Patho Final Study Notes Review, Study notes of Pathophysiology

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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

8. physiologic atrophy: -Thymus gland in early childhood, normal event -ovaries atrophy -aging in brain cells
9. pathologic atrophy: -due to decrease in workload, pressure, use, blood supply, nutrition, hormonal stimulation,
10. hypertrophy: Increased cell size due to stress or mechanical load -cells of heart and kidneys -Left ventricular hypertrophy:
11. physiologic hypertrophy: runners heart, increased enlargement due to aero- bic exercise
12. pathologic hypertrophy: -results from chronic hemodynamic overload, such as hypertension or heart valve dysfunction -LVH secondary to hypertension
13. 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
14. compensatory hyperplasia: -enables organs to regenerate -liver -A callus, or thickening of the skin
15. hormonal hyperplasia: -occurs in organs that respond to endocrine hormonal stimulation -hyperplasia and endometrial proliferation during menstrual cycle
16. Pathologic Hormonal Hyperplasia: -uterine endometrium that occurs from an imbalance in estrogen and progesterone

-prostatic hyperplasia -Thyroid enlargement

17. Dysplasia: -deranged cellular growth -atypical hyperplasia -not a true adaptive change -common in epithelial tissues of uterus, endometrium, GI
18. Metaplasia: -Reversible replacement of a mature cell type by another less mature cell type -tissue damage, repair, regeneration -long term cigarette smoker causes normal ciliated columnar to become replaced by stratified squamous cells
19. metabolic acidosis s/s: Early symptoms: headache and lethargy.... then pro- gresses to confusion and coma in severe acidosis. Other symptoms: decreased BP, warm flushed skin, n/v/d, dysrhythmias, DROWSINESS, DECREASED BP COMPENSATED: Kussmaul's respirations: deep and rapid ventilations
20. Metabolic alkalosis s/s: -weakness, muscle cramps, hyperactive reflexes, tetany, confusion, DIZZINESS, convulsion, TACHYCARDIA, tingling of fingers and toes. COMPENSATED BY: shallow, depressed breathing.
21. respiratory acidosis s/s: DROWSINESS -DECREASED BP headache, blurred vision,

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

22. Respiratory Alkalosis S/S: ·-dizziness, -light-headedness, -confusion, -headache, -tingling of extremities, -convulsion, coma, hypocalcemia (spasms of fingers and toes (tetany), tachycardia, hyperventilation.
23. 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
24. ECF: -all the fluids outside of the cell (1/3 TBW) -includes interstitial fluids, intravascular fluids, and transcellular fluids
25. intravascular fluid: fluid within blood vessels (blood plasma)
26. transcellular fluid: -fluids found within epithelial lines cavities ex: spinal fluid, synovial fluid, GI fluids, urine
27. 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

28. memory cells: Both B and T cells differentiate and proliferate into long-lived memory cells which remain inactive until exposed to same antigen again.
29. innate immunity: -"dumb" immunity -1st and 2nd line of defenses -non-specific -short lived
30. Acute signs of inflammation: 1. Rubor (redness) 2.Calor (heat 3.Tumor (swelling) 4.Dolor (pain) 5.Loss of function (functio lasea)
31. Protective components of inflammation: Prevents infection Limits scope of inflammatory process Prepare injured site for healing/repair Facilitates development of adaptive immunity
32. 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

-other chemicals found in our epithelial cells include antimicrobial peptides and defensins -collectins are produced by other various organs- surfactant in lungs

33. AIDS (acquired immune deficiency syndrome): -most ADVANCED stage of infection that is caused HIV
34. HIV: -depletes body's helper T cells -creates generalized immunodeficiency
35. HIV is...: -blood borne pathogen -heterosexual activity is the most common route worldwide -women affected more often -no cure- however people are living longer and has become a manageable chronic health condition
36. HIV incidence: -Worldwide: 2/3 of people living with HIV in WHO African Region, HETEROSEXUAL transmission most common route -US: 70% of cases were among gay and bisexual men -Region most affected: WHO African region
37. HIV transmission routes: -by body fluids -blood/blood products -IV drug use -heterosexual and homosexual activity -maternal-child transmission before or during birth
38. HIV development: -AIDS is a result of HIV -HIV infects and destroys CD4+ and Th cells, resulting in cellular

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

39. AIDS diagnosis: -made when CD4-T cell numbers are < 200 mm -AIDs defining opportunistic infections and cancers
40. Treatment of AIDS: -chemokine receptor inhibitors -HIV fusion inhibitors -reverse transcriptase inhibitors -HIV integrase inhibitors -HIV protease inhibitors *Death reduced *not curative
41. 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
42. 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
43. 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

44. macrocytic normochromic anemia: -large, abnormally shaped, normal Hgb Ex: pernicious anemia, folate deficiency anemia
45. microcytic hypochromic anemia: · small, abnormally shaped RBC, reduced Hgb Ex: Iron deficiency anemia, sideroblastic anemia
46. normocytic normochromic anemia: · normal size, normal hemoglobin ex: Sickle cell anemia, aplastic anemia, posthemorrhagic anemia
47. iron deficiency anemia (IDA): -most common nutritional disorder (microcytic hypochromic)

• Common in toddlers, adolescent girls, women of childbearing age, poverty, poor restricted diets

48. Causes of IDA include:: - dietary deficiency -impaired absorption

• increased requirement -chronic blood loss, -chronic diarrhea

49. IDA pathophysiology: iron stores are depleted and reduce Hgb synthesis OR delivery of iron stores inadequate to maintain heme

synthesis. Develops over 3 stages: 1.Decreased bone marrow iron stores 2.Iron transportation to bone marrow diminished.

3. Small hgb-deficient cells begin to replace normal erythrocytes-where manifesta- tion becomes apparent.
4. IDA treatment: -Eval: Hgb, Hct -Determine cause to guide treatment: *stop bleeding *provide replacement therapy -serum ferritin best measurement of improvement

• hct levels improve in 1-2 months

51. IDA manifestations: - fatigue

• weakness, -shortness of breath
• pale conjunctivae, earlobes, palms, -Koilonychia (spoon shaped fingernails), brittle, thin nails, -cheilosis (scales fissure of mouth), -stomatitis ( inflammation of mouth)

52. pernicious anemia: -macrocytic normochromic -result of lack of intrinsic factor, which is necessary for absorption of B12, caused by vitamin B12 deficiency -associated with end stage of type A chronic atrophic gastritis (autoimmune)

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

53. 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.

54. 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

55. 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

56. 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

57. 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)
58. 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
59. Thrombocytopenia: low platelet count

• Platelets < 150,000/μl of blood

• < 100,000 significant
• < 50,000 high risk
• < 15,000 DANGER! Spontaneous hemorrhage

60. Thrombocytopenia causes: -congenital acquired, primary secondary causes -Acquired most common: *Heparin induced thrombo (HIT) *Immune idopathic thrombo (IIT) *Thrombotic thrombo purpura (TTP)
61. Manifestations of thrombocytopenia: -easy bruising -bleed gums -minor wounds with bleeding thats hard to stop -petechiae -purpura -blood in stool, urine, vomit -headaches or behavior changes (bleeding in brain)
62. thrombocythemia: too many platelets

• Platelets > 450,000/μl of blood
• Typically asymptomatic until...

• 1 million = spontaneous clot formation

63. Thrombocythemia causes: • Primary (essential) or secondary (reactive) types

• Essential thrombocythemia (ET) is a chronic myeloproliferative neoplasm (MPN)

• Secondary thrombocythemia often occurs post-splenectomy
• Reactive thrombocythemia may occur d/t rheumatoid arthritis or cancers (reaction to an inflammatory condition)

64. 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
65. 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.

66. Virchow's Traid consists of: 1. Injury to blood vessel endothelium 2.Abnormalities of blood flow 3.Hypercoagulability of blood
67. injury to blood vessel endothelium: -atherosclerosis

-hypertension -radiation injury -chemical agents -bacterial toxins

68. 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)
69. Hypercoagulability: -primary causes are genetic -secondary: disseminated intravascular coagulation -liver disease -infection -ARDs

70. 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
71. 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

ex: COPD, pneumonia, ARDs

72. Left sided heart failure (systolic): • Ejection fraction less than 40%

• Inability of the heart to generate adequate cardiac output to perfuse tissues.
• Stroke volume: contractility, preload, afterload
• Disruptions decrease cardiac output.
• Falling cardiac output progressively worsens heart failure.

73. Manifestations of systolic LHF: • Dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output, and edema

• Pulmonary edema, hypotension/hypertension, S3 gallop

74. Diastolic LHF: -pulmonary congestion despite normal stroke volume and car- diac output -major causes: hypertension induced myocardial hypertrophy and myocardial is- chemia induced ventricular remodeling -decreased compliance of left ventricle -abnormal diastolic RELAXATION
75. Manifestations of diastolic LHF: • Dyspnea on exertion, fatigue

• Pulmonary edema may develop over time, S4 gallop.

76. MI structural changes: -Myocardial stunning- injured cells -hibernating myocardium-ischemic cells -myocardial remodeling
77. 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
78. MI is caused by: coronary blood flow is interrupted for more than 20 minutes causing necrosis of myocardial cells
79. NSTEMI: non-ST elevation myocardial infarction -occurs when thrombus disrupting blood flow disintegrates prior to complete distal tissue necrosis occurring -troponin elevated
80. STEMI: ST elevation myocardial infarction -thrombus lodges permanently, causing necrosis to entire section of endocardium, severe cardiac dysfunction
81. 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

• Abnormal extra heart sounds d/t LV dysfunction
• Pulmonary congestion
• Peripheral vasoconstriction
• ECG changes, dysrhythmias

82. acute pericarditis: inflammation of the pericardium

• Most often caused by viral infection or is idiopathic
• Often accompanied by a fever
• Sudden onset of severe retrosternal chest pain that worsens with breathing & lying down
• Can hear a friction rub when auscultating heart sounds

83. pericardial effusion: accumulation of fluid in the pericardial cavity

• Can occur with any type of pericarditis
• Pericardiocentesis done to determine source of fluid
• Can result in tamponade (cardiac compression)

• Distant/muffled heart sounds, DOE, dull chest pain

84. 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.

85. Sepsis: -overreaction or dysregulated response to bacteremia (bacterial infec- tion in the blood) -life threatening organ dysfunction
86. 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.

87. 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

88. 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.

89. MODS cont.: • Oxygen delivery impaired

• Results in significant imbalance between oxygen supply and oxygen demand
• Symptoms may not appear for 24 hours.

90. MODS manifestations: -low grade fever -tachycardia -dyspnea -altered mental status -hyperdynamic and hypermetabolic states -ARDS (tachypnea, pulmonary edema, accessory muscles)
91. MODS organ dysfunction: • Signs of liver and kidney failure will start appear- ing.

• Jaundice, ascites, liver tenderness, muscle wasting, hepatic encephalopathy, low albumin levels

• Oliguria, azotemia (high BUN & creatinine levels), edema, hyperkalemia, metabolic acidosis

• GI system prone to ischemia
• Hemorrhage, ileus, malabsorption, diarrhea/constipation, vomiting, anorexia, abd. Pain
• Ischemia & inflammation lead to CNS symptoms
• Apprehension, confusion, agitation, restlessness, decreased LOC, seizures, coma

92. Treatment of MODs: • Treatment is aimed at resolving the original infection and management of signs and symptoms, making it difficult to resolve.

• Early identification of sepsis & septic shock to prevent MODS is vital

93. How is sepsis treated?: antibiotics, fluids, vasopressors, oxygenation
94. rheumatic heart disease cause: • Rheumatic fever is a systemic inflammatory disease caused by an exaggerated response to infection by group A ²-hemolytic streptococcus (strep throat)

• Affects joints, skin, nervous system, & heart
• Can cause scarring & deformity of cardiac structures, resulting in rheumatic heart disease (RHD)

95. RHD symptoms: • RHD involves damage to the endocardium & swelling of valve leaflets with vegetative growth.

• Carditis w/ murmur, chest pain, pericardial friction rub, valve

dysfunction

• Cardiomegaly & L heart failure, a-fib can occur if untreated/recurrent.

96. Treatment of RHD: • Treatment; no cure, require surgery to replace or repair damages to valves
97. acute pain: - Protective mechanism

• Alerts an individual to a condition or experience that is immediately harmful to the body -Mobilizes individual to take prompt action -Transient -Begins suddenly and relieved after pain stimulus removed

98. somatic pain: -Arises from skin, joints, and muscles -Can be sharp or dull pain
99. Visceral pain: - Arises from internal organs and body cavity linings

• Poorly localized with aching, gnawing, throbbing, or cramping quality
• Often radiates or is referred

100. referred pain: - Felt in an area removed or distant from its point of origin -The area of referred pain is supplied by the same spinal segment as the actual site

• Can be acute or chronic

101. chronic pain: -Pain lasting longer than the expected healing time -Usually defined as lasting at least 3 to 6 months

• May be ongoing or intermittent
• Manifestations thought to be due to stress

• Produces behavior and psychologic changes -Persistent pain causes physiologic adaptation

102. neuropathic pain: -Dysfunction that causes long-term changes in pain path- way structures and abnormal processing of sensory information

• Amplification of pain without stimulation -Often described as burning, shooting, shock like, or tingling Classifications:
• Peripheral neuropathic pain -Central neuropathic pain

103. Fever: -temporary resetting of hypothalamic thermostat to a higher level -increase in heat production, conservation -exogenous, endogenous pyrogens -feels colder, dresses warmly or curls up to get warm -FUO: >101 for longer than 3 weeks undiagnosed -96.2-99.4 normal
104. benefits of fever: kill microorganisms, decreases iron, zinc, copper, lysosomal breakdown of cells, increase lymphocytic transformation and phagocyte motility, augments antiviral interferon production phagocytosis
105. Hyperthermia: - Elevation of body temperature without increase in hypothala- mic set point.

• Produce nerve damage, coagulation of proteins, death.

• Stroke or head trauma
• Therapeutic hyperthermia: warms to destroy microorganisms or tumor cells

106. accidental hyperthermia: -heat cramps: spasmodic cramps in abdomen and extremities from sweating (sodium loss)

• Heat exhaustion: profound vasodilation, sweating, from prolonged high core or environmental temps
• Heat stroke: failure of heat loss mechanisms 104 degrees