Unit 3 -Nutrition and hematology Flashcards
Hemoglobin
Amount of oxygen carrying proteins
Hematocrit
Percent of blood volume occupied by RBC vs other things
MCV
Mean cell volume
MCH
Mean cell hemoglobin
RDW
% of red cell distribution width, the RBC size variation
Where are RBC regulated
The kidneys
Microcytic anemias
MCV under 80 (RBC are too small)
-iron deficiency
-Anemia of chronic disease
Normocytic anemia
80-200 MCV
Less then 3% Correted reticulocyte
-Blood loss, early stage iron deficit, aplatic anemia, renal disease, malignancy
More then 3% Corrected reticulocyte
-Membrane defects, abnormla hemoglobin, deficient enzyme
Macrocytic anemia
over 100 MCV
Megaloblastic: Folate deficiency Vit B deficency
Nonmegaloblastic: Liver disease, alcoholism, reitculocytosis, drugs
what is anemia
a deficency in teh number of erythrocytes. The quanity adn volume of hbg
What can anemia lead to
tissue hypoxia, tired, weak, SOB, Serious problems
Primary anemia
Rises due to a direct defect in the blood forming process
Secondary anemia
Occurs as a result of another underlying disease or condition such as chronic illness/infection
3 main causes of Anemia
Decreased RBC production, blood loss, increased RBC destruction
Decreased RBC production is caused by
GI tract: deficent in iron, cobalamin, rolic acid
Kidney: decreases RBC production
Liver: Decreased Iron avaible
Chronic blood loss
Bleeding from gastric ulcer, colorectal cancer, liver disease, chronic hemorrhage
Acute blood loss
GI bleed, rupture AA, trauma
What causes increased RBC destruction
Intrinsic: Sickle cell, G6PD deficency
Extrinsic: trauma, autoimmune, infection, meds
patho of iron deficient anemia
Stem cells, to erythroblast, to reticulocytes, to erythrocytes. This is called erythropoiesis, this is RBC replacement, Iron is essentail for this to happen
possible casues of iron deficient anemia
decreased dietary intake, decreased GI absorbtion, increased body demand, increased loss
patho of pernicious anemia
Vit B12 bound to protiens in foos. THis is called intrinsic factor. Made in stomach helps the intestines absorb. In this anemia IFA binds to intrinisc absorption of vit B12
Presentation of pernisious anemia
Re, sore, shiny tongue, N and V, anorexia, ABD pain after eating drining, muscle weakness, paresthia (damage to neurone) all because O2 is not getting to tissue
tests and treatment for pernisious anemia
blood smear, gastroscopy, B12, folate
Anemia of chronic disease is associated with
not enoigh RBC production, too small, body is destroying, cytokines take up iron
aplastic anemia
the boen marrow fails to produce enough RBC, WBC, and platelets
Chemo, radiation, adn herediatry can casue what anemia
aplastic anemia
Assessment for aplastic anemia
low WBC, HGB, Platelets
System assessments: resp, cvs, inf, bleeding
Do for aplastic
ID cause, transfusions, antibiotics, Chronic immunosuppressant, bone marrow transplant, anti T-cell
Patho of acute anemia
sudden hemorrhage, diminished volume, diminished O2
Chronic anemia pathogen
Iron deficient, GI bleed, menstuation
Sick cell disease
mosts common is African/asian decent they mutated to fight malaria, joint swelling nad pain
-Abnormal adult hemoglobin. RBC are stiff and changing shape into sickles
Clinical manifestation of sickle cell anemia
brain (paralysis, thrombosis) , lungs (pulmonary hypertension, pnuemonia), kidneys(renal failure), bones, joints (hand-foot syndrome), liver (hepatomegaly), skin (ulcers), penis, spleen, heart, eyes (Blindness, retinopathy)
Sickling event
triggered by O2, inf, low atmospheric O2, stress, dehydration
Sickling crisis
severe painful, acute, blood flow occluded, hypoxia, clot formation, shock
treatment for sickle cell anemia
stem cell transplant, bone marrow transplant, transfusion, fluids, pain releive, O2, antibiotics, vaccines, assess sttroke risk
Aquired anemia
caused by nutritional deficites, chronic disease, bone marrow disorders
Thrombocytopenia
reduction of platelets to an ampunt below 150.
Acute or prolonged state. Caused from abnormal homeostasis
Heparin induced thrombocytopenia
a complication caused by heparin that casuses a decrease in platelets in the blood. Stop heparin!!!
Hemophilia
genetic bleeding disorder in which blood does not clot properly
Hemarthorisis
bleeding into hoints that causes pain, swelling, and long term joint damage
assess for hemophilia
bleeding, bruising, joints, bleeding into brain
Do for hemophilia
factors, PTT, INR, Platelets, transfuse, replace missing factor
Von Willebrands
blood glycol protien protmotes hemostasis. specifically platelet adhesion. Most common congenital bleeding disorder, affects males and females,
Von Willebrands types
Type 1: most common, levels are low
Type 2: Factor sosen’t function properly
Type 3: Rare, the factor is completely absent
Symptoms of Von Willebrand
Excessive bleeding, nose bleeds that don’t stop in 10 mins, heacy or long mestural bleeding, blood in urine or stool, easy bruising lumpy
Teaching for Von willebrand
Razors, aspirin, toothbrushes
Optimum nutrition
The amoutn od nutrients are enough to meet the metabolic needs. Lowers the risk of chronic disease
Under nutrients
nutritional needs depleted, inadequete to meet metabolic demand
Risk for Undernutrition
socail isolation, disease processes, homelessness, poverty, emotional, can’t eat or won’t eat
Food affordability
adequate income is avaible to obtain nutitious foods
Food availibilty
adequate ampounts of nutrious foods are consistently available
Malnourishment symptoms in adults vs children
adults: feeling cold, unintended weight loss, chronic exhaustion, slow wound healing, weak muscles, reduced concentration.
Kids: Stunted growth, reduced enegery, unusual irritability, delayed developement
Obesity
above normal increase in proportion of fat cells in the body, genetics, food availability, mental, physical, socail
primary obesity
calorie intake is greater than metabolic need
Secondary obesity
congenital/chronimosmal/metabolic
Leptin
adipocytes, supresses appetite and hunger, regulates eating behaviour. obeisity is associated with high leptin levels, have dofficulty suppression
Insulin
Pancreas produces, decreases appetite, levels are frequenlty high
Ghrelin
Stimulates appetite, normal does not decline
Peptide YY
Decending colon and rectum. Inhbits appetite by slowing Gi motality and gatric emptying
non modifiable obeisity
genetics, age, endocrine disorder hypothyroidism, cushings, prayer-wili syndrome
Prader-willi syndrome
rare genetic disorder, key feature is a constatn sense fo hunger, want to eat constanly because you never feel, defects chromome 15
Gynoid obeisity and possible complication
Glutofemoral adipose tissue accumulation
-osteoporosis, varicose veins, cellulite, elevated triglycerides
Android obeisity and possible complications
abdominal adipose tissue accumulation
-Heart disease, diabetes, metablolic syndrome
Common disease caused by over nutrition
diabetes, sleep apnea, CVD, Cancer, liverdisease, osteoporosis, gull bladder, gut, arthritis
ABCD nutritional assessment
A: anthropometric measurements
b: Biochmical tests
C: Clinical observation
D: Det
Anthropometric measurements
Height, weight, BMI
Goals for BMI
18.5-24.9
Waist to hip ratio
wast in CM/Hip by cm goal is below 0.
Clinical observations for obeisity
vital signs, head to toe, nutritional, systems
Do for diabetes
Weight loss (meds), nutritionist, Bariatric surgery, gastric banding, diversion surgery, gastric bypass
