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92 Cards in this Set
- Front
- Back
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Risk Factors for HTN
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1) Family history
2) Advancing age 3) Gender 4) Black race 5) High dietary sodium intake 6) Glucose intolerance (DM) 7) Cigarette smoking 8) Obesity 9) Heavy alcohol consumption 10) Low dietary intake of K, CA, and Mag |
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Very-Low-Density Lioproteins (VLDL)
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triglyceride. You want this less than 200. Borderline is 150-199
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Low-desnity lipoproteins
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mostly cholesterol. This is responsible for the delivery of cholesterol to the tissues.
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High Density lipoproteins (HDL)
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reverse cholesterol transport. Also part of endothelial repair.
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Total Cholesterol
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Desireable: less than 200. Borderline: 200-239. High is >240
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LDL
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Optimal <100, Near Optimal 100-129. Borderline 130-159, High is 160-189, and Very High is >190
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Triglycerides
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Desirable <150, Borderline 150-199, High is 200-499, Very High is >500
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HDL
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low <40, high >60
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Infarction
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- Results when there is prolong ischemia causing irreversible damage to the heart
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Inschemia
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temp. blocked to the heart
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Stable angina
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transienta that only last 3 to 5 minutes
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Prinzmental Angia
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this occurs mostly at night during rapid eye movement, and vasopsam.
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Systolic heart failure-
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-inability of the heart to generate an adequate cardiac output to perfuse vital tissues. This is a failure of CO which depends on contractility, preload, and afterload.
Increased Preload-excess plasma volume, and a certain amount of increase fluid is good to a point, that it starts causing stretching Increased afterload-commonly a result of increase PVR (HTN). |
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Renin-Angiotensin-Aldosterone system
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-when a decrease in BP to the kindey, the Renin is released that turns into angiotensin 1, which turns in angiotensin 2. The Angiotensin 2 causes retention of sodium/water, increase in blood pressure, and hypertrophy and dilation of the ventricle.
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Aldosterone
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which increase sodium, and fluid retention.
Stimulates the release of vasopressin (anti-diuretic hormone). Inflammatory cytokines are released |
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Endothelial hormones
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potent vasoconstrictor. Sign of bad CHF
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signs of Systolic Left sided Heart failure
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S/S: Pulmonary Vascular Congestion and Inadequate perfusion of systemic circulation.
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Diastolic heart failure
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- pulmonary congestion with a normal stroke volume and cardiac output.
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Patho of Diastolic heart failure
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due to decreased compliance of the left ventricle and abnormal diastolic relaxation (lusitropy). Caused by an increase in LVEDP but normal LVEDV. Symptoms made worse with exercise. They have dyspnea with exertion and fatigue.
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Right side heart failure
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inability of the right ventricle to provide adequate blood flow into the pulmonary circulation. Right heart failure in absence of left heart failure is common caused by COPD, ARDS, and Cycstic Fibrosis
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High-Output Failure
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Patho: caused by the inability of the heart to adequately supply the body with blood-bourn nutrients, despite adequate blood vlume and normal. Causes are anemia, septicemia, hyperthyroidism, and beriberi.
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Anemia
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the body goes into metabolic acidosis as the cell goes into anaerobic metabolism. The HR and SV increase. But unable to keep up
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Septicemia
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the toxins cause systemic vasodilation and fever. Vasodilation the biggest problem
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Hyperthyroidism
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due to the body burning through so much more energy it needs more energy
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Beriberi (thiamine deficiency)-
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caused by chronic EOTH abuse
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Ductus Venosus
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closes within first days. This ductus helps the umbilical vein to byass liver to to get blood directly to the heart/brain
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Ductus arteriosus
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closes more gradually. Due to increase oxygen saturationcause vasoconstriction at the shite, plus a decrease in the amoung of prostaglandins promote closer of the ductus. Permanent closure within 10 to 21 days after birth.
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Neonate when it starts
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Cardiogenesis starts at 3 weeks, but cardiovascular happen fourth and seventh week.
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Atrial Septal Defect (ASD)/PFO
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Patho: hole between the atra allowing a LEFT to RIGHT shunt of blood flow
s/s: Right atrial/Ventricular enlargement. Wide fix splitting of the second heart sound treatment: closure via cath, bypass, and better if treated before school age |
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Ventricular septal defect
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Patho: Shunting from LEFT to RIGHT due to hole in ventricular wall. Pulmonary HTN is common
s/s: Loud, Harsh, Holoystolic murmur and systolic thrill that can be dected at the left lower sternal border. Treatment: Most close on their own before first year. But if the Left to right shunting with a ratio greater than 2:1 or increasing pulmonary vascular resistance are indications for closure. Surgrey with bypass, or possible Cadiac Cath Over time causes Reverse to Right to Left shunt |
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Atrioventricular Canal Defect (AVC)
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Complete AVC: inlet VSD, priumum type of ASD, defects in both the mitral and tricuspid values.
Partial AVC defect (PAVC)-consist of a priumum type of type defects in both the mitral and tricuspid value Transitional AVC (TAVC)-defects involve partial fusion of the endocardial cushions, resulting in variable AV valve abnormalities. Patho: LEFT to RIGHT shunting after neonatal period. Hole inbetween the Atria/Vent with the AV values invlovded also. This is common in Down’s Treatment: repair between 3 and 6 months of life |
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Coarctation of the Aorta (COA)
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Patho: narrowing of the lumen of the aorta
Two types Preductal (before the ductus arteriosus) Postductual (after the ductus arteriosus) s/s: in newborns after the ductus closese rapid CHF which is hypotension, acidosis, and chock. In older children not till HTN in upper extremities and decreased/absent pulses in the lower extremities. They may have cramps in the legs. Treatment: Surgery |
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Ventricular septal defect
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Patho: Shunting from LEFT to RIGHT due to hole in ventricular wall. Pulmonary HTN is common
s/s: Loud, Harsh, Holoystolic murmur and systolic thrill that can be dected at the left lower sternal border. Treatment: Most close on their own before first year. But if the Left to right shunting with a ratio greater than 2:1 or increasing pulmonary vascular resistance are indications for closure. Surgrey with bypass, or possible Cadiac Cath Over time causes Reverse to Right to Left shunt |
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Aortic Stenosis
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narrowing of the aortc outflow tract
Patho: causes LVH s/s: mild-moderate asymptomatic mostly just exertional chest pain and exercise intolerance. An Ejection click with valvular AS treatment: Valve replacement |
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Atrioventricular Canal Defect (AVC)
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Complete AVC: inlet VSD, priumum type of ASD, defects in both the mitral and tricuspid values.
Partial AVC defect (PAVC)-consist of a priumum type of type defects in both the mitral and tricuspid value Transitional AVC (TAVC)-defects involve partial fusion of the endocardial cushions, resulting in variable AV valve abnormalities. Patho: LEFT to RIGHT shunting after neonatal period. Hole inbetween the Atria/Vent with the AV values invlovded also. This is common in Down’s Treatment: repair between 3 and 6 months of life |
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Pulmonic Stenosis
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Narrowing of the pulmonary otuflact flow
Patho: causes backflow into the RA from the RV due to CHF. This can cause the reopening foramen ovale. Right to Left |
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Coarctation of the Aorta (COA)
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Patho: narrowing of the lumen of the aorta
Two types Preductal (before the ductus arteriosus) Postductual (after the ductus arteriosus) s/s: in newborns after the ductus closese rapid CHF which is hypotension, acidosis, and chock. In older children not till HTN in upper extremities and decreased/absent pulses in the lower extremities. They may have cramps in the legs. Treatment: Surgery |
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Aortic Stenosis
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narrowing of the aortc outflow tract
Patho: causes LVH s/s: mild-moderate asymptomatic mostly just exertional chest pain and exercise intolerance. An Ejection click with valvular AS treatment: Valve replacement |
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Patent ductus arteriosus (PDA)
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Patho: open patent ductus (aortra). LEFT to RIGHT shunt
s/s: continuous-machinery murmur heard best in the left upper sternal border. Thrill, bounding pulses, and pulmonary overcirculation. Treatment: indomethacin (prostaglandin inhibitor) to close the duct. IF that doesn’t work they will use. CAth or Surgrey if that doesn’t work |
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Pulmonic Stenosis
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Narrowing of the pulmonary otuflact flow
Patho: causes backflow into the RA from the RV due to CHF. This can cause the reopening foramen ovale. Right to Left |
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Pernicious anemia-patho
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There is a lack of intrinsic factor (if) which is a transporter that is required for Vit b12. Vit b12 is needed in DNA systhesis. IF is made and produced in the Gastric Parietal cells (stomach). Gastric Atrophy is very common. Can be auto-immune. Loss of the parietal cells results in the loss of IF.
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Patent ductus arteriosus (PDA)
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Patho: open patent ductus (aortra). LEFT to RIGHT shunt
s/s: continuous-machinery murmur heard best in the left upper sternal border. Thrill, bounding pulses, and pulmonary overcirculation. Treatment: indomethacin (prostaglandin inhibitor) to close the duct. IF that doesn’t work they will use. CAth or Surgrey if that doesn’t work |
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Pernicious anemia-enviromental factors
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excessive EOTH, hot tea, smoking. Gastrectomy. H. Pylori. PPI’s.
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Pernicious anemia-patho
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There is a lack of intrinsic factor (if) which is a transporter that is required for Vit b12. Vit b12 is needed in DNA systhesis. IF is made and produced in the Gastric Parietal cells (stomach). Gastric Atrophy is very common. Can be auto-immune. Loss of the parietal cells results in the loss of IF.
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PA s/s
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: Early signs include infections, mood swings, gastriointestinal, cardiac, or kidney problems. Once the H & H hit 7 to 8 they will have weakness, fatigue, paresthesias of the feet/fingers, difficulty in walking, loos of appetite, abdominal pains, and weight loss. Sore, smooth, beefy red tongue. Lemon yellow (swallow) due to pallor or icterus.
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Pernicious anemia-enviromental factors
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excessive EOTH, hot tea, smoking. Gastrectomy. H. Pylori. PPI’s.
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Pernicious anemia-testing
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Schilling test-a test that administering radioactive b12 and measuring what comes out in urine. If low, they have this. Second test is given IF, and see any chances in urine.
These test has been replaced by measuring the methylmalonic and homocysteine levels (will be seen early on). |
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PA s/s
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: Early signs include infections, mood swings, gastriointestinal, cardiac, or kidney problems. Once the H & H hit 7 to 8 they will have weakness, fatigue, paresthesias of the feet/fingers, difficulty in walking, loos of appetite, abdominal pains, and weight loss. Sore, smooth, beefy red tongue. Lemon yellow (swallow) due to pallor or icterus.
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Pernicious anemia-testing
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Schilling test-a test that administering radioactive b12 and measuring what comes out in urine. If low, they have this. Second test is given IF, and see any chances in urine.
These test has been replaced by measuring the methylmalonic and homocysteine levels (will be seen early on). |
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Pernicious anemia treatment
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weekly cobalamin shots till fix, then once a month. May give oral at high doses due to small bowel obs. Return to normal in 5 to 6 weeks.
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Folate Deficiency Anemia Patho
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: A lack of intact of folic acid. More common in EOTH, and chronic malnourishment. This cause megaloblastic cells (large cells).
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Folate Deficiency Anemia-s/s
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s/s: similar to PA, but also svere cheilosis (scales and fissures on the lips/corners of the mouth), stomatitis (inflammation of the mouth), and painful ulceration of the buccual mucosa and tongue. Problems swallowing, watery diarrhea, gas.
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Folate Deficiency Anemia-treatment
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Treatment: one milligram per day up to 5mg per day in EOTH. After treatment will dispear in 1 to 2 weeks. 400 mcg/day recommend.
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Iron deficiency anemia (IDA)-patho and sources
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causes abnormally small cells with less amounts of hemoglobin
Sources: NSAID, PICA, Chronic Parasite Infestations. Iron is needed for hemoglobin sythesis Patho: can be caused by not eating enough, blood loss. Also can be caused by metabolic or functional iron deficiency. |
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Iron deficiency anemia (IDA) stages
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Stage 1: body iron stores are depleted, but everything is normal
Stage 2: iron transportation to bone marrow is diminished, resulting in iron deficiency erythropoiesis Stage 3: small number of hemoglobin-deficient cells enter circulation with sufficient numbers to replace the normal. S/S happens here |
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Iron deficiency anemia (IDA) s/s
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Fatigue, weakness, Sob, pale earlobes, palms, and conjunctivae. The nails become thin, brittle, coarsely ridge, sppon-shaped/concave (koilonychias). Tongue becomes red, sore, and painful. Dryness/soreness at the corners (angular stomatitis). Difficulty in swallowing due to a “web”. Later on numbness, headache, mental loss/confusion
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Iron deficiency anemia (IDA) testing
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Testing: Best is a serum ferritin which 1mc/L is equal to 80 to 10 mg. can also use serum transferrin receptor (sTfR).
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Iron deficiency anemia (IDA) treatment
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150 to 200 mg per day, and H & H should come up in 1 to 2 months. Once the serum ferritin levels reach 50 mcg/L that you are good.
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Hemolytic Anemia
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premature accelerated destruction of erythrocytes
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Paroxysmal nocturnal hemoglobinuria
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caused by complement-mediated damage, causing lysis and release of hemoglobin. s/s include red urine, abdominal pain, and thrombosis. Cause of death is thrombosis of abdominal/cerebral veins. NO likes hemoglobin causing increased plately vascular adherence and clot formation.
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Autoimmune hemolytic anemia (AIHA)
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caused by autoimmune disease against RBC. Three subtypes
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Warm autoimmune hemolytic
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anemia is caused by IgG that binds optimally to erythrocytes at normal body temp.
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Cold agglutinin autoiummune hemolytic anemia
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caused by antibodies that optimally bind to RBC lower than 87.7 degrees and best at 39.2.
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Cold hemolysin autoimmune hemolytic anemia
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just like above but also results in hemoglobulinuria
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Drug-induced hemolytic anemia
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caused due to drug binding to RBC, and antibotics against the drug atak the RBC also. Can be caused by PCN, Cephalosporins (mostly these ones), and hydrocortisone. Usually happens 1 to 2 weeks after large IV of antibitoics
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Hemolytic Anemia s/s
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of all of them: jaundice, splenomegaly
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Hemolytic Anemia testing
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erythroid hyperplasia (many fragile and immature erythrocytes).
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Hemolytic Anemia treatment
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Treatment: transfusions, folate, rituxiamab
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Thalassemia
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Patho: a genetic disease (similar to sickle cell) that causes reduce or no synthesis of the globin chains that make up hemoglobin of the A or B golbin. Happens mostly in African patients
s/s: no major s/s treatment: transfusion, splenectomy, iron chelation. |
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Eosinophilis
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increase in numbers of total of these. Associated with allergic disorders (type 1) with asthma, hay fever, drug reactions, parasitic.
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Basophilis
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increase in these is rare, but related to inflammation and immediate hypersensitivity. These have the histamine. Also measles/chickenpox, Hodgkin, Myxedema or antithyroid therapy
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Neutrophils
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released in early stages of inflammation or infection. This is where the left shift is happening whe the bands start to go up.
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Infectious Mono-
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acute self limiting caused by a viral infection of B Cells. The kissing disease cuased by EBV
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Infectious Mono s/s
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s/s: headache, malaise, fatigue, arthralgia, fever, chills which last 7 to 20 days. Incubation period of 4 to 8 weeks. Splenomegaly is clinically evident 50% of the time
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infectious mono testing
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testing: Hoagland criteria of 50% lymphocytes and 10% atypical lympohcytes in the blood in presence of fever, pharyngitis, and adenopathy with a possible serologic test. The Heterophile antibodies. Monospot test
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Acute Lymphocytic (ALL)-patho
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Patho: Mostly in children with 30% lymphoblast in one marrow or blood. Lymphoblast are baby WBC that spill over from the marrow into the blood. In ALL most comes from precursor B Cells. Effected by MLL gene
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Acute Lymphocytic (ALL)-s/s
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s/s: fatigue, bleeding, fever. Spleen in largement. Pain in bones/joints
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Acute Myelogenous (AML)-patho
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Patho: abnormal proliferation of myeloid precursor cells, decrease rate of apoptosis, and an arrest in cellular differentiation. This leads to anemia, unable to fight infections, and bleeding problems. Mutation flt3
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Acute Myelogenous (AML)-s/s
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Patho: abnormal proliferation of myeloid precursor cells, decrease rate of apoptosis, and an arrest in cellular differentiation. This leads to anemia, unable to fight infections, and bleeding problems. Mutation flt3
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Hodgkin Lymphoma (HL) Patho:
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Patho: Progression from one group of lymp nodes to another, the development of systemic symptoms, and the presence of Reed-Sternberg RS) cells. These cells are large, binucleate with occasional mononuclear variants. Can be linked to EBV virus.
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Hodgkin Lymphoma (HL) s/s
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The cells release cytokines and other growth factors. First signs are enlarged painless lympd node in the neck, or mediastinal mass in a chest X-ray. Fever (without infection), drenching night sweats ,itchy skin, fatigue.
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Non-Hodgkin Lymphoma Patho
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progressive clonal expansion of B Cells, T Cels, NK cells. Mostly a middle age disease , and mostly a B Cell disease. There is no RS Cells. Mostly caused by environmentally induced gene changes
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Non-Hodgkin Lymphoma s/s
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Swelling, enlarged nodes mostly in cervical, axiallary, inguinal, and femoral chains. These may have regression of the nodes (like infections). Night sweets. Adenopathy
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Non-Hodgkin Lymphoma evaluation/treatment
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: uses mostly the Ann Arbor staging system. Chemotherapy and radiation.
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Burkitt Lymphoma Patho
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EBV caused tumor of the B-cells mostly in Eastern-Central Africa or New Guinea characterized by a rapidly growing tumor primarily I the jaw/facial bones.
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Disseminated intravascular coagulation (DIC)- patho
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rapid miniclotting everywhere in the body. Happens often with Sepsis. Caused by damage to vascular endothelium
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Disseminated intravascular coagulation (DIC)
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s/s: Bleeding from enipuncture sites, arterial lines, surgical sounds, bleeding in eyes, epistaxis
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Disseminated intravascular coagulation (DIC)-testing
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D-dimer
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Fetal Blood
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Monocytes-High in first year of life, and then decrease to adult levels
Eosinophil- High in first year, and Higher in children than in teengers/adults |
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Hemolytic Disease of a Newborn-HDN-patho
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Patho: caused by antigenically incompatible erthroycites. The first pregnancy with RH incompatibly problems is ok because few fetal erthroytes across the . Worse than ABO incompatibility. If thebaby can’t surivce the anemia they are stillborned wti hgross edema called hydrops fetalis
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Hemolytic Disease of a Newborn-HDN-testing
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Coombs test indirect (measures antibody already bound to the surfaces to fetal erthroytes). Direct coombs (used to measure the antibodies already bound to the surfaces
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Hemolytic Disease of a Newborn-HDN-treatment
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Giving RH-Negative women RH immune globulin within 72 hours of exposure to to RH positive. Mom must get these injections after ever RH positive baby or miscarriage. RH-Negative women and RH-postive partners may geet it prophylaxis.
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