exam 9 Flashcards
Mb vs Hemoglobin
fx:
structure :
o2 dissociation curve:
which one has a higher percent saturation in tissues? In lungs?
Mb
fx: bind and transport o2
structure: Monomer tertiary stucture folded alpha helices
1 heme group per 1 02
O2: hyper bolic
Hemoglobin
fx: transport and store CO2 and O2
structure : tetramer (between 2 alpha globulin and 2 beta glob)
quaternary structure
4 heme groups per (1 per glob chain ) so binds 4 02.
o2 dissociation curve: sigmoidal
Mb has a higher percent saturation in tissue?
percent saturation is about the same in lungs
what is allosterism and does it work with Hb or Mb and why
what kind of curve does an allosteric protein have
it is regulation of proteins by binding effector molecules
it works with quaternary structures only so Hb
sigmoidal
Homotropic effector:
Heterotropic effector:
Homotropic effector: effector is identical to true ligand o2 and positive effector of Hb
Heterotropic effector:
effector chemical different
Name POSITIVE effectors that are important for Hb
what happens to the to the dis. curve
what does it do to O2 (hold release)
CO
O2
shifts to the left
Decrease O2 release ,
holds O2 INCREASES AFFINITY
R>T state
Name NEGATIVE effectors that are important for Hb
what happens to the to the dis. curve
what does it do to O2 (hold release)
-H+ (low pH) stable doexy form
this is because histadine side chains like Protons
-Co2
-2,3 bisphosphatglycerate (2,3 GPG)
-increase in temperature
increases realease of O2 decreases affintiy
shifts curve to right
T> R state
List 3 fates of CO2
- bicarb HcO3 (increases H+ which can protanate Hb and stabilize the T state. 60%
- carbinohemoglobin ….HbCO2…. co2 binds to alpha of hemoglobin. 30%
- disolve 10 %
what is bohr effects
talkabout how it relates to Lungs and tissue
change in Hb Oxygen due to pH
Lungs
have increase pH so CO2 is released and oxyhb is favored
Tissues
have a decrease in pH so [CO2] increases and deoxyHb is favored
2,3BPG affects what affinity and how
increases affinity of FHb so that the maternal Hb can give o2 to the baby
2,3BPG binds less tightly to HbF than to HbA
what two cells does erthopoiesis start with
what cell is the cell right before rbc
what is reticulocytosis
BFU-E
CFU- E
reticulocyte
reticulocytosis is when the body releases reticulocytes early (48 hrs in Bm and 48 in circulation) instead of the normal time it takes for rbc to mature which is 48 in bm and 24 in circulation
EPO is released by what organ
where does it bind
what are its effects
kidneys
it binds to epo receptor in BM to increase RBC
effects
-increases BFUE (increase proliferation)
-increase CFUE (decreasing cell death)
-increase hb syntheeis
-increas FE absorption
-increase erythroid differentiation
- release and production of reticulocytes
memorize
what is red cell distribution width (RDW)
what does low and high RDW indicate
measure of distribution of individual values for rbc volumes
shows cells of uneven size
low =
roughly the same size but doesnt mean healthy
can all be micro or macrocytic
high=
uneven sizes anisocytosis may be due to anemia
compare severe acute malnutrition (SAM)
Marasmus
-deficiency
-body looks like
-albumin levels
-viceral organ involved?
Kwashiorkor
Marasmus
-deficiency: calories all nutrition
-body looks like : broom stick loss of fat
-albumin levels: normal to slight
-viceral organ involved? no
Kwashiorkor
-deficiency: protein malnutrition
-body looks like: distension of stomach, spare sub cut fat and muscle
-albumin levels: large decrease
-viceral organ involved? yes
which on is associated with these sx (Bulimia or anorexia nervosa)
- <30 yo
-amenorrhea
- electrolyte imbal
-risk of cardiac arrythmias
- <30 yo - B
-amenorrhea - A - electrolyte imbal-B
-risk of cardiac arrythmias - B
vit A
purpose:
deficiency causes:
hyper vitaminosis
vit A (FAT SOLUBLE)
purpose:
- lipid matabolism
-vision (rhodospin in rod need)
-immune
deficiency causes:
-squamous metaplasia
*bitot spots, keratomalacia,
cornea ulcers
-nighblindness
-infection
Hyper:
(acute)
-yellow skin (not sclera)
-papilledema
-cerebral hypertension
(chonic)
-liver injury with fibrosis and death bone and joint pain
-
Vit D
fx:
deficiency dx:
hypervitaminosis D:
Vit D
fx: reabsorption of calcium , raise calcium from bone , absorption of phosphorous and calcium in stomach
deficiency dx:
causes decreased serum calcium and phosphate.
- rickets
-osteomalcia
hypocalcemic tetany
hypervitaminosis D:
calcification of kidneys due to hypercalcemia
premature babys may have what vit deficiency
vit e due to underdeveloped gut , causes neurogical dz and hemolysis
vit K due to lack of intestinal bacteria
causes bleading ,
caused by deficiency of coagulation factors
Ptprolonged initially and PTT also prolonged
what happens with thiamine deficiency vit B1
think neuro heart and nystagmus
-dry beriberi (peripheral neuropathy(
-wet beriberi (heart failure makes edema)
-wenicke-korsakoff syndrome (sever chronic deficiency) nystagmus ataxia defective memaory
who get riboflavin deficiency or B2
anorexia nervosa patient
niacin deficiency vit B3
dz and signs
pellegra
3 d’s
dementia
diarrhea
dermatitis (tips of fingers spared)
pyridoxine b6 deficiency
convulsions
seborrheic dermatitis (scaling) glossitits peripheral neuropathy
Vit C ascorbic acid deficiency
Vit C overdose
scurvy
lack of tensile strength hollagen joint pain, loss of teath bad wound healing
overdoes
increased kidney stones
increased absorption of iron
copper deficiency
myelonueropathy numbness difficulty using legs anemia
Zinc Deficiency
acrodermatitis enteropathica oozing rash around eye nose and mouth peranal perioal
poor night vision
diarrhea
selenium deficiency
myopathy including cardiomyopathy
what does ferritin do
what does transferrin do
ferritin: it stores iron in enterocyte
transferrin: transfers 2 ferric iron Fe 3+
1 ml of blood has how much iron
0.5 mg
what is ferrous is it toxic
unbound iron Fe2+ toxic that catalyzes ffenton reation to make free radicals
name the three places iron is
- in use with globin 75 % (3g)
- storage in ferritine hemosiderine 25% 1g
- in circulation 0.1% 4000mg
list least to most bio available heme iron from food
now list non heme free iron that comes from plants , list from least to most
heme iron» ferrous iron Fe2+» ferric Fe3+> Elemental iron Fe0
Ferric Fe3+
Ferrous (Fe2+) supplements
Elemental iron Fe0
what is transferrin
what causes its synthesis
it transportes Fe3+ Ferric iron
prevents fenton reaction
low iron levels cause synthesis
describe absorption of iron
cell uptake of iron
wh
at is the usual cause of deficiency anemia
period blood loss
when iron levels are low what happens to the amount of transferin and ferritin
low feratin
high transferrin (measured by TIBC)
describe signs of deficient anemia
spoon shapped nails (koilochia)
anisocytosis ( different sized cells)
target cells
cause of macrocytic anemia
decrease in folic acid (either by absoprtion or diet)
decrease in B12 (by absorption or diet) * causes nueroapthy if not tx)***
look at other side of this card
what is pernicious anemia PA
caused by
malabsorption of B 12
caused by autoimmune destroying perietal cells (resposible for making IF or intrinsic factor) this creates Ab that bind to I and prevents b12 binding
MALABSORPTION AND MEGOBLASTIC ANEMIA
tx with b12 shot or folate allows for synthesis of dTMP by passing need to recycle folate
what is gold standard to detect if b12 or folate deficiency
methylmalonic acid
how do we test for jaundice
give equation
what is kernicterus
when unconjigated biliruben get stuck in the brain due to untreated neonatal jaundice
tx with blue lit to make plana structure (DOESNT CHANGE TO CB)
what is B-flucaronidase
gut bacteria to help conjugate biliruben . babys lack this and are unalt to comfort UCB to CB so they get jaundice
a decrease in UCB uptake causes what
increase in UCB and jaundice
why is DBIL normal in pre hepatic jaundice
cause CB is not released into circulation due to healthy live
hepatic and post hepatic…
increase of decrease fecal urobillinogen
both are decrease
