1. Neutrophils clear the wound of debris
2. Seal, Fibrin Clot replaced by scar tissue, 4th day of injury
3. Scar tissue is thinner, firm, inelastic
4. approximated, closed no dead space
5. Tissue loss, require filling of dead space w/connective tissue
26
1. Folate
2. S/Sx Folate Deficiency
3. Iron deficiency
4. Iron & RBCs
5. Aplastic Anemia Etiology
1. Required for DNA & RNA synthesis, Bone marrow production of Platelets
2. Dysphagia, watery diarrhea, stomatitis, fissures of the mouth
3. Hemoglobin deficiency in RBCs
4. Microcytic & hypochromic (anemia)
5. chronic exposure to viruses, infection autoimmune, allergic states
27
1. Pancytopenia -leukemia, aplastic anemia
2. Aplastic Anemia Treatment
3. Mononucleosis
4. Mono relationship
5. What should you monitor in mono?
1. deficient RBCs, WBCs, platelets, arrested development of bone marrow
2. Bone Marrow transplant
3. B lymphocytes\> receptor EBV
4. Bacteria, virus, Lymphadenopathy, Hematosplenomegaly, Strep
5. Splenic Rupture (LUQ, Left shoulder, Ab)
28
1. What is leukemia
2. Manifestation of leukemia
3. Chronic Myeloid Leukemia
4. Patient that might have lymphadenopathy
5. Malignant Lymphomas possible linkage
1. Overcrowding bone marrow with WBCs, decreased everything else
2. bone pain, inc hr (low h/h), SOB, pallor, dec cap refill, low BP, **WEIGHT LOSS**, inc INR, prolonged PTT, **BLEEDING**
3. Philadelphia chromosome
4. HIV, syphilis, leukemia, Hodkin TB, Mono
5. Mono
29
1. Malignant Lymphoma Cells
2. Manifestation of malignant lymphoma
3. Treatment for Malignant lymphoma
4. Splenomegaly
5. Splenomegaly indicitave of
1. RS
2. pruritis, drenching night sweats, fever
3. chemotherapy, radiation stem cell transplant
4. Sequestering of all three blood components (anemia)
5. Leukemia, TB, Sphyilis, Thalssemai R. HF, Mono Esophageal Varices, Fungal
30
1. Vitamin K deficit
2. Outcome of Vitamin K deficit
3. Trasmission of Hemophilia
4. Etiology of hemophilia
5. Factors of DIC
1. inability to coagulate for synthesis of prothrombin
2. impaired hemostasis associted w/ LIVER dysfunction
3. X-linked recessive disorder by females to males
4. abnormal bleeding, epistaxis
5. Infection, OB complications, Neoplastic disease (leuk), necrosis, heat stroke/shock
31
1. What happens in DIC
2. Treatment for DIC
3. Components needed to make RBC
4. Intrinsic Factor
5. Pernicious Anemia
1. damage to endothelium, activate X factor, Excess Fibrin, occulsion of organs from thromboembolus formation
2. Heparin, oxygen
3. Iron, B12, Folate
4. secreted by the stomach that enables body to absorb b12
5. deficiency of intrinsic factor necessar to absorb b12
32
1. Why injections for Pernicious anemia
2. How long for injections
3. Structure of RBC in Sc.Anemia
4. Sickle Cell Crisis
5. SCAnemia Diet
1. Can't absorb in the GI tract
2. every week until deficiency is correctly, monthly for life
3. lack of o2 causes cell to make a s shape, Rigid, clumped
4. anything that will cause increase need for oxygen
5. high calorie, high protien, folic acid supplement
33
1. Why vaccines for Sc.Anemia
2. Sickling Conditions
3. Conditions associated with Sickle Crisis
1. Absence of normal spleen function
2. hemoglobin A replaced w/ hemoglobin S (sensitive to o2 changes)
3. vasoocclusive crisis, splenic sequestration, hyperhemolytic, aplastic
1. Hypoventilation Excess CO2,
2. Hyperventilation (compensating HC03 decreases) Similar to m. acidosis
3. hydrogen ion DONORS, end product of metabolism
4. Kussmauls, hypotension, headache
5. vomiting, gastic suction, cardiac dysrythmias, twitching
35
1. Order of Compensation Acid/Base Balance
2. RAAS controls...
3. When renin is released
4. What is Angiotensin II
5. Aldosterone stimulates...
1. Buffer, Lungs, Kidneys, Potassium
2. reabsorption of sodium
3. BP or fluid concentration is LOW
4. vasoconstrictor, secretes ALDOSTERONE
5. absorb NA secrete K
36
1. Where is ADH produced
2. What stimulates ADH
3. ADH + Aldosterone inc BP
4. 3rd spacing
5. Risk for 3rd spacing
1. Hypothalamus
2. dehydration or high sodium, decreased blood volume
3. Increase Sodium and water
4. trapped fluid in interstitial space (nonfunctional), fluid LOSS
5. Burn patients, preeclampsia
37
1. Osmotic Pressure
2. Hydrostatic pressure/Filtration
3. HTN and Coronary Disease
4. Which cardiac ensymes are affected in MI
5. Stimulation of baroreceptors
1. low concentration to high concentration
2. higher pressure to lower pressure
3. CDA is loss of oxygen, HTN increase oxygen demand
4. Creanin Kinase, NP, Troponins, Myoglobin
5. hypoperfusion in MI
38
1. Where can MI stem from
2. EKG changes MI
3. Signs Right sided HF
4. Signs Left sided HF
5. What type of HF happens first
1. athrosclerosis, thrmobsis platelet, stenosis
2. ST elevated
3. Jug vein distention, peripheral edema
4. pulmonary edema, paroxysmal nocturnal dyspnea
5. Left sided
1. chronic hypoxemia, pulmonary HTN, hypertrophy of muscle
2. hepatomegaly, RUQ discomfort, weight gain, dyspnea
3. sodium water enters the lungs, can lead to ARDS
41
1. Arthus define
2. Aplastic define
3. Kinin system define
1. Edema-Abscesses-Gangrene
2. Ineffective development
3. Hormones-BP control-Coag-Pain