Problems Flashcards
S/Sx of iron deficiency anemia
- Pallor
- Glossitis (inflamed tongue)
Cheilitis (inflamed lips)
Parasthesias
Headache
Fatigue
Palpitations
Sensitivity to cold
What is thalassemia? What are 2 types?
Do not make enough Hemoglobin, which leads to RBC deficit
Genetic disorder
Two types: Minor (one parent)
Major (two parents)
Happens to people of certain ethnicities that live around the equator.
S/Sx of thalassemia
Minor type: Same as anemia
Major type: Life threatening anemia
Symptoms develop by age 2. If untreated leads to growth and developmental deficits.
Jaundice
Splenomegaly (from high RBC death)
Cardiomegaly (from iron deposits)
Hepatomegaly (from iron)
Tx for severe thalassemia
Blood exchanges regularly
Chelating meds that bind iron and remove it
What is pernicious anemia?
Risk factors?
No intrinsic factor (made in stomach)
So cannot absorb B12
Risk factors: GI problems, like surgery. Malabsorption (like Crohns or celiac), Alcoholism, smokers, long term proton pump inhibitors, vegetarians
S/sx of pernicious anemia
Tx?
Typical anemia s/sx with:
Beefy, red, shiny tongue
Anorexia, N/V
Tx: IM Vitamin B12
What is aplastic anemia?
Decrease of all blood cell types (pancytopenia) AND hypo cellular bone marrow.
This is autoimmune (70% of time)
What is meant by hemolytic anemia?
RBCs are being destroyed faster than can produce
This is a broad term that can involve many subtypes of anemia.
Sickle cell in most common
What is sickle cell anemia?
Most severe type of SSD
Inherits gene from both parents
What is sickle cell cycle?
Hypoxia (many causes but usually infection)
leads to
RBCs become rigid, sickle shaped
leads to
Vascular occlusion
leads to
More Hypoxia
Cycle starts again
What happens to the spleen in SSD?
Sickle cells have high turn over rate
Spleen become overworked and can’t handle infections (infection is common cause of death in SSD)
Anemia worsens
Spleen atrophies
S/sx of SSD
Pallor (look at mucous membranes)
Gray coloring
Jaundice
Pain (this is main symptom)
Fever
HTN
Tachypnea
N/V
Complications of SSD
Vaso-occlusive crisis
Kidney damage
Infection (pneumonia common)
Immunocompromised
HF
PE
CVA
Leg ulcerations
Priapism
Gallstones/Hepatomegaly
Spleen atrophy
Eye vascular problems
What is hemochromatosis?
Tx?
Too much iron
Iron overload leads to liver enlargement
Iron deposits in different organs
Skin bronzing
Tx: removing blood
Chelating meds
What is polycythemia?
Two types?
Too much blood cells (RBCs, WBCs, platelets)
Two types: Primary: Polycythemia vera (JAK2 gene mutation)
Secondary polycythemia (driven by hypoxia) (think resp. or CV chronic illness)
S/Sx of polycythemia
This patient will be clogged up and overloaded:
Headache, vertigo, dizziness, tinnitus, visual changes
Itching (caused by increased basophils)
paresthesias
erythromelalgia (painful burning/redness of hands/feet)
Thrombosis
Tissue hypoxia
Hypertension
Engorgement may cause bleed out
Hepatomegaly-feel full and bloated
Splenomegaly-feel full and bloated
Plethora (ruddy complexion)
Tx for polycythemia
Phlebotomy q 2-3 months
Hydration
Baby aspirin
Myelosuppressive agents
Nutrition
What is thrombocytopenia?
What are some potential causes?
Lack of platelets
1. Acquired Immune disorder (ITP)
2. Heparin induced (HIT)
What is pathos in immune thrombocytopenia?
Autoimmune attack on platelets
Acute condition in kids
Chronic in adults
What is pathos of HIT (heparin induced thrombocytopenia?
Body’s immune system responds to heparin by binding platelets to heparin then forming an antibody to it and destroying it. This removes the platelets from your blood.
What is a surprising complication of HIT?
Thrombi can form as all the platelets are used up and then are in hypercoag state. Have an increased D-dimer and low platelet count
What is the common complication of HIT?
Uncontrolled bleeding
Tx for HIT
Stop heparin
Warfarin
Plasmapheresis (if clotting severe)
Treatment for immune thrombocytopenia
Corticosteroids
What is Von Willebrand?
Similar to hemophilia
Patient does not make the clotting factor Von Willebrand
The most common congenital bleeding disorder.
Risk factors for DIC
Sepsis
Cancer
Trauma/burns
Abruptio placentae
HELLP syndrome
Pathos for DIC
Some trauma (most commonly sepsis) triggers an abnormal response in clotting cascade.
This puts them in a state of hypercoaguablity with platelet and fibrin deposits everywhere, causing thrombosis.
Then after these clotting factors are depleted, the blood becomes unable to clot. Massive bleeding to all systems.
What is the most important thing we can do for DIC?
Early detection
This is key to survival
Must detect early and correct under lying cause
Be alert to:
Petechaie, bruising, oozing IVs
Tachycardia, Change in LOC, pain, increased abdominal girth, renal output
What is the goal when treating DIC?
Balance clotting factors they are missing ASAP
Why is neutropenia a serious finding? Most common cause?
Neutrophils are our primary macrophages.
Chemo and immunosuppressants
What is considered an emergency in a neutropenic patient?
Low grade fever
S/sx of infection
The most important measure to prevent infection?
Hand hygiene
What is leukemia?
General term
Proliferation of immature WBCs that crowd out healthy bone marrow.
This leads to a lack of blood cell production. Anemia, thrombocytopenia, leukopenia.
What are the 4 main classes of leukemia?
Acute Myeloid (AML)
Acute Lymphocytic (ALL) (from lymphocytes, the agranulocyte that makes T and B cells)
Chronic myelogenous (CML)
Chronic lymphocytic (CLL)
Which type of leukemia is most common in kids?
ALL
Acute lymphocytic
Small immature lymphocytes proliferate in bone marrow (most from B cells)
What is the Philadelphia chromosome?
A genetic mutation present in 98% of CML cases
What are general S/Sx of leukemia?
Decreased RBC, HGB, HCT, Platelets, WBC can be high or low,
Bone pain
Splenomegaly
Hepatomegaly
Lymphadenopathy
Oral lesions
Fatigue
Weakness
Fever
What is lymphoma?
Two types?
Cancer originating from bone marrow and lymphatic structures and resulting in proliferation of lymphocytes (these are agranulocyte WBCs that make T and B cells)
Hodgkin and Non Hodgkin
What are main differences between Hodgkin and NHL?
Hodgkins is usually localized while NHL is more disseminated
If Hodgkins continues it will infiltrate other organs
What is usually the initial sign of Hodgkins?
Enlargement of cervical, axillary, inguinal lymph nodes
Movable and non tender
What are “B symptoms”?
More common in Hodgkins
Night sweats, fever, weight loss
Poorer prognosis
What is the overlap with lymphomas and leukemia?
Both involve the proliferation of lymphocytes and their precursors
Both originate from hematopoietic stem cells. One differentiates into myeloid (bone marrow, leukemia) and one into lymphoid (lymphocytes which come from lymph nodes, lymphoma)
What is HELLP syndrome?
Hemolysis, Elevated Liver Enzymes, Low Platelets
Risk when severe HTN, preeclampsia in pregnancy
Hemolysis»fibrin clots»liver damage»enzymes elevated»fibrin depletion»low platelets
—-Can lead to DIC—
S/Sx of HELLP
Liver pain (don’t palpate!!)
Hepatomegaly, abdominal distention
N/V
Severe edema (especially hands, face)
Jaundice
Vision changes
Headache that won’t go away
Tx for HELLP
Antihypertensives
Delivery
Blood transfusions
Mag sulfate
