Patho Final Study Notes Review, Study notes of Pathophysiology

Patho Final Study Notes Review

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Patho Final Study Notes Review
1.histone modification: -what happens when there are CHEMICAL
changes to the histone proteins that DNA is wrapped around
-histones are basic proteins that work to compress DNA in the nucleus to
form chromatin and then there is a platform for regulating gene
transcription
2.Histone modification cont.: -histone modification can be a consequence
of DNA methylation
-indirectly affects DNA
-proteins can attach chemical tags to histones
-cell's proteins detect these tags to determine if that region of DNA
should be turned on or off
3.Prader-Willi Syndrome: -deletion of 4 mb pairs of long arm of
chromosome 15
-inherited from father
4.Prader-Willi characteristics: short stature, hypotonia, small hands
and feet, obesity, mild to moderate mental retardation, and
hypogonadism.
5.Angelman Syndrome: -deletion of 4mb from chromosome 15
-mother
6.Angelman syndrome symptoms: severe intellectual disability, seizures,
ataxic gait
7.Atrophy: decreased cell size, shrinkage
-occurs most in skeletal muscle, heart muscle, secondary sex organs,
and the brain
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Patho Final Study Notes Review

  1. histone modification: -what happens when there are CHEMICAL changes to the histone proteins that DNA is wrapped around -histones are basic proteins that work to compress DNA in the nucleus to form chromatin and then there is a platform for regulating gene transcription
  2. Histone modification cont.: -histone modification can be a consequence of DNA methylation -indirectly affects DNA -proteins can attach chemical tags to histones -cell's proteins detect these tags to determine if that region of DNA should be turned on or off
  3. Prader-Willi Syndrome: -deletion of 4 mb pairs of long arm of chromosome 15 -inherited from father
  4. Prader-Willi characteristics: short stature, hypotonia, small hands and feet, obesity, mild to moderate mental retardation, and hypogonadism.
  5. Angelman Syndrome: -deletion of 4mb from chromosome 15 -mother
  6. Angelman syndrome symptoms: severe intellectual disability, seizures, ataxic gait
  7. Atrophy: decreased cell size, shrinkage -occurs most in skeletal muscle, heart muscle, secondary sex organs, and the brain
  1. physiologic atrophy: -Thymus gland in early childhood, normal event -ovaries atrophy -aging in brain cells
  2. pathologic atrophy: -due to decrease in workload, pressure, use, blood supply, nutrition, hormonal stimulation,
  3. hypertrophy: Increased cell size due to stress or mechanical load -cells of heart and kidneys -Left ventricular hypertrophy:
  4. physiologic hypertrophy: runners heart, increased enlargement due to aero- bic exercise
  5. pathologic hypertrophy: -results from chronic hemodynamic overload, such as hypertension or heart valve dysfunction -LVH secondary to hypertension
  6. Hyperplasia: Increased cell number due to increased rate of cell division -occurs when damage is severe or prolonged or results in cell death -requires cells to undergo mitosis
  7. compensatory hyperplasia: -enables organs to regenerate -liver -A callus, or thickening of the skin
  8. hormonal hyperplasia: -occurs in organs that respond to endocrine hormonal stimulation -hyperplasia and endometrial proliferation during menstrual cycle
  9. Pathologic Hormonal Hyperplasia: -uterine endometrium that occurs from an imbalance in estrogen and progesterone

-breathlessness -restlessness, apprehension, lethargy, disorientation, - ventricular fibrillation -warm flushed skin, coma, seizures, muscle twitching, hypoventilation with hypoxia.

  1. Respiratory Alkalosis S/S: ·-dizziness, -light-headedness, -confusion, -headache, -tingling of extremities, -convulsion, coma, hypocalcemia (spasms of fingers and toes (tetany), tachycardia, hyperventilation.
  2. ICF: All the fluids within the cells -2/3 total body water -females is less due to larger amounts of Sub-Q tissue and smaller muscle mass
  3. ECF: -all the fluids outside of the cell (1/3 TBW) -includes interstitial fluids, intravascular fluids, and transcellular fluids
  4. intravascular fluid: fluid within blood vessels (blood plasma)
  5. transcellular fluid: -fluids found within epithelial lines cavities ex: spinal fluid, synovial fluid, GI fluids, urine
  6. Clonal selection definition: -the processing of antigen for a specific immune response -antigens must be shown to immune cells to elicit response -APC: dendritic cells, macrophages, B-cells
  1. memory cells: Both B and T cells differentiate and proliferate into long-lived memory cells which remain inactive until exposed to same antigen again.
  2. innate immunity: -"dumb" immunity -1st and 2nd line of defenses -non-specific -short lived
  3. Acute signs of inflammation: 1. Rubor (redness) 2.Calor (heat 3.Tumor (swelling) 4.Dolor (pain) 5.Loss of function (functio lasea)
  4. Protective components of inflammation: Prevents infection Limits scope of inflammatory process Prepare injured site for healing/repair Facilitates development of adaptive immunity
  5. Biochemical means innate immunity: -perspiration, saliva, tears **contain enzyme called lysozyme which attacks cell wall of gram + bacteria -sebaceous glands secrete fatty acids, lactic acids, killing bacteria and fungi and create acidic pH on skin surface -mucous and earwax

and humoral immunity deficiencies -AIDS is most advanced stage of HIV -AIDS diagnosis is made when HIV becomes associated with various clinical con- ditions

  1. AIDS diagnosis: -made when CD4-T cell numbers are < 200 mm -AIDs defining opportunistic infections and cancers
  2. Treatment of AIDS: -chemokine receptor inhibitors -HIV fusion inhibitors -reverse transcriptase inhibitors -HIV integrase inhibitors -HIV protease inhibitors *Death reduced *not curative
  3. Weakened - attenuated vaccine: · derived from wild viruses or bacteria. These wild viruses or bacteria are weakened in a laboratory by repeated culturing. Ex. Measles, mumps chickenpox
  4. dead pathogen vaccine: use of the killed version of the germ that causes disease. Inactivated vaccines don't provide immunity that as strong as live vaccines, may need several boosters. · Ex: hep A, polio, rabies, flu
  5. recombinant viral protein vaccine: · made by using bacterial or yeast

cells to manufacture the vaccine. A small piece of DNA or protein is taken from the virus or bacteria against which we want to protect. Ex: Hep B, HPV

  1. macrocytic normochromic anemia: -large, abnormally shaped, normal Hgb Ex: pernicious anemia, folate deficiency anemia
  2. microcytic hypochromic anemia: · small, abnormally shaped RBC, reduced Hgb Ex: Iron deficiency anemia, sideroblastic anemia
  3. normocytic normochromic anemia: · normal size, normal hemoglobin ex: Sickle cell anemia, aplastic anemia, posthemorrhagic anemia
  4. iron deficiency anemia (IDA): -most common nutritional disorder (microcytic hypochromic)
  • Common in toddlers, adolescent girls, women of childbearing age, poverty, poor restricted diets
  1. Causes of IDA include:: - dietary deficiency -impaired absorption
  • increased requirement -chronic blood loss, -chronic diarrhea
  1. IDA pathophysiology: iron stores are depleted and reduce Hgb synthesis OR delivery of iron stores inadequate to maintain heme

-individuals over 30 and northern European descent -once considered fatal due to lack of treatment

  1. Patho of PA: - Absence of IF which is secreted from gastric cells and forms a complex with Vitamin B12 In small intestine.
  • Vit B12 for nuclear maturation and DNA synthesis in RBCs
  • Congenital or acquired: surgical removal of stomach, resection of ileum, tape- worms.
  • Demand more B12: pregnancy, hyperthyroidism, chronic infection, disseminated cancer.
  1. Manifestations of PA: Early: infections, mood swings, GI/kidney/cardiac ail- ments Classic: Hgb 7-8, weakness, fatigue, paresthesia of fingers and feet, ataxia, loss of appetite, weight loss, sore tongue that is smooth and beefy red, sallow skin (lemon yellow)
  • hepatomegaly and splenomegaly can result -RHF can result if not treated
  1. PA treatment and evalutation: -blood test, bone marrow, -gastric biopsy should reveal total absence of HCL. -replacement of Vit B12 with injections, weekly injection until corrected,

then monthly for life, oral high doses don't work as well

  1. Folate deficiency anemia: -macrocytic normochromic caused by folate defi- ciency
  • folate is vital for RNA and DNA synthesis in RBCs -dependent on nutritional intake 50-200 mg/day -increased for lactating mothers, occurs more often than PA
  1. folate patho: -folate absorbed from upper small intestine is not dependent on another factor for absorption -folate is stored in the liver -most common in alcoholics and malnourishment -decreased incidence because of fortified foods in US (cereal)
  2. Folate manifestations and treatment: -cheilosis, stomatitis, burning mouth syndrome, dysphagia, flatulence, watery diarrhea, neurologic manifestations d/t thiamine deficiency -eval based on folate levels and manifestations -treatment is oral folate and increase in folic acid rich foods
  3. Thrombocytopenia: low platelet count
  • Platelets < 150,000/μl of blood
  • Secondary thrombocythemia often occurs post-splenectomy
  • Reactive thrombocythemia may occur d/t rheumatoid arthritis or cancers (reaction to an inflammatory condition)
  1. Manifestations of thrombocythemia: -blood clots in hands, feet, brain -TIA -headaches -visual changes -easy bruising -bleeding from nose, gums, GI tract -blood stools -weakness -swollen lymph nodes
  2. Virchow's triad: • Virchow's triad used to assess an individual's risk for devel- opment of thrombi.
  • Do not have to have all 3 factors present to develop thrombi.
  • Identifying risk factors based on triad can direct interventions or preventative strategies.
  1. Virchow's Traid consists of: 1. Injury to blood vessel endothelium 2.Abnormalities of blood flow 3.Hypercoagulability of blood
  2. injury to blood vessel endothelium: -atherosclerosis

-hypertension -radiation injury -chemical agents -bacterial toxins

  1. Abnormalities of blood flow: -Turbulence: may activate platelets and endothe- lial cells, leading to thrombus -Stasis: may cause the platelets to remain in contact with endothelium too long, leading to clots (surgery, limb paralysis, spinal injury, postpartum period, bed rest)
  2. Hypercoagulability: -primary causes are genetic -secondary: disseminated intravascular coagulation -liver disease -infection -ARDs
  1. right sided heart failure: -blood backs up into the body/periphery -inability of right ventricle to provide adequate blood flow at a normal venous pressure -can result from an increase in left ventricular filling pressure that is reflected back into pulmonary circulation
  2. Causes of RHF: -most commonly caused by a diffuse hypoxic pulmonary dis- ease-anything that impeded blood flow through the lungs and backs up the blood into the right side of the heart
  1. MI structural changes: -Myocardial stunning- injured cells -hibernating myocardium-ischemic cells -myocardial remodeling
  2. causes of myocardial infarction: -Genetic -Hypertension -Atherosclerosis -Hyperlipidemia -Stress -Endocrine hormone disorders (type I and II diabetes) (excess glucose destroys walls of blood vessels) -CAD
  3. MI is caused by: coronary blood flow is interrupted for more than 20 minutes causing necrosis of myocardial cells
  4. NSTEMI: non-ST elevation myocardial infarction -occurs when thrombus disrupting blood flow disintegrates prior to complete distal tissue necrosis occurring -troponin elevated
  5. STEMI: ST elevation myocardial infarction -thrombus lodges permanently, causing necrosis to entire section of endocardium, severe cardiac dysfunction
  6. MI outcomes: • Sudden severe chest pain
  • Heavy, crushing, radiates to neck, jaw, back, shoulder, arm.
  • Nausea/vomiting d/t vagal nerve stim.
  • Can be "silent" in older people, diabetes.
  • Temporary increase in HR & BP d/t SNS compensation
  • Distant/muffled heart sounds, DOE, dull chest pain
  1. Restrictive/ constrictive pericarditis: -fibrous scarring and calcification of peri- cardium
  • Encases heart in a rigid shell
  • Develops gradually, reduces cardiac output
  • Symptoms are exercise intolerance, DOE, fatigue, anorexia, edema distention of jugular vein, hypotension.
  1. Sepsis: -overreaction or dysregulated response to bacteremia (bacterial infec- tion in the blood) -life threatening organ dysfunction
  2. septic shock: • Septic shock is a progression of sepsis which substantially increases the risk of death.
  • Profound underlying circulatory and cellular/metabolic abnormalities
  • Damage could be irreversible.
  1. symptoms of sepsis: S—Shivering, fever, or very cold E—Extreme pain or general discomfort ("worst ever") P—Pale or discolored skin S—Sleepy, difficult to rouse, confused I—"I feel like I might die" S—Short of breath
  1. Multiorgan dysfunction syndrome: • Ultimately, caused by anything that trig- gers a massive systemic inflammatory response (SIRS)...typically sepsis
  • Stress hormones released: epi, norepi, cortisol
  • Inflammatory mediators released into circulation.
  • 4 major plasma enzyme cascades initiated resulting in hype coagulant & hyperin- flammatory state.
  1. MODS cont.: • Oxygen delivery impaired
  • Results in significant imbalance between oxygen supply and oxygen demand
  • Symptoms may not appear for 24 hours.
  1. MODS manifestations: -low grade fever -tachycardia -dyspnea -altered mental status -hyperdynamic and hypermetabolic states -ARDS (tachypnea, pulmonary edema, accessory muscles)
  2. MODS organ dysfunction: • Signs of liver and kidney failure will start appear- ing.
  • Jaundice, ascites, liver tenderness, muscle wasting, hepatic encephalopathy, low albumin levels