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Patho Renal/Heme/GI
| Question | Answer |
|---|---|
| Functions of the kidneys | Erythropoeitin Renin Activation of Vitamin D |
| Erythropoetin | Hormone released in response to hypoxia- stimulates RBC production |
| Renin | Released by nephron for decrease in arterial pressure or increase in Na. Converts Angio I to II- stimulates aldosterone and vasoconstriction. |
| UTICervical carcinoma in situ: | Infection that can happen anywhere along the |
| Cystocele | Descent of the bladder and anterior vaginal wall into the vaginal canal. |
| Who usually gets cystocele? | Women with pelvic organ prolapse. Childbirth, heavy lifiting, menopause, constipation. |
| Rectocele | rectum and back wall of the vagina into the vaginal space. |
| Who usually gets rectocele? | Women with pelvic organ prolapse. Childbirth, heavy lifiting, menopause, constipation. |
| Risk factors for ovarian cysts | NO KNOWN RISK FACTORS |
| Who gets ovarian cysts? | Women from pubery to menopause. |
| Ovarian Cyst | sacs filled with fluid or a semisolid material that develops on or within the ovary |
| Pathology of ovarian cyst | During the days preceding ovulation, a follicle grows. At the time of expected ovulation, the follicle fails to rupture and release an egg. Instead of being reabsorbed, the fluid within the follicle persists and forms a cyst. |
| Follicular cysts: | Occur when the dominant follicle fails to rupture and release the ovum, or when the nondominant follicles fail to regress Can be as large as 10 cm in cycles |
| Luteal cysts: | Occur because of abnormal LH and progesterone responses during the menstrual cycle such that the corpus luteum does not develop normally |
| Dermoid cysts: | Are ovarian tumors that contain elements of skin, hair, glands, muscle, cartilage, and bone. Are usually asymptomatic but must be removed to prevent the development of ovarian cancercorpus luteum does not develop normally |
| Causes of PCOS | Cushing syndrome, thyroid disorders, adrenal disorders, adrenal and ovarian tumors. It is also associated with endocrine disorders. Low levels of follicle-stimulating hormone, increased levels of luteinizing hormone, and elevated estrogen |
| Cystocele | is the name for a hernia-like disorder in women that occurs when the wall between the bladder and the vagina weakens, causing the bladder to drop or sag into the vagina. |
| What happens in cystocele | two kinds of problems to occur, urine leakage incomplete emptying of the bladder The dropped bladder stretches the opening into the urethra, and urine may leak when a woman does any action that causes pressure on the bladder, such as coughing. |
| rectocele | is a bulge of the front wall of the rectum into the vagina. |
| What happens in rectocele | The rectal wall may become thinned and weak, and it may balloon out into the vagina when pushing to have a bowel movement. |
| The two kinds of vaginal cancer. | Squamous cell Adenocarcinoma |
| Squamous | Women from 60-80 |
| Adenocarcinoma | Women from 12-60 |
| Vaginal Cancer Risk factors | History of cervical cancer HPV VAg irritation Vag prolapse |
| S&S Vaginal cancer | Ulcer, thickening or lump Usually on the labia majora May be anywhere on the vulva Local itching, pain, burning, bleeding Pain with urination Pain with intercourse Unusual odor |
| Uterine cancer | Endometrial cancer 95%= adenocardinomas |
| Risks of determiner cancer | Early menarche:. Late menopause: Obesity Tamoxifen: Ovarian diseases A diet high in animal fat Diabetes Family history: Breast or ovarian cancer:. Prior pelvic radiation therapy: |
| S&S of Uterine Cancer | Prolonged periods or bleeding between periods Any bleeding after the time of menopause A pink, watery or white discharge from your vagina Pelvic pain, especially late in the disease Weight loss |
| Survival rate- Prognossis | Survival Rate by Stage I 90% to 95% II 75% III Cervical 60% IV 15% to 26% |
| Cervical cancer | Cervical cancer develops in the lining of the cervix, the lower part of the uterus |
| Cellular dysplasia: | Confined to original site |
| Cervical intraepithelial neoplasia [CIN] | Cell changes: Some epithelial cells replaced by atypical, neoplastic cel. Often associated with human papillomavirus (HPV) infection |
| Cervical carcinoma in situ: | Progresses to this stage within 10-12 years.Cell changes: All or most of cervical epithelium replaced by atypical, neoplastic cells |
| Invasive carcinoma: | Metastatic spread—invasion into adjacent tissues and metastasis through lymphatics; can spread to rectum, bladder, lungs, and bone |
| Causes of cervical cancer | HPV human papilloma virus multiple partners (STD) Sexual intercourse at a young age Estrogen replacement therapy Early menarche Late menopause Never having children Failure to ovulate Diabetes Hypertension Obesity |
| S&S of Cervical Cancer | Abnormal vaginal bleeding Abnormal (yellow, odorous) vaginal discharge Low back pain Painful sexual intercourse (dyspareunia) Painful urination (dysuria) |
| Dispareunia | Pain during intercourse |
| Ovarian cancer | Accounts for the most deaths. It occurs in older women, with a peak incidence in the eighth decade. ovarian cancers arise from the surface epithelium of the ovary and spread intra-abdominally over the surface of the peritoneum |
| Risks for ovarian cancer | Family history of gynecologic cancer Personal history of breast cancer Mutations of the BRCA1 or BRCA2 genes Infertility Early menarche or late menopause Nulliparity (never having given birth) |
| S&S Ovarian cancer | asymptomatic,with advanced disease. painless ascites Abdominal or pelvic pain Vomiting Constipation Vaginal discharge or bleeding Hypercoagulability with venous and arterial clot formation Abnormal skin pigmentation |
| BC:Carcinoma in situ | early stage cancer, confined to where it started. is confined to the ducts or the lobules, depending on where it started. It has not gone into the fatty tissues in the breast nor spread to other organs in the body. |
| BC:Ductal carcinoma in situ | most common type of noninvasive breast cancer. the cancer is confined to the ducts. It has not spread through the walls of the ducts into the fatty tissue of the breast. Nearly all women with cancer at this stage can be cured. |
| BC:Lobular carcinoma in situ | his condition begins in the milk-making glands but does not go through the wall of the lobules. Although not a true cancer, having LCIS increases a woman's risk of getting cancer later |
| BC:Infiltrating (invasive) ductal carcinoma | most common breast cancer. It starts in a milk passage or duct, breaks through the wall of the duct, and invades the fatty tissue of the breast. From there it can spread to other parts of the body. IDC is the most common type of breast cancer. |
| BC:Infiltrating (invasive) lobular carcinoma | This cancer starts in the milk glands or lobules. |
| Causes of breast cancer | Gender Age Genetic risk factors Family history Personal history of bc Race Menstrual periods Not having children Birth control pills Hormone replacement Breast-feeding and pregnancy Alcohol Diet. Exercise |
| Genetic Mutations of BC | Acquired: p53ERBB2myc Inherited: BRCA1 BRCA2p53 (Li Fraumeni) |
| Reproductive causes of BC | Nulliparity Late pregnancy Early menarche Late menopause No breast- feeding |
| Hormonal causes of BC | High levels of endogenous estrogens Hormone replacement therapy Increased insulin-like growth factor |
| Environmental causes of BC | Cigarette smoke Ionizing radiation High-fat diet Lack of physical exercise Chemicals |
| When do you start mamograms? | Age 40 |
| Self Breast exam | Age 20 |
| Symptoms of BCs | a swelling of part of the breast or painless lump skin irritation or dimpling nipple pain or the nipple turning inward redness or scaliness of the nipple or breast skin a nipple discharge other than breast milk a lump in the underarm area |
| Prostatitis | is a general term for inflammation of the prostats Researchers don't know the exace gland |
| Causes of Prostatitis | Bacterial infection Heavy lifting. Physical activity. Uri Pelvic muscle spasm. Structural abnormalities of the urinary tract. Narrowings (strictures) of your urethra |
| Benign prostatic hyperplasia BPH | is non-malignant enlargement of the prostate. The prostate is a walnut-sized gland located at the neck of the bladder surrounding the urethra. It is part of the male reproductive system. |
| Cause of BPH | idiopathic |
| The main risk factor for BPH | is being over 50 years old. |
| S&S BPH | Difficulty starting to urinate Weak urination stream Dribbling at end of urination Sensation of incomplete bladder emptying Urge to urinate frequently, especially at night Deep discomfort in lower abdomen Incontinence |
| Causes of prostate cancer | Age increases rapidly after age 50. Race Fam History Diet Vasectomy |
| S&S Prostate Cancer | Frequent urination Pain/burning during urination Weak/interrupted urine flow Blood in the urine Nocturia Metastasis= a man may experience: Pain in the back, hips, thighs, shoulders, or other bones Weight loss Fatigue |
| What kinds of cancer does HPV cause? | Cervical, vulvular in women in men anorectal and squamous cell carcinoma of the penis. |
| Characteristics of Urine | Straw colored, Amber pH= 4.6- 8 protien= less than 0.1g glucose= less than 0.3g in 24 hours= 600-2500ml may be voided. |
| Sign of prostate cancer | Nocturia |
| Spinal cord injury sign | retention of urine |
| Kidney/gallstones sign Bladder cancer | Hematuria |
| Infection (WBC up) | Cloudy urine |
| UTI | is an infection that can happen anywhere along the urinary tract -- the kidneys, the ureters, the bladder, or the urethra |
| Who gets UTIs? | Women tend to get them more often because their urethra is shorter and closer to the anus, Elderly people (especially those in nursing homes) and people with diabetes |
| Cause/pathology of UTI | Usually caused by a bacteria from the anus entering the urethra and then the bladder. This leads to inflammation and infection in the lower urinary tract. |
| What is the biggest cause for UTIs? | Escherichia coli (about 80% of uncomplicated and 20% of complicated cases) Most common cause of UTI |
| Cystitis | People with interstitial cystitis have a bladder wall that is inflamed and irritated (red and sore). This inflammation can scar the bladder or make it stiff. In some cases, the walls of the bladder may bleed slightly. |
| Who gets cystitis? | Women its idiopathic |
| S&S of Cystitis? | rgent need to urinate. only passing small volumes of urine Pain in the lower abdomen between the vagina and anus in women or the scrotum and anus in men (perineal). Chronic pelvic pain mimic UTI |
| Polynephritis | An infection of the kidney and the ducts that carry urine away from the kidney (ureters). |
| Cause of Polynephritis | Bacterial infection Viral or fungal infection |
| S&S of Polynephritis | Flank pain or back pain Fever Chills with shaking Increased frequency or urgency nocturia Cloudy or abnormal urine color Blood in the urine Foul or strong urine odor Mental changes or confusion Warm skin Flushed skin diaphoresis Fati |
| Pathology of of Polynephritis | Inflammation/infection of the ureters. |
| No fever, no chills, no CVA tenderness Not due to bacteria | Cystitis |
| No urgency but always fever and always bacterial, possibly sepsis. | Polynephritis |
| Polynephritis can cause _________ in the elderly | Septic shock |
| Glomerulonephritis | Inflammation of the kidney hampering the kidneys' ability to remove waste and excess fluids. It can be acute, referring to a sudden attack of inflammation, or chronic, which comes on gradually. Can be part of a systemic disease, lupus,diabetes, |
| Glomerulonephritis causes | Infections or Immune diseases causing antigen antibody complexes to damage the kidney most common cause Inflammation of the blood vessels (vasculitis) Conditions that scar the glomeruli. Often, however, the exact cause is initially unknown |
| Glomerulonephritis S&S | Tea-colored urine from hematuria Foam in the toilet water from proteinuria Notproducing erythropoeitin High blood pressure (hypertension) Fedema in face, hands, feet and abdomen Fatigue from anemia or kidney failure Less frequent urination than |
| Goodpasture S&S | Hemoptysis Crackles and rhonchi Pulmonary hemorrhage Renal involvement Hematuria Acute renal failure Weakness Pallor |
| Goodpasture cause | idiopathic possibly autoimmune attack basement membrane. |
| Goodpasture Disease | autoimmune disease characterized by glomerulonephritis (inflam capillary loops in the glomeruli of the kidney), pulmonary hemorrhage (bleeding in the lungs), and autoantibodies to the glomerular and alveolar basement membranes (anti-GBM) antibodies. |
| What tests measure the functionality of the kidenys? | BUN, Creatinine, 24 hour urine for Creatinine clearance |
| Nephrotic Syndrome | form of glomerular dysfunction. Its clinical presentation is primarily massive proteinuria, specifically defined as 3.5 grams or more in 24 hours. In some cases, patients may excrete as much as 10 grams in 24 hours |
| Pathology of Nephrotic Syndrome | fatty degeneration of the tubules associated with normal appearing glomeruliCharacterized by massive loss of urinary protein (primarily albuminuria) leading to hypoproteinemia and edema |
| Nephronic Syndrome | Idiopathic |
| Signs of Nephrotic Syndrome | Proteinuria Hypoalbuminemia Edema Hyperlipidemia Lipiduria Decreased vitamin D |
| Tests for Nephrotic | Urinalasys, Protein in urine lipid profile BUn, Creatinine elevated |
| S&S of Renal Calculi | Classic presentation of renal colic is excruciating unilateral flank or lower abdominal pain of sudden onset that is not related to any precipitating event and is not relieved by postural changes or nonnarcotic medications |
| Who does Renal Calculi occur in? | Three times more common in males. |
| What are Renal Calculi made out of? | Calcium oxalate Calcium phosphate |
| Kidney Stone | Vague flank pain, hematuria |
| Proximal ureter | Vague flank pain, hematuria |
| Middle section of ureter | Renal colic, anterior abdominal pain, flank pain |
| Distal ureter | Renal colic, dysuria, urinary frequency, anterior abdominal pain, flank pain |
| Acute Glomerulonephritis | Damage to the epithelial and endothelial cells of basement membrane |
| Chronic Glomerulonephritis | Glomerulosclerosis and interstitial injury |
| Causes of bladder cancer | Smoking. Exposure to certain toxic chemicals and drugs Treatment with the anti-cancer drugs Use of the herb Aristolochia fangchi. Use of chlorine in water and artificial sweetners such as Saccharin and Cyclamate |
| Bladder Cancer | Hematuria Pelvic pain Pain during urination Frequent urination or feeling you need to urinate without being able to do so Slowing of your urinary stream |
| Bladder cancer tests | cysto w/ biopsy MRI CT Scan- more for metastasis Bone Scan ultrasound- fluid/pain meds |
| Renal Stones whos at risk? | Adults, men, whites, in hot temperatures |
| Acute renal failure | udden loss of the ability of the kidneys to excrete wastes, concentrate urine, and conserve electrolytes. |
| Pre-renal azotemia | a problem in a part of the body before the kidneys that is causing a ↓ in renal blood flow |
| Intra-renal azotemia | intrinsic) – there is a problem within the kidneys |
| Post-renal azotemia | an obstruction after the kidney |
| Azotemia | an elevation of the nitrogenous waste products (creatinine and urea nitrogen) |
| Uremia | is the clinical syndrome resulting from azotemia and is characterized by anorexia, N/V, and mental status changes |
| Causes of Pre-renal azotemia | Hypotension from any cause CHF or severe pulmonary dz Volume depletion: vom/dia/burns, dehydration, hemorrhage -Hypercalcemia (which may result in afferent arteriolar vasconstriction) -Medications: cyclosporine, ACE-I, NSAIDs, osmotic diuretics |
| Causes of intra-renal azotemia | schemia: thromboembolism, hypoperfusion from systemic hypotension, vasoconstriction Toxins: endogenous, exogenous, Inflammation: acute glomerular nephritis, acute tubular nephritis, pyelonephritis, infection Tumor infiltration, myeloma kidney |
| Causes of post-renal obstructions | -prostatic hypertrophy -malignancy – cervical cancer -urethral stricture -ureter obstruction: stone or crystals (uric acid, Ca oxalate), papillae, fibrosis, tumor *may require renal imaging to determine obstruction |
| Phases of ARF | Onset or initiating: Time of insult until symptoms appear Oliguric: Reduction in GFR and oliguria of < 400 ml in 24 hours Diuretic: Increase in urine output but not in filtration of toxins. ↑BUN Creat Recovery with normalization of BUN and Creat |
| ARF S&S | Nocturia edema lower limbs generalized swelling lower sensation hands or feet decreased appetite metallic taste in mouth persistent hiccups changes in mental status or mood slow, sluggish, movements seizures hand tremor n/v flank pain |
| Renal Diet | Low sodium, Low potassium, low protein, fluid restrictions |
| Chronic Renal Failure | Chronic renal failure is a gradual and progressive loss of the ability of the kidneys to excrete wastes, concentrate urine, and conserve electrolytes. |
| Causes of chronic renal failure | Diabetes Hypertension Glomerulonephritis of any type (one of the most common causes) Polycystic kidney disease Obstructive uropathy Kidney stones and infection |
| S&S Chronic Renal failure | weight loss n/v General ill feeling Fatigue Headache nocturia Decreased alertness coma Muscle twitching or cramps Seizures Uremic frost -- deposits of white crystals in and on the skin Decreased sensation |
| Polycystic Kidney Disease | Cysts take over functional part of the kidney |
| What kind of disease it PKD? | Autosomal dominant |
| S&S PKD | pain in the back and lower sides headaches urinary tract infections blood in the urine cysts in the kidneys and other organs |
| Wilm's tumor | s a cancerous tumor of the kidney. It generally occurs in children under the age of seven. |
| Blood Cell Production (Hemopoiesis) | Red bone marrow produces RBCs, WBCs and platelets |
| Stimulus for erythropoiesis | low levels of atmospheric O2 increase in exercise hemorrhaging Kidneys- regulates production |
| key nutritional requirement for erythropoiesis | iron,B12 & folic acid (for rapid cell division) and C & copper for cofactors for enzymes synthesizing RBCs |
| plaelets | Their sticky surface lets them, along with other substances, form clots to stop bleeding |
| Leukocytes divide in two categories: | granulocytes (esino, baso, neutro)and l ymphoid cells or agranulocytes (lymphocytes) |
| leukocytosis | Increase in WBC- l |
| Neutrophils | are very active in phagocyting bacteria and are present in large amount in the pus of wounds. |
| Basophil | secrete anti-coagulant and vasodilatory substances as histamines and serotonin. Even if they have a phagocytory capability, their main function is secreting substances which mediate the hypersensitivity reaction. |
| Eosinophils | attack parasites and phagocyte antigen-antibody complexes |
| Lymphocytes | T and B lymphocytesWBC |
| WBC rates | 4.5-10 |
| Agranulocytes (or mononuclears) | Lymphocytes Moncytes |
| Lymphocytes | 25-35% |
| Monocytes | 4-6% |
| Granulocytes | Neutro Baso Esino |
| Neutro | 50-70% |
| Esino | 1-3% |
| Baso | 0.4-1% |
| Male/Female numbers of RBC | male: 4.7 to 6.1 million cells/mcl female: 4.2 to 5.4 million cells/mcl |
| Platelets | Normal Value 150-400/ ul |
| Hemoglobin | oxygen-carrying pigment and predominant protein in the RBC Hemoglobin forms an unstable, reversible bond with oxygen. oxygenated state it is called oxyhemoglobin and is bright red.reduced state it is called deoxyhemoglobin and is purple-blue. |
| Adult males: Hemoglobin | 14-18 gm/dl |
| Adult females: Hemoglobin | 12-16 gm/dl |
| Hematocrit | Hematocrit is the proportion, by volume, of the blood that consists of red blood cells. The hematocrit (hct)is expressed as a percentage. For example, an hematocrit of 25% means that there are 25 milliliters of red blood cells in 100 milliliters of blood |
| Adult women: hematocrit | 38-46% |
| Adult men: hematocrit | 42-54% |
| Anemia | lower than normal number of red blood cells (erythrocytes) in the blood, usually measured by a decrease in the amount of hemoglobin. |
| Pernicious Anemia | Lack of vitamin B, abnormal DNA and RNA synthesis in erythroblast, premature cell death. |
| Pernicious Anemia Cause? | Congenital or acquired deficiency of intrinsic factor, ill not be absorbed because of gut problems |
| Folate deficiency anemia | lack of folate, premature cell death |
| Folate anemia cause? | Dietary folate deficiency. |
| Iron deficiency anemia | lack of iron from hemoglobin, insufficient hemoglobin MACROCYTIC |
| Iron deficiency anemia cause? | Chronic blood loss, dietary iron deficiency, disruption of iron metabolism cycle. MICROCYTIC |
| Microcytic | iron deficiency anemia |
| Macrocytic | vitamin B12, folic acid deficiency, liver disease. |
| Normocytic | cute blood loss, chronic renal disease, aplastic anemia |
| Pernicious anemia | large immature megoblasts |
| Sickle cell anemia | Crescent shaped, distorted, fragile cells |
| Thalassemia | Low hemoglobin |
| Diet needs for RBC | Vitamin B12: red meats, liver Folic acid: green leafy vegetables meat fish legumes& whole grain Vitamin B-6:meats,potatoes,bananas,legumes Amino acids: Eggs, meat, milk, milk products, poultry, fish, nuts, Vitamin C: citrus fruits strawberries |
| Microcytic anemia | thick, curved (spoon) nails |
| TIBC | Iron binding capacity |
| For vitamin B12 to be absorbed by the body, | must bind to intrinsic factor, a protein secreted by cells in the stomach. |
| Vit b12 def | a strict vegetarian diet that excludes all meat, fish, dairy products, and eggs Chronic alcoholism Abdominal or intestinal surgery Crohn's disease Intestinal malabsorption disorders Fish tape worm Pernicious anemia |
| Sickle Cell disease | inherited blood disorder that affects RBC. RBC contain mostly hemoglobin* S (abnormal)become sickle-shaped w/difficulty passing through small blood vessels. When sickle-shaped cells block small blood vessels, causes tissue damaged |
| S&S sickle cell anemia | Stroke ACS-similar ro pneumonia- chest= blocked blood vessel chest pain, fever, blocked vessels in the lungs Over time. effects on body, blindness, organ damage, |
| Sickle cell crisis | Demand for o2 up, low o2= greater production of RBC, produce more quickly, more sickled cells, more blockage from abnormal cells. |
| Sickle cell genetics | autosomal recessive |
| Clotting | capillary is injured and blood leaks out. capillary tightens up to help slow the bleeding. blood cells called platelets make a plug to patch lotting factors in plasma form a clot over the plug. This makes the plug stronger and stops the bleeding. |
| Hemophelia genetics | x linked recessive |
| hemophilia A. | People with low levels of factor VIII (eight) have |
| hemophilia B. | People with low levels of factor IX (nine) have |
| Pathology of hemophelia | In hemophilia, one clotting factor is missing, or the level of that factor is low. This makes it difficult for the blood to form a clot, so bleeding continues longer than usual, not faster. |
| Other effects of hemophelia | Joint pain, crippling pain because of bleeding into the joints |
| S&S of hemophelia | bleeding can happen anywhere after an injury or surgery. or no clear reason. When babies start to walk, they bruise easily. They also bleed longer than usual after an injury, especially to the mouth and tongue. spontaneous bleeding becomes |
| Polycythemia | Overproduction of red blood cells |
| Relative polycythemia | Result of dehydration Fluid loss results in relative increases of red cell counts and Hgb and Hct values |
| CAuse of Polycythemia | It is a protein switch that tells the cells to grow. Specifically it's a mutation in the protein JAK2 (the JAK2 V617F mutation). |
| S&S of Polycythemia | Headache visual disturbances Neurologic deficits Angina, and heart failure. Severe itching when they take a warm shower or bath because of mast cell stimulation in the skin. |
| Diagnostic tests polycythemia | what do you measure? hemoglobin hemo greater than 12, phlebotomize, |
| What happens in polycythemia | strokes- heart faliure- so much blood, moving slower, increased BP, feel like having stroke. take it out. |
| leukemia | one blood cell goes awry (in the majority of cases this cell is a white blood cell) and the body produces large numbers of this cell. |
| acute leukemias | he white blood cells multiple very rapidly and are very immature, and therefore cannot function properly (immature cells are called blasts). |
| chronic leukemia | the blasts form more slowly, allowing the body to continue to produce functional cells, causing fewer symptoms for the patient. These cases are often diagnosed during a routine physical. may cause the spleen to become enlarged, |
| myelogenous, or myeloid, leukemia | If the cancerous blood cells are primarily granulocytes or monocytes, the leukemia is |
| lymphocytic leukemia | If the cancerous blood cells are primarily lymphocytes |
| Acute myeloid leukemia (also called AML) - | occurs in both children and adults. |
| Acute lymphocytic leukemia (ALL) | the most common type seen in children before age 14 peak age 2-9 yrs, but also seen in adults over 65. Effects T and B cells and invades the lymph nodes |
| Chronic myelogenous leukemia (CML) | occurs mostly in adults 29-60 yrs old. mutation= Philadelphia chromosome,exchange of chromosomal materials between chr9 and 22. Effects the B and T stem cells in the bone marrow and decreases the other cellular lines ie erythrocytes and thrombocytes |
| Chronic lymphocytic leukemia (CLL) | most often seen in people over age 55, can affect younger adults, but almost never seen in children |
| Specific thing about CML, | translocation between 9& 22 |
| Pathology of Leukemia | leukemia is believed to occur in individuals with an inherited chromosomal vulnerability to mutagens such as radiation, toxins, or chemotherapeutic agents. Point mutations, frame shift mutations, and chromosomal aneuploidy and translocations have |
| blasts | immature cells |
| Causes of leukemia | High-energy radiation, Some genetic syndromes, such as Down's syndrome, put a person at higher risk. the chemical benzene epistien barr Exposure to electromagnetic fields |
| S&S leukemia | Fevers or infections that won't go away. Tiredness or appears pale. As the number of immature cells (blasts) increases, the normal cells are crowded out. This leads to anemia. Bleeding or bruise easily from low platelet counts. |
| Other S&S Leukemia | Leg pain in the long bones petchiea cross blood brain barrier/ spinal tap headaches/vom/confus swollem lymph nodes night sweats |
| Hodgkins Lymphoma | malignancy of lymphocytes that reside in the lymph node and these malignant cells have a characteristic appearance and are called Reed-Sternberg cells |
| Hodgkins Lymphoma S&S | Swelling of the lymph nodes, starting in the neck Night sweats Low-grade fevers Weight loss |
| Causes of lymphoma | viruses, transplant immunosuppression Radiation chemical exposure Numerous types of cellular DNA mutations have been documented in these malignancies Non-Hodgkin lymphoma tends to involve many peripheral nodes and extends into extranodal tissues. |
| who is at risk for Multiple Myeloma? | nset of multiple myeloma occurs most commonly in individuals between the ages of 50 and 60 years old and is more common in African Americans. |
| Multiple Myleoma | plasma cells grow out of control in the bone marrow and form tumors in the areas of solid bone. The growth of these bone tumors makes it harder for the bone marrow to make healthy blood cells and platelets. |
| CRAB | C- increase in calcium- bone dest R-renal disease due to BJP destroying kidney A-anemia- bone marrow impacted with these cells decrease RBC production, B-bone disease |
| Pathology of multiple myleoma | Lysis of bone=increased cytokines= stimulate myleoma growth Bone lesions are accompanied by malignant transformed plasma cells that produce an abnormal protein monoclonal immunoglobulin immunoglobulin fragments called Bence Jones proteins excret in urin |
| S&S of multiple myleoma | Bone pain (especially ribs, sternum, skull, vertebrae, and femur) Pathologic fractures Hypercalcemia (lethargy and confusion) Renal disease Recurrent and overwhelming infection (which may be fatal) |
| Lymphoblastic Lymphoma (LL) | Clone of immature T cells that become malignant in the thymus |
| ITP Immune thrombocytopenic purpura | IgG antibody that targets platelet glycoproteins Antibody-coated platelets are sequestered and removed from the circulation The acute form of ITP that often develops after a viral infection is one of the most common childhood bleeding disorders AUTOIMM |
| Cause if ITP? | Idiopathic sometimes after virus in childhood |
| S&S ITP | Petechiae Purpura Epistaxis Hematuria Menorrhagia Gum bleeding Systemic effects: fever, weight loss, and headache |
| HIT | is an autoimmune disorder that results in intravascular aggregation of platelets and a paradoxical thrombosis in response to heparin administration. HIT is quite common. antibodies to heparin that destroys platelets. |
| Vit K Defficiency | Vitamin K is necessary for synthesis and regulation of prothrombin, the prothrombin factors (II, VII, XI, X), and proteins C and S (anticoagulants) |
| Disseminated Intravascular Coagulation (DIC) | Complex, acquired disorder in which clotting and hemorrhage simultaneously occur Is the result of increased protease activity in the blood caused by unregulated release of thrombin with subsequent fibrin formation and accelerated fibrinolysis |
| Cause of DIC | Endothelial damage is the primary initiator - SEPSIS! Sepsis Trauma Shock Obstetrical accidents Some viral infections Hematologic disorders Some cancers |
| Clinical S&S of DIC | Clinical signs and symptoms demonstrate wide variability Bleeding from venipuncture sites Bleeding from arterial lines Purpura, petechiae, and hematomas Symmetric cyanosis of the fingers and toes Runny faucet all of the time. |
| Pathology of DIC | Look at blood levels fibrinogen- activated split fib levels= decreased over time- damage to all organs- end organ failure. |
| Why DIC with liver failure? | Liver produces most clotting factors, so when it is not functioning, it will cause clotting problems. |
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