Test3 Flashcards
Spleen
- filtration-removes old/defective RBCs from the circulation.
- immunological-filters circulating bacteria, has rich supply of lymphocytes, monocytes and stored immunoglobulins.
- storage-stores RBCs and platelets (person with a splenectomy has higher circulating platelets).
Remove for: sickle cell,thrombocytopenia, ITP, trauma; thalassemia; observe for hemorrhage post-op bc spleen is very vascular; increased risk for infection
polycythemia vera
=primary polycythemia
results from chronic myeloproliferative disorder arising from chromosomal mutaion–involving RBCs and WBCs and platelets
age of dx=60 yo males
splenomegaly, hepatomegaly
Tx=phlebotomy
angina, heart failure, intermittent claudication, and thrombophlebitis
Thrombocytopenia
Platelets below 150,000
usually acquired
immune (ideopathic) thrombocytopenia=abnormal destruction of circulating platelets (ITP)
platelets are destroyed by macrophages (autoimmune)
Tx=corticosteroids to supress the phagocytic response of splenic macrophages; increases life-span of platelets;splenectomy
If heparin induced-protamine sulfate
Thalassemia
decreased erythrocyte production
autosomal recessive
abnormal hemoglobin production
common: Mediterranean, equitorial Asia, Middle East, Africa
can cause growth and development defecits
Tx: transfusions to keep Hgb>10; remove spleen
Iron Supplements
give 1 hour before meals with acidic drink
changes stool dark, not tarry
Hemoglobin and transfusions
Transfuse if Hgb is 6-7
Normal Hgb 13-17 men, 12-15 women
normal platelets 150,000-450,000
Megaloblastic Anemia
- B12 deficiency (pernicious anemia)-give coalbumin injections (B12) bc they don’t have intrinsic factor
- Folic Acid deficiency-foods: whole grains
Aplastic Anemia
- pancytopenia (decreased RBCs, WBCs, platelets)
- 70% ideopathic
- 30% chemical, congenital, meds (antisiezure)
- whole blood transfusions or just platelets
- bleed, infected
Sickle Cell Anemia
- spleen starts to not work (remove by age 2-3)
- worry about kidney failure, brain (stroke), lungs, heart (ischemia), eyes (retinal detachment)
- hydration!!!
- pain-past jam
- fever, swelling (joints), increased RR, HR, N/V
- pneumonia
- keep still, rest, ice, pressure, no aspirin
- morphine is drug of choice
Disseminated Intravascular Coagulation
- pallor, petechiae, purpura, oozing blood, hematomas, GI bleed, tachy, hypoTN, cry blood, urine bright red
- id quickly!
- O2, fluids-fresh frozen plasma, blood, give clotting factors.
- occurs in PG, septic, illness
Neutropenia
- neutrophils < 1500 (first responders to infection) normal is 4,000-11,000)
- usually due to immunosuppressive therapy
- masks signs of infection (bc there’s no immune response)
- strict infection prevention-reverse isolation, no fresh fruits, veggies, flowers
- fever of 100.4 is a huge deal
Blood Transfusions
- 2 RNs must check
- bracelet, chart and blood
- 18 guage needle
- y-tubing with filter
- saline flush (NO dextrose)
- VS #1 priority-for baseline
- use blood within 30 minutes
- infuse over 2-4 h
(plasma/platelets-much faster)
- reactions usually within first 15 minutes: SOB, throat closing, itchy, HA, flushing, anxiety, vomiting
- circulatory overload
- Acute hemolytic reactions-rare=fever, chills, back pain
- TRALI-transfusion related acute lung injury (fever, chills, SOB. Caused by leukocytes from donor.
Prediabetes
fasting glucose
>100 but < 126
prediabetics should check BS once a day
Type II DM
fasting glucose >126
blurry vision
polydypsia, polyuria
fatigue
recurring infections
weight loss
slow healing cuts/bruises
loss of feeling in the feet/tingling (damage to endothelial lining)
Rapid Acting Insulin
(lispro, aspart, glutiene)
Onset: 15 minutes
Peak: 60-90 minutes
Duration: 3-4 hours
Short Acting Insulin
(Regular)
Onset: 30 min-1hour
Peak: 2-3 hours
Duration: 3-6 hours
regular insulin is the only one that can be given IV
Intermediate Acting
(NPH or Lente)
Onset: 2-4 hours
Peak: 4-10 hours
Duration: 10-16 hours
Long-acting
(glargine (Lantus), detemir)
Onset: 1-2 hours
Peak: no peak
Duration: 24 hr
Cannot be mixed with anything!
Oral Drug Therapy for Type II DM
- Sulfonylureas (Glipizide) - squeeze the pancreas
- Biguanides (Glucophage) - decreased gluconeogenesis in liver
- Alfa Glucosidase Inhibitors (Acarbose) - starch blockers - block the conversion of starch
- Thiazolidinediones (Actos, Avandia) - make the tissue more susceptible to the insulin that’s there.
Somogyi Effect
A rebounding high blood sugar that is a response to low blood sugar. When managing the blood glucose level with insulin injections, this effect is counter-intuitive to insulin users who experience high blood sugar in the morning as a result of an overabundance of insulin at night. Give them less at night so they don’t drop so low and then rebound..
Caused by too much insulin at bedtime
Dawn Phenomenon
An early-morning (usually between 2 a.m. and 8 a.m.) increase in blood sugar
Different from Somogyi rebound in that dawn phenomenon is not associated with nocturnal hypoglycemia.
Treat by increasing the insulin dose and an appropriate bedtime snack.
AC/HS
Before Meals / Before Bed
DKA
(diabetic ketoacidosis)
lethargy, weakness
severe dehydration
abd pain, anorexia, vomiting
labored breathing
polyuria, polydypsia
breath odor (ketones)
BG > 300
pH < 7.3
positive ketones (blood, urine)
elevated anion gap
usually Type I
ABCD
give fluids, IV access
IV drip insulin 0.1 U/kg/hr
HHS
(hyperosmolar / hyperglycemic state)
life threatening-enough insulin to prevent DKA, but not enough to prevent hyperglycemia and hypovolemia
no ketones, pH is normal
type II
extreme hyperglycemia > 400
severe osmotic diuresis-profound dehydration
low Na, K, P
decreased renal perfusion, hypotension, hemoconcentration
pump fluids, insulin drip
