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IHO Final > Heme, Iron, Blood Plasma > Flashcards

Heme, Iron, Blood Plasma Flashcards

1
Q

Name 2 types of congenital methemoglobinemia

A

Congenital - lack of NADH cyctochrome b5

Inherited hemoglobin M disease - mutation in heme pocket which stablizes ferric F3 iron.

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2
Q

Causes of acquired methemoglobinemia

A

Sulfa drugs (TMP), lidocaine, benzocaine, Dapsone

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3
Q

Treatment methemoglobinemia

A

reducing agents - methylene blue or ascorbic acid

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4
Q

Explain the Bohr effect

A

Increase in pH (decrease in CO2) hemoglobin affinity increases

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5
Q

An increase in temperature does what to hemoglobin’s oxygen binding affinity?

A

Decreases it

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6
Q

What is the role of bicarbonate in the transport of oxygen and CO2 between the lungs and tissues?

A

Tissues - CO2 converted to bicarb and H+ the H+ then binds the heme and release O2 to tissues
Lungs - H+ released from hemeglobin to bind to O2 - the H+ binds bicarbonate forming water and CO2 which is expired.

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7
Q

Most common deficiency in hereditery spherycytosis?

A

ankyrin

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8
Q

Symptoms of spheryocytosis?

A

splenomegaly, jaundice, secondary to hemolytic anemia. typically follows EBV or intense physical work

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9
Q

Treatment for spherocytosis?

A
  1. Give vaccines for HIB, PCV, meningcocal
  2. Remove spleen
  3. Folic acid supplement
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10
Q

Difference between oncotic and hydrostatic pressure?

A

Hydrostatic pressure created by beating of the heart

Oncotic pressure is based on the amount of proteins in the blood

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11
Q

List causes of ascites

A

Alcoholism (cirrhois), CHF, Kwashiorkor (lack of proteins)

Also some cancers where the tumors produce fluid

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12
Q

Treatment for Ascites

A

Periscentesis - give albumin if remove more than 5 L

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13
Q

What is genetic heredibility of G6PD

A

x-linked

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14
Q

If you have G6PD you are unable to reduce this cofactor

A

NADP+ to NADPH

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15
Q

List stressers of G6PD and what do they cause

A

Infection, Fava beans, drugs like antimalarials, Dapsone, and sulfa, Henna tattoos. Oxidative stress

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16
Q

Histologic findings for G6PD

A

Heinz bodies, bite cells and blister cells

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17
Q

Sx of G6PD

A

Dark urine, skin pallor, jaundice, hepatosplenamegaly, fever

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18
Q

What cofactor is required for Glutathione reductase to make glutathione

A

FAD

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19
Q

What pathway does G-PD enter into?

A

Pentose Phosphate Pathway

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20
Q

Why is selenium required in diet?

A

Allows conversion of H202 to H+ and H20

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21
Q

What type of anemia is associated with lead poisoning?

A

microcytic anemia

22
Q

What enzymes does Pb2+ block in the heme synthesis pathway?

A

Delta- ALA - dehydratase and ferrochetalase

23
Q

What is porphyria?

A

Inherited disorder of heme production

24
Q

Name symptoms of acute porphyria

A

constipation, diarrhea, n/v, back, chest and neck pain, AMS, tachycardia

25
Q

Diagnostic signs of acute porphyria

A

Increase in intermediates (porphobilinogen), increased ALA if lead poisoning

26
Q

What defect in heme synthesis pathway is not a porphyria?

A

delta -ALA synthase deficiency (also Autosomal recessive)

27
Q

Describe Cutena Tarda.

A

Hepatic URO-D deficiency, linked to Hep-C (acquired) - congenital is HFE C282Y homozygous

28
Q

Symptoms of cutaneous porphyria

A

Deposits in the skin, scarring, hyperpigmention, hyper trichosis, bullous dermatosis

29
Q

B6 deficiency manifests as this.

A

Microcytic hypochromatic anemia

30
Q

What supplement is needed for a patient on Isoniazid?

A

B6 - pyridoxal phosphate

31
Q

What populations are at high risk for B6 deficiency?

A

Pregnant people, alcoholics, diabetes, HIV+, seizure disorders

32
Q

If a pt. presents with excess unconjugated bilirubin there is a problem with this reaction?

A

Glucorination in the liver

33
Q

Bilirubin is converted to this form for excretion in the urine, stool

A

Urobilinogens, stercobilinogens

34
Q

List significant lab findings for hemochromatosis

A

Increased serum Fe, ferritin, transferrin iron sat.

Decreased total iron binding capacity

35
Q

List significant lab finding for iron deficiency anemia

A

Increased total iron binding capacity.

Decreased serum iron, ferritin and transferrin iron

36
Q

What AOCD?

A

Anemia of chronic disease - too much stored iron, can’t access it.

37
Q

Confirmation of hemochromatosis diagnosiss is done with these procedures/tests

A

Liver biopsy and T2star MRI

38
Q

What is the mutation associated with Type I hereditary hemochromatosis?

A

Cysteine to Tyrosine substitution at 282, C282Y

39
Q

Effect of C282Y mutation

A

Decreased hepciden and increased iron absorption

40
Q

Triad of symptoms for hemachromatosis or iron overload

A

Diabetes, hepatomegaly, hyperpigmentation, leads to cirrhois, hepatocellular carcinoma and CHF

41
Q

Treatment for hemochromatosis

A

Ferritin < 1000 mg/L - phelbotomy

Ferritin > 1000 mg/L - add liver biopsy - check for HCC

42
Q

Causes of iron deficiency anemia

A

Blood loss, increased requirement, and decreased absorption

43
Q

Symptoms of iron deficency anemia

A

Fatigue, irritability, pica, koilonychia (spooned nails), glossitis. kids - impaired psychomotor development

44
Q

Treatment of iron deficency includes in this steps

A

Look for source of blood loss, rule out intervascular hemolysis. If negative supplement with Iron

45
Q

Disease states associated with AOCD

A

Infectious - TB, Malignant - Hodgkins, NHL, Autoimmune - RA, trauma and heart disease

46
Q

Release of what 2 immunologic factors results in increased hepcidin

A

IL6 and IL1B

47
Q

Treatment of AOCD

A

Treat the underlying process and give EPO

48
Q

Why is heme iron absorbed more readily than non-heme iron

A

Heme does not have to converted to be absorbed.

49
Q

List 2 transporters for heme

A

Ferrous +2 - HPC1

(Ferric +3 converted to Ferrous) - DMT1

50
Q

What enzyme converts ferric iron to ferrous iron?

A

Duodoenal cytochrome B reductase

51
Q

List promotors of iron absorption

A

Ascorbic acid, citric acid, beta carotene, alcohol

52
Q

Describe Sprue

A

Disorder of duodenum which inhibits absoprtion of iron (often called Celiac)

IHO Final (40 decks)

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