Patho final exam study guide.pdf

Alyssa Carter; 4/19/23 - 4/25/23 ; Pathophysiology ; Dr. King 1) Key Concepts Homeostasis/Feedback mechanisms: Homeostasis→ A dynamic, steady state of achieving internal balance o things that can be homeostatically regulated are nutrient concentrations, O2 and CO2 concentration, concentration...

Alyssa Carter; 4/19/23 - 4/25/23 ; Pathophysiology ; Dr. King 1) Key Concepts Homeostasis/Feedback mechanisms: Homeostasis→ A dynamic, steady state of achieving internal balance o things that can be homeostatically regulated are nutrient concentrations, O2 and CO2 concentration, concentration of waste products, pH, concentration of water and salt and other electrolytes, volume and pressure, and temperature oWhen homeostasis is disrupted, illnesses may occur(i.e. injury, lack of nutrients, infections) oHomeostasis is maintained using Feedback mechanisms. Feedback Mechanisms oFeedback mechanisms have 3 components→ * Sensor mechanism(senses the disruption in Homeostasis) *Control Center(regulates the response to the disruption) * Effector Mechanism(acts to restore homeostasis) oThere are 2 main types of Feedback Mechanisms: *Negative(works to restore homeostasis by correcting the disruption in it Ex: High Blood Glucose levels) *Positive(moves the system further away from homeostasis Ex: intensifying labor contractions) 2) Altered Cell Function Features of hypoxic cell injury - This is the decrease of Oxygen getting into the blood cells(which is often caused by lung injury). - - Ischemia is what happens when oxygen isn’t getting to tissues. This is the single most common cause of cell injury. hyponia ischemia Cillinjurydeath Causes of irreversible cell injury - The causes of irreversible cell injury are: cell membrane damage, lysosomal membrane injury(which causes leakage of enzymes into the cytoplasm and is the main cause), and then this can all lead to cell death/necrosis. Causes of cellular swelling - 4088 A.K.A Reversible Cell injury; Dec. 402duetowww.fbuwodssuppyy ATP prod. →which then causes an inc. in anaerobic glycolysis→accumulation of Lactic Acid(because of glycolysis)-->decreased/more acidic pH→ an impairment of cell volume regulation(basically, there’s a failure of Na+/k pump, which leads to accumulation of Na and, thus, cell swelling)--> disruption of ribosomal interactions with E.R. Effectors of cell injury - Oxygen and Oxygen-derived free radicals, an inc. in cytosolic calcium and loss of calcium homeostasis, ATP depletion, defects in membrane permeability(necrosis which results in cell death and ischemia/dec. amount of O2 getting to cell) 3) Inflammation Define nonspecific vs. specific immune responses - Non-specific/Innate immunity consists of Inflammation and natural barriers(i.e.skin, epithelial membranes). On the other hand, specific/acquired/adaptive immunity is your humoral immunity(i.e. B-lymphocytes) and your cell-mediated immunity(T-lymphocytes). anodilation increased vascularpermeability Describe components of the vascular response - Basically, the vascular response causes vasodilation, which then increases vascular permeability, and then the WBCs a start to migrate to the site of injury. It ends up resulting in: prevention of infection or further damage, limit and control migrahm over the inflammatory process, interaction with components of the adaptive immune system, and preparing the area of ABL injury for healing. toof - Your components of the Vascular response are the Plasma Protein cascade(which consists of the complement system, the clotting system, and the Kinin system), the cellular elements(like your mast cells, your dendritic cells, leukocytes),unify and your mediators(such as Cytokines that are further divided into interleukins and interferons, and Chemokines which consist of Peptides). Define chemotaxis - Chemotaxis is the movement of an entity or organism in response to a chemical stimulus. Cytokines are often the attractant to get WBCs to travel to the site of infection. Describe the role of the following in inflammation: ○ Complement system: This is the initial frontline, and it’s what will recruit the WBCs to the site of injury. - Can sometimes destroy pathogens directly; it causes fragmentation of complement components(like proteins), then there’s vasodilation, followed by increased vascular permeability, then rapid mast cell degranulation/destruction, chemotaxis of neutrophils/the neutrophils travel to the site, next comes opsonization(where pathogens are marked for phagocytosis), and then, finally, cell lysis(the breaking down of the cell membrane).  - Overall the Complement functions are: 1)Lysis 2)Chemotaxis 3)Opsonization ○ Clotting cascade/Coagulation:(On the next page) - This is what will help form this fibrinous meshwork, which is able to prevent the spread of infection to nearby tissues. It will trap microorganisms and foreign bodies to the site of inflammation so that they can be removed by infiltrating cells(like Neutrophils). There’s then the formulation of a clot, which will stop any bleeding, and it will provide a framework for future repair and healing. ○ Bradykinin: Part of the Kinin system which will cause strong vasodilation. This vasodilation will increase the microvascular permeability—allowing for Neutrophils to migrate, and then the pain receptors are activated; Bradykinin is the primary Kinin produced. ○ Mast cells: are involved in histamine release; they are an inflammatory response mediator/initiate the inflammation response ○ Dendritic cells: antigen processing cells; they process antigen material and then present it on the cell surface so that the T-cells of the immune system can come get it/so they activate the T-cells; they act as messengers between the innate and adaptive immune systems. ○ Leukocytes: Consists of Granulocytes, Monocytes/Macrophages, Lymphocytes - Neutrophils→ Involved with phagocytosis; the 1st WBCs to the scene; make up 60-70% of total WBCs - Eosinophils→ Responsible for Allergies and fighting parasites; control the mechanisms assoc. with Asthma - Basophils→ These are responsible for inflammatory reactions during the immune response; are involved in hypersensitivity reactions. - Monocytes/Macrophages→ migrate and differentiate into tissue macrophages for Phagocytosis - NK Cells→ Provides for direct cytotoxic activity against virus-infected cells and cancer cells - B-Cells→ Make antibodies - T-Cells→ Fight off infections, diseases, and help to boost the immune system ○ Natural Killer Cells: Provides direct cytotoxic activity against virus-infected cells and cancer cells 4) Fluid and Electrolytes Compare Osmosis vs. Hydrostatic pressure - Osmosis is a passive process, requiring no energy expenditure, that involves movement of water molecules from a region of high concentration to lower concentration until the concentrations become equal on either side of the partially permeable membrane. On the other hand, Hydrostatic pressure is the mechanical force of water pushing against cellular membranes. Know the ion composition of cytoplasm (potassium) and the ECF (sodium) - Na+, K+ and A-(proteins) are the major cations. Extracellularly/in the ECF, Na+ is the major cation at 150. Intracellularly/in the ICF, K+ is the major cation at 150. So, Sodium basically remains outside of the cell while Potassium is largely inside of the cell. Proteins tend to stay in the cell and never leave. Describe the role of Aldosterone and ADH in water balance - Aldosterone: produced by the adrenal cortex; alters the reabsorption of Na+ in the Kidneys, and since water follows solute, it stimulates water reabsorption as well; also has the ability to regulate K+ levels; will raise B.P. - ADH/Vasopressin: secreted by the Hypothalamus and stored and released from the Posterior Pituitary; controls water excretion in the kidneys in response to the increased osmolality(solute concentration) and decreased B.P. ; It will increase Blood pressure; if you’re dehydrated you’ll see increased ADH to try and conserve water List the 4 problems that result in edema - 1.)Increased capillary permeability that is caused by inflammation/the immune response - 2)Increased capillary Hydrostatic pressure(often caused by Na+ and Water retention that you’ll often see in those w/ CHF, Renal failure, Cirrhosis, or venous obstruction w/ thrombophlebitis) - 3)Decreased Capillary Oncotic Pressure(which is due to a dec. in the production of plasma proteins—the decrease in production is often caused by liver disease and/or protein malnutrition) - 4)The loss of Plasma proteins mnnm Holymnanosman df.fifhhmIfhm ffanofk.ms *Lymphatic Obstruction is a 5th problem that causes edema, but it’s not as common; any time you have Pulmonary edema it’s gonna fall into one of these categories. Describe the causes of the following alterations in sodium and water balance: Isotonic Hypertonic Hypotonic Change in Total Body Water {Hypernatremia} Na > 145 results in Osmolarity of ECF/Extracellular Fluid is accompanied by changes in Intracellular dehydration less than normal concentration of electrolytes.(So Causes: Na 145) Na+ is 26 Common causes: lungs) -HCO3 levels are 40 in. for men; >35 for women) (2)Plasma Triglycerides >150 mg/dL (3)HDL-C: Men 100mg/dL (* won’t be asked specific numbers but understand the concepts) Risk factors for coronary heart disease Modifiable Non-Modifiable Hyperhomocysteinemia, dyslipidemia Older age, male gender/women after menopause, HTN, smoking, obesity, DM, sedentary lifestyle, stress, genetic predisposition, being Black/Asian alcohol Factors involved in the development of the atherosclerotic plaque - First, you have your initiating event, which is injury to the endothelium - Then, injury to endothelium causes endothelial dysfunction & inflammation. - After that, Inflammatory cytokines are released draws monocytes - These Monocytes adhere to damaged endothelium and proceed to migrate between endothelial cells into intima. - Monocytes differentiate into macrophages and release enzymes & toxic oxygen free radicals which causes more damage—eventually leading to oxidation of LDL - Macrophages engulf oxidized LDL which leads to the formation of foam cells and foam cells form fatty streaks **Oxidation of LDL is central to the development of atherosclerotic plaque** plague Clinical manifestations of the different types of chest pain (e.g. stable angina, unstable angina, etc.)  -semirimintight platiguisoB.it Stable angina Prinzmental angina Silent /asymptomatic Unstable angina Short lasting chest pain Chest pain due to transient - presence of regional Reversible myocardial that may radiate , ischemia occurs exclusively at abnormality in left ischemia & is a harbinger commonly mistaken for rest ventricular sympathetic of impending infarction. indigestion -caused by vasospasm of afferent innervation -symptoms with no -associated with pallor, coronary artery w/ or wo -nfhPy can arise from ymanyeliabiffypnt apparent trigger diaphoresis, dyspnea atherosclerosis metabolic dysfunction in -long duration and cannot -caused by gradual luminal -cyclic pattern of occurrence DM, following be relieved by nitrates. narrowing and hardening -results from hyperactivity of CABG/cardiac transplant, -caused by rupture of of arterial walls SNS, increased ca+ influx in following ischemic nerve plaque in coronary artery -relieved by rest & arterial smooth muscle, injury by MI nitrates impaired prod. of Prostaglandin/thromboxane - Etiology and pathophysiology of right-sided and left-sided heart failure Left Sided HF diastoricodimandumptions of Right Sided HF - CPU Systolic/diastolic ventricular ventricp dysfunction most common cause is left side HF , in the absence of LHF, - ↓ left ventricular emptying & abnormal diastolic it is caused by COPD, cystic fibrosis, ARDS relaxation - ↑ pulmonary vascular resistance - ↑ volume & pressure in left ventricle - ↓ right ventricular emptying - ↑ volume & pressure in left atrium - ↑ volume & pressure in right ventricle, - ↑ volume in pulmonary veins & pulmonary capillary - ↑ volume & pressure in atrium bed - ↑ volume & pressure in great veins - Pulmonary edema - ↑ volume in systemic venous circulation - ↑ pulmonary vascular resistance - ↑ capillary pressure resulting in peripheral edema - Right ventricular failure CM- external & nocturnal dyspnea, blood-tinged sputum, cough, cyanosis, fatigue Factors that increase or decrease peripheral resistance and cardiac output (see chart) - a.) Blood Volume: the higher the blood volume, the greater the amount of work is needed for the heart to pump blood through the circulatory system; ↑Blood Volume = ↑Blood Pressure - b.) Overall Compliance: the elastic characteristics of the vessels contribute to the overall pressure in the vessels; the more elastic the blood vessels are, the lower the blood pressure is; ↑Blood Vessel Elasticity=↓Blood Pressure - c.) Cardiac Output(CO): this is related to heart rate and stroke volume; ↑H.R. and Stroke Volume= ↑C.O= ↑B.P. - d.) Peripheral Resistance: the resistance of the arteries is related to the overall compliance characteristic; ↑Peripheral Resistance = ↓Overall Compliance = ↑Arterial Blood Pressure Classification of blood pressure (see table) CATEGORY SYSTOLIC(mmHg) DIASTOLIC(mmHg) Normal Angiotensinogen→ Angiotensin I→ Angiotensin II→ Vasoconstriction—> Aldosterone→ H2O and Na Inc→ inc. in Peripheral Vascular Resistance→ inc. in B.P. Compare the etiology and pathophysiology of the following types of shock: Cardiogenic Hypovolemic Neurogenic Anaphylactic Septic -Decreased C.O. -Loss of whole -Massive vasodilation Hypersensitivity Infection that progresses to -Tissue hypoxia blood(hemorrhage), loss (decreased Systemic reaction bacteremia, then SIRS with -Adequate of plasma(burns), Vascular Resistance) -You can get sepsis, and ends with multiple -intravascular -Interstitial fluid (DM, DI, -Parasympathetic vasodilation, relative organ dysfunction syndrome. volume emesis, diarrhea, overstimulation, hypovolemia, -Associated w MI, sweating) sympathetic under decreased tissue Most common sources of HF, dysrhythmias, -When intravascular stimulation perfusion, impaired infection are: lungs, Urinary acute valvular volume has decreased Can be Caused by… cellular metabolism tract, GI, wounds, indwelling dysfunction, by 15% - trauma to spinal vascular catheters massive PE cord/medulla -interruption of O2 supply or supply of glucose to medulla -bradycardia may contribute to reduced C.O. 7) Pulmonary Alterations Know the normal values for PO2 and PCO2 - The normal values for PCO2 is 35-45, and for PO2 it’s between 80-100mmHg Definition of: hypoxemia, hypercapnia, hypoventilation, hyperventilation, dyspnea - Hypoxemia: reduced oxygenation of arterial blood(↓PaO2); causes of Hypoxemia are dec. O2 content(high altitudes), hypoventilation(C.O.P.D), diffusion abnormalities(Edema), abnormal ventilation-perfusion ratios(asthma), and pulmonary shunts(RDS/Respiratory Distress Syndrome) - Hypercapnia:increased CO2 that can end up resulting in an acid-base imbalance that may cause dysrhythmias; caused by a dec. drive to breathe, an inadequate ability to respond to ventilatory stimulation; Hypercapnia can cause Hypoventilation; very high levels of CO2 may even result in a coma. - Hypoventilation:inadequate ventilation(due to pulmonary mechanics or impaired neurological control); CO2 removal isn’t matching CO2 production, so you get Hypercapnia (when PaCO2 is greater than >45mmHg) - Hyperventilation: this is when alveolar ventilation/breathing exceeds demands; Hypocapnia causes PaCO2