

A

Made by fat cells
Stimulates POMC/CART, inhibits NPY/AgRP
Stimulates energy expenditure
Can be a proinflammatory cytokine

19
Q

Adiponectin

A

Produced by adipocytes

Binds to AdipoR1:muscle and AdipoE2:liver

20
Q

Ghrelin

A

Only hormone that increases food intake

Stimulates NPY/AgRP

21
Q

PYY

A

Secreted by ileum
Depresses appetite
Low in Prader Willi
Stimulates POMC/CART

22
Q

Hydrops fetalis

A

Edema of fetus during intrauterine growth

- immune or nonimmune

23
Q

Immune hydrops fetalis

A
  • type II hypersensitivity
  • blood group incompatibility (Rh)
  • consequences:
    — hemolytic anemia -> hypoxic injury to heart and liver -> decrease proteins and heart failure -> edema
    — jaundice -> kernicterus
    — erythroblastosis fetalis
    — extramedullary hematopoiesis in the liver
    — hepatosplenomegaly
24
Q

Nonimmune hydrops fetalis

A
  • CV defects
  • Chromosomal abnormalities
  • fetal anemia
    — alpha-thalassemia (most common cause of non immune)
    Clinical features: pallor, hepatosplenomegaly, jaundice, neuro injury, edema, extramedullary hematopoiesis in the liver
25
Q

PKU

A
  • autosomal recessive
  • due to decreased phenylalanine hydroxylase of decreased BH4 (malignant PKU)
  • Symptoms: intellectual disability, growth retardation, seizures, fair complexion, eczema, musty body odor
  • Treatment: decrease phenylalanine and increase tyrosine
  • malignant treatment: supplement BH4
26
Q

Maternal PKU

A

Due to improper dietary therapy during pregnancy

Symptoms in infant: intellectual disability, growth retardation, congenital heart defects

27
Q

Galactosemia

A
  • galactokinase Deficiency or classic galactosemia
  • galactokinase deficiency
    — autosomal recessive; milder
    — symptoms: galactosemia, galactosuria, infantile cataracts
  • classic galactosemia
    — absence of galactose-1-phosphate uridyltransferase
    — autosomal recessive
    — symptoms develop when infant begins feedings
    — symptoms: failure to thrive, jaundice, hepatomegaly, infantile cataracts, intellectual disability, predisposed to E. Coli sepsis
28
Q

Cystic Fibrosis

A
  • bicarb cannot be excreted -> acidic fluids -> increased mucin/plugging of ducts/increased bacteria -> pancreatic insufficiency
  • Meconium ileus
  • class II most common
  • heterozygote is at risk for pancreatic issues, pulmonary disease, obstructive azoospermia
29
Q

Wilms tumor is associated with what syndromes?

A

WAGR, Denys-Drash, Beckwith-Wiedemann

30
Q

WAGR syndrome

A

Wilms tumor, Aniridia (absence of iris), Genitourinary malformations, mental retardation/intellectual disability (WT1 deletion)

  • autosomal dominant PAX6
31
Q

Denys-Drash syndrome

A

Wilms tumor, diffuse mesangial sclerosis (early onset nephrotic syndrome), dysgenesis of glands (male pseudohermaphroditism), WT1 mutation

  • At risk for: gonadoblastoma
32
Q

Beckwith-Wiedemann Syndrome

A

Wilms tumor, macroglossia, organomegaly, omphalocele, large cells, genomic imprinting, hemipheryplasia (WT2 mutation)
- IGF2 - solely expressed on paternal allel when maternal is silenced, uniparental disomy = overexpression of IGF2 (growth factor)

  • at risk for: hepatoblastoma, pacreatoblastoma, adrenocortical tumors, rhabdomyosarcomas
33
Q

Morphologic features of Wilms tumor

A

Sheets of small blue round cells
Anaplastic cells: large hyperchromatic pleomorphic nuclei
Large circumscribed mass
Tumor is soft, tan to gray color with cysts and hemorrhage
Class triphasic combo: blastemal cells, stromal cells, epithelial cell types observed

  • clinical course: abdominal mass, hematuria, pain in abdomen, intestinal obstruction, HTN, increased risk of developing second primary tumors

MOD II Exam 1 (2 decks)

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