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310 Cards in this Set
- Front
- Back
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erythrocyte sedimentation rate in old age indicates
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a disease process
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enhancement of liver cytochrome P450 system
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increased synthesis of GGT...excellent marker for alcoholic liver disease
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what is an excellent marker for alcoholic liver disease?
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enhancement of cytochrome P450 system
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increased production of NADH causes
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lactic acidosis-pyruvate --> lactate
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fasting hypoglycemia
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pyruvate is not available for gluconeogenesis
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hypertriglyceridemia
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1,3 biphosphoglycerate-->dihydroxyacetone phosphate-->glycerol 3-phosphate-->triglycerides
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lab test alterations in alcoholics
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enhancement of liver cytochrome p450 system, increased production of NADH causes lactic acidosis and fasting hypoglycemia and hypertriglycceridemia...also causes increase in ketoacid synthesis and increase in fatty acid synthesis and hyperuricemia and increased anion gap metabolic acidosis
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acidosis or alkalosis with alcoholics?
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anion gab metabolic acidosis because of lactate
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lab test alterations in smokers
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respiratory acidosis, hypoxemia, increased CO, secondary polycythemia, absolute neutrophilic leukocytosis
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acidosis or alkalosis in smokers?
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respiratory acidosis
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plasma/serum turbidity due to
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increase in triglycerides, NOT cholesterol
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triglycerides are carried by
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lipoproteins (85% chylomicrons) and 55% VLDL
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triglycerides are falsely increased after
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eating
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chylomicrons are __- dense than VLDL
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less dense
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chylomicrons form a ___ in plasma
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wsupranate
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VLDL forms a ___ in plasma
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supranate (more protein, so it doesn't float on surface of plasma)
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increased turbidity inteferes with
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measuring enzymes and serum Na, so it's falsey low values
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albumin binds
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40% of total calcium in blood
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how much calcium is free, ionized calcium and metabolically active?
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47%
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low serum albumin ___ calcium bound to albumin
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decreases, so it's hypocalcemia...PTH is normal
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normal females have __ Barr bodies. Males have __ Barr bodies
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females = 1 ; males = 0
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Klinefelter syndrome has __ Barr body
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1
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Turner syndrome has __ Barr body
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0
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cystic fibrosis = deletion of
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3 nucleotides coding for phenylanine
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|
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cystic fibrosis on chromosome
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7
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|
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Cystic fibrosis transmembrane regulator is defective and
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degraded before reaching the cell membrane after it leaves the Golgi apparatus
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Tay sachs is
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4 base insertion produces a frame shift
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tay sachs codes for defective
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hexosaminiadase
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sickle cell disease/trait is what type of mutation?
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point mutation involving thymidine replaceed by adenine
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sickle cell codes for __ instead of ___
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valine instead of glutamic acid in 6th position of B globin chain
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B thalassemia major is what type of mutation?
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point mutation produces a stop codon leading to termination of DNA transcription of B globin chain
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trinucleotide repeat disorders gets progressively worse in future generations. This is called
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anticipation
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Huntington's is wat type?
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autosomal dominant
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Fragile X syndroms is
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SXR, female carriers with trinucleotide repeats eventually become symptomatic
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Friederich's taxia is
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autosomal dominant
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myotonic dystrophy is
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autosomal dominant
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nondisjunction is due to
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unequal separation of chromosomes in first phase of meiosis
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mosaicism is
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nondisjunction nof chromosomes in mitotic division in the early embryonic period. 2 chromosomally different cell lines are derived from a single fertilized egg
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mosaicism usually involves
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sex chromosomes such as gonadal dysgenesis with XO/XX, XO/XY
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Translocation
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1 part of a chromosome is transferred to a non-homologous or homologous chromosome
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what is balanced translocation?
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if the translocated fragment is functional
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What is Robertstonian translocation?
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in Down's syndrome, the balanced translocation with a translocation between 2 acrocentric chomosomes (chroms 14 and 21 produce 1 long chromosome)
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In Down's, all of the #___ are functioning
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all #21s are functional. Get 1 #21 from father, 1 14-21 and 1 normal 21 from affected mother
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cri-du-chat is
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deletion of short arm of chromosome 5. mental retardation, cries like a cat
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microdeletion syndromes
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loss a small part of 1 chromosome. You can only identify it with high resolution
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Prader-Willi syndrome
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microdeletion of chromosome 15
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chromsome 15 deletion is of what origin?
|
paternal
|
|
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Prader Willi syndrome involves
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obesity, hypogonadism, mental retardation
|
|
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microdeletion of chromosome 15 can also cause
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Angelman syndrome
|
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What is Angelman sydrome?
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child always happy/laughing, but can't talk.
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What diseases are genomic imprinting?
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Angelman and Prader Willi
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genetic disorders in Jews
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factor 12 deficiency, Gaucher's disease, tay sachs
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genetic disorders in Northern Europeans
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cystic fibrosis, MC genetic disease interfering with ability to reproduce
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genetic disorders in Mediterranean
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GP6D, sickle cell, B thalassemia
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genetic disorders in african americans
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sickle cell, B/alpha thalassemia, G6PD, hereditary persisitence of HgbF
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genetic disorder in southeast asians
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alpha thalassemia
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genetic syndrome associated with advanced maternal age
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21
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Down's syndrome folds
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epicanthal with upward slanting
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Down's reproductive
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all males are sterile, and females have 50% chance of having a child with Down's
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Trisomy 18
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Edward's syndrome = severe mental retardation, clenched hands with overlapping 2nd and 5th fingers. rocker bottom feet
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Trisomy 13
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Patau's syndrome = cleft/lip palate, severe mental retardation, polydactyly, cystic kidneys
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|
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disorders in dexcending order of frequency
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AD>AR>sex linked recessive>sex linked dominant
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Sex linked recessive
|
affected males transmit disease to both daughters, but no sons. daughters are asymptomatic carriers.
Female carrier transmits to 50% of boys and 25% of females |
|
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sex linked dominant
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males and heterozygous females both express disease
|
|
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what is the most common autosomal dominant disease?
|
von williebrand's
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|
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familial hypocholesterolemia is
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autosomal dominant
|
|
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most autosomal recessive are
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enzyme deficiencies
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most autosomal dominant disorders are
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strucutural defects in proteins and receptors
|
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inborn errors of metabolism are
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autosomal recessive
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|
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acute intermittent porphyria is
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autosomal dominant
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|
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C1 esterase inhibitor deficiency is
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autosomal dominant
|
|
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G6PD is
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Sex linked recessive
|
|
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lesch-nyhan is
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sex linked recessive
|
|
|
cystic fibrosis is
|
autosomal recessive
|
|
|
sickle cell trait/disease is
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autosomal recessive
|
|
|
hemochromatosis is
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autosomal recessive
|
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wilson's disease is
|
autosomal recessive
|
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the most common sex linked recessive disorder is
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fragile X
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SCID is
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sex linked recessive
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Wiskott-aldrich syndrome is
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sex linked recessive
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esticular feminization is
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sex linked recessive
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|
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chronic granulomatous disease of childhood is
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sex linked recessive
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|
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Bruton's agammagloulinemia is
|
sex linked recessive
|
|
|
fragile X is a
|
MC mendelian disorder associated with mental retardation and macroorchidism at puberty
|
|
|
what is the repeat in Fragile X?
|
CGG
|
|
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Lesch nyhan symdrome
|
deficiency of HGPRT = no inhibition of PRPP in purine metabolism. there is hyperuricemia, mental retardiation, and self mutilation
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|
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sex linked dominant disorders. affected women transmit symptomatic disease to
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50% of her daughters and 50% of her sons
|
|
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sex linked dominant disorders. affected males transmit symptomatic disease to
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all daughters and no sons
|
|
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what are sex linked dominant disorders?
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familial hypophosphaternia (defect in proximal reabsorption of phosphate and conversion of 25(OH)D3 to 1,25 OH-D3... and alport's syndrome
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|
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multifactorial polygenic inheritance are
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multiple small mutations plus the effect of the environment.
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what are examples of multifactorial polygenic inheritance?
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cleft lip or palate, congenital heart disease, coronary artery disease, gout, type 2 diabetes, essential hypertension, open neural defects, congenital pyloric stenosis
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mitochondrial DNA disorders - women transmit symptomatic abnormal allele to
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all the children
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mitochondrial DNA disorders - men transmit symptomatic abnormal allele to
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none of the children
|
|
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Leber's hereditary optic neuropathy
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mitochondrial DNA disorder. myoclonic epilepsy. lactic acid with stroke
|
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cystic fibrosis prevalence is
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1/2500
|
|
|
the number of couples at risk for cystic fibrosis
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1/25 x 1/25 = 1/625
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|
|
what is the carrier rate of cystic fibrosis?
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1/25
|
|
|
deformations occur in
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the last 2 trimesters after organs have developed
|
|
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oligohydramnios produces
|
facial and limb abnormalities (called Potter's facies)
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|
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What is a malformation?
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distrubance (drugs, infection) that occurs in morphogenesis of an organ
|
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what is hypospadias?
|
faulty closure of urethral folds
|
|
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what is epispadias?
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a defect in geital tubercle
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when does the neural tube normally close?
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days 23-28
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|
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what do teratogens do?
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interfere with formation of mitotic spindle, interfere with production of ATP, interfere with gene production
|
|
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what does cocaine do on the mother?
|
hypertension and abruptio placenta
|
|
|
hemochromatosis is
|
autosomal recessive
|
|
|
wilson's disease is
|
autosomal recessive
|
|
|
the most common sex linked recessive disorder is
|
fragile X
|
|
|
SCID is
|
sex linked recessive
|
|
|
Wiskott-aldrich syndrome is
|
sex linked recessive
|
|
|
esticular feminization is
|
sex linked recessive
|
|
|
chronic granulomatous disease of childhood is
|
sex linked recessive
|
|
|
Bruton's agammagloulinemia is
|
sex linked recessive
|
|
|
fragile X is a
|
MC mendelian disorder associated with mental retardation and macroorchidism at puberty
|
|
|
what is the repeat in Fragile X?
|
CGG
|
|
|
Lesch nyhan symdrome
|
deficiency of HGPRT = no inhibition of PRPP in purine metabolism. there is hyperuricemia, mental retardiation, and self mutilation
|
|
|
sex linked dominant disorders. affected women transmit symptomatic disease to
|
50% of her daughters and 50% of her sons
|
|
|
sex linked dominant disorders. affected males transmit symptomatic disease to
|
all daughters and no sons
|
|
|
what are sex linked dominant disorders?
|
familial hypophosphaternia (defect in proximal reabsorption of phosphate and conversion of 25(OH)D3 to 1,25 OH-D3... and alport's syndrome
|
|
|
multifactorial polygenic inheritance are
|
multiple small mutations plus the effect of the environment.
|
|
|
In addition to increased birthweight and hyperinsulinism in diabetes, what are other effects of diabetes?
|
open neural tube defects, cleft lip/palate, respiratory distress syndrome (because less surfactant production)
|
|
|
What does DES do?
|
interferes with mullerian structures in female fetus causing abnormalities in tubes, uterus, cervix, upper 1/3 of vagina, clear cell adenocarcinoma of vagina/cervix, fertility problems and implantation problems with problems in uterus and fallopain tubes
|
|
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what is the most common teratogen in the US?
|
alcohol
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|
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what does alcohol do during pregnancy?
|
mental retardation, intrauterine growth retardation, maxillary hypoplasia, microcephaly, atrial septal defects, hypoglycemia
|
|
|
what does heroin do in pregnancy?
|
small for gestational age, irritability/hyperactivity, high pitched cry with excessive hunger, salivation, sweating, tremors, fist sucking. temperature instability, seizures
|
|
|
what does isotretinoin do?
|
3Cs:
craniofacial abnormalities = small ears, micrognathia, cleft palate cardiac defects CNS malformations - hydrocephalus, microcephaly |
|
|
What does phenytoin do during pregnancy
|
nail hypoplasia, CNS abnormalities, cleft lip/palate, congenital heart disease
|
|
|
what does smoking do during prengnacy?
|
placental ischemia, increased risk for thrombosis in placental vessels, low birth weight
|
|
|
what happens during pregnancy with mothers with lupus?
|
complete heart block
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What does thalidomide do during pregnancy?
|
limb abnormalities, absent limbs (amelia) and phocomelia (seal like limbs)
|
|
|
what is amelia?
|
absent limbs
|
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what is phocomelia?
|
seal like limbs
|
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What does valproate do during pregnancy?
|
open neural tube defects
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what does warfarin do during pregnancy?
|
CNS defects and nasal hypoplasia
|
|
|
what are congenital infections?
|
toxoplasmosis, other (HBV, AIDS< parvovirus, syphilis), Rubella, CMV, herpes TORCH
|
|
|
what infections can be transmitted by breast feeding?
|
HIV, HBV, CMV
|
|
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what infections can be transmitted by cervical infection?
|
HSV2, chlamydia
|
|
|
what infection can be transmitted during delivery?
|
HBV
|
|
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what is the most common in utero viral infection?
|
CMV
|
|
|
what is the most common complication from CMV?
|
bilateral sensorineural hearing loss
|
|
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what does CMV do to fetuses?
|
bilateral sensorineural hearing loss
periventricular calcification hepatosplenomegaly chorioretinitis-->blindness |
|
|
what does urine culture reveal in newborns born with CMV?
|
large, basophilic intranuclear inclusions (owl eyes) in renal tubular cells
|
|
|
how do you treat newborns with CMV?
|
gancliclovir. if that doesn't work, then foscarnet
|
|
|
how is rubella transmitted to the fetus
|
transplacental
|
|
|
when is the highest incidence of congential abnormalities in fetuses with mothers with rubella?
|
first 8 weeks
|
|
|
what does rubella do to fetus?
|
interveres with protein synthesis and produces vasculitis. it causes sensorineural deafness, cataracts, and patent ductus arteriosus
|
|
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what does rubella do to fetuses heart?
|
patent ductus arteriosus
|
|
|
how is toxoplasmosis transmitted to a fetus?
|
transplacental
|
|
|
when does toxoplasmosis most commonly get transmitted?
|
later in pregnancy
|
|
|
what does toxoplasmosis do to fetus?
|
chorioretinitis-->blindness
calcifications in basal ganglia |
|
|
how do you identify toxoplasmosis in fetus?
|
Sabin Feldman dye test that uses live organisms
|
|
|
How is HSV2 transmitted to fetus?
|
through birth control in women actively shedding the virus. so they should deliver via c section
|
|
|
what does HSV2 do to newborn?
|
local or systemic disease: encephalitis, skin infections
|
|
|
how is HSV2 treated in newborns?
|
acyclovir
|
|
|
how is syphilis transmitted to the fetus?
|
transplacental
|
|
|
when is syphilis transmitted to fetus?
|
usually NOT during the first 5 months because anatomical barriers prevent access to the fetal circulation
|
|
|
what is the most common sign of syphilis in a newborn?
|
hepatomegaly
|
|
|
what are signs of syphilis in newborns?
|
osteochondritis, hepatomegaly, mucocutaneous lesions, pneumonia alba (lobar pneumona) sniffles,
|
|
|
what are common signs of late neonatal syphilis (more than 2 years)
|
frontal bossing is most common. also saber shins, rhagades (perioral linear scars), Hutchinson's triad-teeth (notched upper central incisors called Hutchinson's teeth and malformed molars called mulberry molars...interstitial keratitis (blindness), sensorineural hearing loss
|
|
|
how do you treat syphilis in children?
|
penicillin
|
|
|
What does congenital chicken pox cause?
|
chorioretinitis = potential for blindness
limb hypoplasia cortical atrophy in the brain vesicular skin lesions |
|
|
when you get old, what happens to immune system?
|
decreased T cell function, loss of isohemagglutinins to blood antigens (may not develop hemolytic transfusion if blood is mismatched)
|
|
|
what is a common skin change in old people?
|
senile purpura over the dorsum of hands and lower legs where bumping into objects occurs, decreased sweating
|
|
|
what is common in the GI tract when you get old?
|
decreased gastric acidity, decreased colonic motility (constipation-->diverticulosis), decreased activity of hepatic cytochrome P450 (danger of drug toxicities)
|
|
|
what is common renal problems when you get old?
|
decreased GFR with reduction in creatinine clearance (risk of drug toxicity due to slow clearance of drugs)
|
|
|
what is the usual cause of pneumonia in old people?
|
strep pneumonia
|
|
|
what is the most common type of stroke in old people?
|
aterhosclerotic type
|
|
|
what is the most common cause of lbindness in the elderly?
|
macular degeneration
|
|
|
what is the precursor to squamous skin cancer?
|
actinic (solar) keratosis
|
|
|
what are the top 5 causes of death in males and females?
|
heart disease, cancer, stroke, COPD, motor vehicle
|
|
|
what are the 3 top causes of death in children 1-14?
|
accidents (motor vehicle, falls, burns); cancer; congenital anomalies
|
|
|
what are the 3 top risk factors for morbidity and mortality in the US?
|
cigarette smoking, dietary factors/activity patterns, high saturated fat/lack of exercise/alcohol abuse
|
|
|
when drowning, what is destroyed in the lungs?
|
surfactant --> leads to atelectasis with intrapulmonary shunting --> diffuse alveolar damage and initiates spasm in bronchioles.
|
|
|
what is immediate COD in drowning?
|
cardiac arrhythmia
|
|
|
third degree burns are
|
painless
|
|
|
second degree burns involve
|
entire epidermis
|
|
|
third degree burns include
|
extensive necrosis of epidermis/adnexa
|
|
|
3rd degree burns can cause what type of cancer
|
squamous cell
|
|
|
how do you identify toxoplasmosis in fetus?
|
Sabin Feldman dye test that uses live organisms
|
|
|
How is HSV2 transmitted to fetus?
|
through birth control in women actively shedding the virus. so they should deliver via c section
|
|
|
what does HSV2 do to newborn?
|
local or systemic disease: encephalitis, skin infections
|
|
|
how is HSV2 treated in newborns?
|
acyclovir
|
|
|
how is syphilis transmitted to the fetus?
|
transplacental
|
|
|
when is syphilis transmitted to fetus?
|
usually NOT during the first 5 months because anatomical barriers prevent access to the fetal circulation
|
|
|
what is the most common sign of syphilis in a newborn?
|
hepatomegaly
|
|
|
what are signs of syphilis in newborns?
|
osteochondritis, hepatomegaly, mucocutaneous lesions, pneumonia alba (lobar pneumona) sniffles,
|
|
|
what are common signs of late neonatal syphilis (more than 2 years)
|
frontal bossing is most common. also saber shins, rhagades (perioral linear scars), Hutchinson's triad-teeth (notched upper central incisors called Hutchinson's teeth and malformed molars called mulberry molars...interstitial keratitis (blindness), sensorineural hearing loss
|
|
|
how do you treat syphilis in children?
|
penicillin
|
|
|
What does congenital chicken pox cause?
|
chorioretinitis = potential for blindness
limb hypoplasia cortical atrophy in the brain vesicular skin lesions |
|
|
when you get old, what happens to immune system?
|
decreased T cell function, loss of isohemagglutinins to blood antigens (may not develop hemolytic transfusion if blood is mismatched)
|
|
|
what is a common skin change in old people?
|
senile purpura over the dorsum of hands and lower legs where bumping into objects occurs, decreased sweating
|
|
|
what is common in the GI tract when you get old?
|
decreased gastric acidity, decreased colonic motility (constipation-->diverticulosis), decreased activity of hepatic cytochrome P450 (danger of drug toxicities)
|
|
|
what is common renal problems when you get old?
|
decreased GFR with reduction in creatinine clearance (risk of drug toxicity due to slow clearance of drugs)
|
|
|
malignant hyperthermia results from
|
defective Calcium channels in the muscle sarcoplasmic reticulum
|
|
|
how do you treat malignant hyperthermia?
|
dantrolene
|
|
|
what is destroyed in lungs during drowning?
|
surfactant
|
|
|
what is the peak sensitivity to ionizing radiation?
|
G2 and M phase
|
|
|
What is G2?
|
synthesis of tubulin for mitotic spindle
|
|
|
What is M phase?
|
assembly and disassembly of mitotic spindle
|
|
|
What tissues are highest radiosensitivty?
|
hematopoietic cells lymphocytes>granulocytes>platelets>mature RBCs
|
|
|
what is the tissue with the lowest radiosensitivity?
|
brain
|
|
|
what is the earliest change from total body irradiation?
|
lymphopenia>thrombocytopenia>bone marrow hypoplasia
|
|
|
what does UVB do to the skin?
|
mutagen - thymidine dimers
|
|
|
what is the most common skin cancer?
|
basal cell carcinoma
|
|
|
what is the precursor to squamous carcinoma?
|
actinic/solar keratosis
|
|
|
__ventilation is essential at high altitude
|
hyperventilation
|
|
|
what type of acidosis/alkalosis is present in high altitude?
|
respiratory alkalosis
|
|
|
what drug prevents acute mountain sickness?
|
acetazolamide, a carbonic anhydrase inhibitor that produces metabolic acidosis - compensates for the respiratory alkalosis that you normally see
|
|
|
what causes rigor mortis?
|
decrease in ATP in muscle
|
|
|
where is ethanol reabsorbed?
|
small intestine (75%), stomach (5%)
|
|
|
what aprtially metabolizes alcohol?
|
alcohol dehydrogenase
|
|
|
what is the liver metabolism of alcohol?
|
alcohol --> acetaldehyde + NADH --> acetate + NADH --> acetyl CoA
|
|
|
what enzymes are involved in liver metabolism of alcohol?
|
alcohol to acetaldhyde is done by alcohol dehydrogenase
then aldehyde dehydrogenase converts it to acetate and then to acetyl coA |
|
|
what blocks aldehyde dehydrogenase?
|
disulfiram
|
|
|
what is legally drunk?
|
100mg/dL
|
|
|
what level of alcohol will cause stupor or coma?
|
300-350 mg/dL
|
|
|
what level of alcohol will cause death?
|
500 mg/dL
|
|
|
when does delirium tremens occur?
|
3-5 days after complete withdrawal
|
|
|
what is delirium tremens?
|
tremulousness, disorientation, visual hallucinations, agitation
|
|
|
what is treatment for delirium tremens?
|
IV diazepam and thiamine
|
|
|
what is Mallory Weiss syndrome?
|
tear of the distal esophagus/proximal stomach from retching
|
|
|
What is Boerhave's syndrome?
|
rupture of distal esophagus/proximal stomach from retching
|
|
|
what is esophageal varicies?
|
effect of portal vein hypertension due to alcoholic cirrhosis
|
|
|
how does alcohol cause hemosiderosis?
|
alcohol increases reabsorption of iron
|
|
|
what type of hyperlipidemia does alcohol cause?
|
type IV. increases synthesis of VLDL
|
|
|
what type of pneumonia is caused by alcohol
|
Klebsiella pneumonia
|
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what type of cancer can be caused by alcohol?
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squamous: oropharynx, midesophagus, larynx,
adenocarcinoma:pancreas, liver |
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what type of cerebellar degeneration occurs in CNS/PNS?
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Hu and Yo antibodies
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how do you measure nicotine intake?
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measure plasma/urine levels of cotinine
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what is the most common genetic defect in smoking-induced cancer?
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nicotine inactivates p53 suppressor gene by a point mutation on chromosome 17
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what drugs cause interstitial pulmonary fibrosis?
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amiodarone, bleomycin, busulfan, cyclophosphamide, nitrofurantoin, nitrosourea, methysergide, methotrexate, procarbazine
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what does methysergide cause?
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pulmonary fibrosis, retroperitoneal fibrosis, Raynauds
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what do meat packers get exposed to?
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polyvinyl chloride. increased risk of hepatic angiosarcoma
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what do dry cleaners get exposed to?
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CCl4 with liver necrosis due to free radicals
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what do rubber/chemical industry get expossed to?
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benzene = aplastic anemia, leukemia
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what do painters get exposed to?
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methylene chloridde = converted into carbon monoxide
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what do petroleum industry people get exposed to?
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benzene, polycyclic hydrocarbons =lung cancer
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what do sewer workers get exposed to?
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hydrogen sulfide gas: sulfhemoglobinemia
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if you overdose on rubbing alcohol
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metabolic end product in the liver is acetone. there is no metabolic acidosis (unlike other alcohols)...deep coma with hyporeflexia
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what if you overdose on methyl alcohol (wood's alcohol)
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increased anion gap meabolic acidosis...optic neuritis and potential for blindness.
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what is wood's alcohol converted to
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formic acid
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what is treatment for wood's alcohol/methyl alcohol poisoning?
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IV ethanol is the competitive antagonist
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what is antifreeze (ethylene glycol) converted into?
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oxalic acid
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if you overdose on rubbing alcohol
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metabolic end product in the liver is acetone. there is no metabolic acidosis (unlike other alcohols)...deep coma with hyporeflexia
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what if you overdose on methyl alcohol (wood's alcohol)
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increased anion gap meabolic acidosis...optic neuritis and potential for blindness.
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what is wood's alcohol converted to
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formic acid
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what is treatment for wood's alcohol/methyl alcohol poisoning?
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IV ethanol is the competitive antagonist
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what is antifreeze (ethylene glycol) converted into?
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oxalic acid
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why does antifreeze cause renal fialure?
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calcium oxalate crystals obstruct the lumens
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how do you treat antifreeze poisoning?
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ethanol IV. it's a competitive antagonist of methyl alcohl for alcohol dehydrogenase
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what does mercury poisoning cause?
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ATN involving proximal tubules
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how do you treat mercury poisoning?
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dimercaprol
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arsenic poisoning smells like
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garlic odor
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arsenic poisoning causes what type of diarrhea?
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rice water, similar to cholera
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what does the skin look like after arsenic poisoning?
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gray skin with dark macules
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arsenic poisoning causes what to the kidneys?
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ATN involving proximal tubules
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what is the treatment for arsenic poisoning?
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dimercaprol
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what does mushroom poisoning inhibit?
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inhibits RNA polymerase
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what are symptoms of mushroom poisoning?
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abdominal pain/vomiting, bloody diarrhea, jaundice, extensive fatty change
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what are symptoms of petroleum product disorders?
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euphoria (drunk acting) when inhaled or ingested. toxic doses cause convulsions, tinnitus, pulmonary edema
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what is strychnine poisoning?
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CNA stimulant that blocks postynaptic inhibition. it's similar to tetanus. it causes convulsions, opishotonus, risus sardonicus, death
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perfusion defect
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pulmonary embolus
no perfusion, only ventilation increase in dead space if give 100% Oxygen, get the PO2 up |
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ventilation defect
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give 100% oxygen, PO2 doesn't go up.
then you have a shunt |
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diffusion defect
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something in interface like fibrosis/sarcoidosis/pulmonary edema/fluid in heart failure
oxygen can't get through. |
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active J(jerk) receptor
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get dyspnea. can't take full breath because you have fluid in interstitium of lung, irritating J receptor
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what produces hypoxemia?
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ventilation defect, perfusion defect, diffusion defect, J receptor activation
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what is hypoxemia?
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decreased PO2
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what is anemia
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PO2 is normal. Oxygen saturation is normal. What is decreased? hemoglobin. still have normal respiration.
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both carbon monoxide and cyanide poisoning occur in
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house fire
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carbon monoxide poisoning
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oxygen saturation decreased. treat with 100% oxygen
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cyanosis
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a decrease in oxygen saturation
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carbon monoxide poisoning symptom
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headache
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methemoglobin poisoning
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Fe+3. oxygen can't bind. oxygen saturation decreased.
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methemoglobin blood drawn looks like
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chocolate
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dude coming out of rocky mountains, he was cyanotic, given 100% oxygen, still cyanotic
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drinking water in rocky mountains, loaded with nitrates/nitrates (oxidizing agents) --> oxidize hemoglobin so that it's Fe+3 instead of +2. oxygen didn't correct cyanosis. so it was probably methemoglobin
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how to treat methemoglobin
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IV methylene blue + vitamin C (reducing agent)
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datsone is used for
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leprosy
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sulfa and nitro drugs do 2 things
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1. produce methemoglobin
2. have potential of GP6D and hemolysis oxidizing agents cause increase in peroxide, which destroys RBC. |
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methemoglobinemia in HIV. why?
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because they're on sulfa drugs
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what type of oxygen curve do you want?
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right shifted, so that it reduces oxygen to tissue
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what happens in high altitude?
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you have to hyperventilate, and right shift curve. that's how you get oxygen up there
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CO causes decreased oxygen saturation and
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left shifted oxygen dissociation curve
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cytochrome oxidase
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last enzyme before transferring electron to oxygen
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cytochrome oxidase, cyanide, carbon monoxide
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inhibit cytochrome oxidase
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methemoglobin causes what shift?
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left
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what does CO block besides oxygen?
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blocks cytochrome oxidase. no electron goes to the oxygen. the whole system shuts down
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uncoupling
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ability of inner mitochondrial membrane to synthesize ATP.
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what is dinitrylphenol?
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uncoupling agent so that protons go right through membrane
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what are uncoupling agents that let protons go right through the mitochondrial membrane? (not cool...draining off all of the protons without much ATP.)
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salicylates, dinitrylphenol (preserves wood), alcohol,
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what happens from draining protons caused by uncoupling agents?
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any reactiont hat makes NADH and FADH gets revved up to make more protons. if you increase the rate of the chemical reaction, temperature goes up --> hyperthermia
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salicylate toxicity
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hyperthermia because it's an uncoupling agent
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alcoholic on a hot day
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develops heat stroke. very susceptible because mitochondria are already screwed up
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what produces tissue hypoxia?
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ischemia, hypoxemia, hemoglobin related things, uncoupling agents. absolute key things on boards
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respiratory acidosis. what happens to hemoglobin?
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nothing.
oxygen saturation = decrease it because PO2 is decreased. partial pressure of oxygen = decrease it |
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anemia
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hemoglobin is affected, but nothing else
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methemoglobin
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oxygen saturation affected
PO2 = no effect |
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what happens when you have decrease in ATP?
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hypoxemia
anaerobic glycolysis-->lactic acid |
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what cells can do anaerobic glycosis?
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any cell, including RBCs.
if no oxygen at end of electron transport system, then you get 2 ATP from anerobic glycolysis, but you get a buildup of lactic cid |
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coagulation necrosis
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tissue hypoxia --> causes coagulation necrosis (infarction). it's caused by a buildup of lactic acid in a cell
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when lack ATP, all ATPase pumps are screwed up because
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they run on ATP. so Na goes into cell and causes swollen cells.
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what drug blocks NaK pump?
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digitalis. so that Na goes into cardiac muscle to open Ca to increase force of contraction
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tissue hypoxia will cause tissue to swell up because
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Na goes into cell (irriversible)
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mature RBC energy source is
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anaerobic glycolysis
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what happens to Ca in tissue hypoxia?
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it enters cells via CaATPase pump. ATPase decreases, so Ca has easy access to cell. When it's in the cell, it activates phospholipases (damages cell membrane) and causes nuclear chromatin disappearance.
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what happens when Ca goes into mitochondria?
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destroys it.
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hypercalcemia causes
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acute pancreatitis because it activates enzymes in pancreas. it does the same thing in cells
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Ca most destroys what?
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cell membrane, irriversable damage
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what is lipofucin?
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wear and tear in old people. when you have free radical damage, the end product is lipofucin. lipofucin is lipids that you can't break down all the way
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what is free radical?
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unpaired electron in outer orbit
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RDS
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oxygen related free radical injury such as retinopathy of prematurity, damage to lungs (fibrosis in lungs)
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