Patho Final Exam Review_FA24 Final PDF

11/26/24 1 Importance of ATP and Oxidative Phosphorylation 2 Acid/Base Balance Interpretation Common conditions associated with imbalances Effects of imbalances on oxygen-hemoglobin dissociation curve 3 4 5 6 7 8 Understanding O2 Carrying: Vocabulary You Need...

11/26/24 1 Importance of ATP and Oxidative Phosphorylation 2 Acid/Base Balance Interpretation Common conditions associated with imbalances Effects of imbalances on oxygen-hemoglobin dissociation curve 3 4 5 6 7 8 Understanding O2 Carrying: Vocabulary You Need to Know ►PaO2 = Partial pressure of oxygen Oxygen content dissolved in arterial blood. Measure of how well O2 is able to move from the lungs into the bloodstream to be transported to the rest of the body. ►Oxygen saturation (O2 sat, SPO2) % of hemoglobin (Hgb) sites in the blood that are carrying oxygen relative to all Hgb. Ex: SPO2 of 99% = 99% of available Hgb sites are saturated with O2. ►O2 Affinity How much does hemoglobin want to bind oxygen to itself. Higher affinity = more binding of O2, less letting it go into tissues. 9 10 Oxygen-Hgb Dissociation Curve – Right Shift ►Oxygen will leave hemoglobin and go to the tissues in cases of: Acidosis –Lactic acid production –Other acid production (e.g. DKA) OR loss of bicarb (e.g. diarrhea) –CO is being retained in lungs and/or being produced in excess High temperature ►Hemoglobin has a lower affinity for oxygen under these 11 1  ►Hemoglobin has a lower affinity for oxygen under these circumstances. It wants oxygen to leave it and go to the tissues where it’s needed BUT…it also makes it less likely to pick up oxygen in the lungs and take it to where it’s needed = hypoxia ► 11 Oxygen-Hgb Dissociation Curve – Left Shift ►Oxygen will stay with or go to hemoglobin when: Alkalosis (e.g. vomiting) Temperature is low Low partial pressure of CO2 ►This means that hemoglobin has a higher affinity for oxygen under these circumstances. It wants oxygen to go to it and stay with it which makes it difficult for oxygen to leave and go to the tissues where it’s needed = hypoxia 12 Hypoxemia Hypo = low or under; ox = oxygen; emia = blood Causes –Hypoventilation – lack of air movement either through slow breathing or shallow breathing –Diffusion impairment –Ventilation/perfusion mismatch (V/Q mismatch) Ventilation – there is a block in the airways somewhere preventing alveoli from having air exchange Perfusion – breathing is fine but lack of blood getting to alveoli so gas exchange isn’t happening and pulmonary arterial blood gets recirculated –Shunt Blood vessel or cardiac malformations 13 Filtration and Reabsorption ►Filtration: movement of fluid moving OUT OF the vascular space (capillaries) Major force is capillary hydrostatic pressure pushing fluid out of the capillary 13 Major force is capillary hydrostatic pressure pushing fluid out of the capillary ►Reabsorption: movement of fluid moving BACK INTO the vascular space (capillaries) Major force is capillary oncotic pressure pulling fluid back into the capillary –Albumin the the protein mainly responsible for this force –Albumin is made in the liver ►There is always a net filtrate (left over fluid in the interstitial space) Where does it go?? Lymph system: drains excess filtrate out of the interstitial space 14 Mechanisms of Edema Formation 15 RAAS 16 RAAS and Hypertension 1 ►In healthy people, the RAAS is an important mechanism to maintain balance BP and tissue perfusion. ►In people with HTN, the RAAS can be overactive, leading to salt and water retention and increased blood vessel tone. 17 ADH 18 RBC’s and Anemia 19 Anemia Classification Microcytic hypochromic = small cell size, low color –Iron deficiencies –Small, chronic bleeds Macrocytic normochromic = large cell size, normal color –A lot of other nutritional deficiencies such as B12 Normocytic normochromic = normal cell size, normal color –Blood loss 20 Plasma Protein System: Clotting 21 Clotting Factors All factors are made in the liver EXCEPT factor 8 –Factor 8 is produced by endothelium Low or missing clotting factors = increased risk for bleeding 20 21 –Factor 8 is produced by endothelium Low or missing clotting factors = increased risk for bleeding Measure with PT/INR and PTT –PT/INR measures extrinsic pathway Helpful to determine effectiveness of warfarin (an anticoagulant) –PTT measures intrinsic pathway Helpful to determine the effectiveness of heparin (an anticoagulant) –Each test measures specific clotting factors so they help us figure out if clotting factors are missing 22 Sickle Cell Disease Autosomal recessive disease (inherited) Proteins undergo polymerization à sickling of RBC’s S&S: bilateral pain, extremity edema, acute chest syndrome, glomerular disease, infection What types of situations will cause a sickle cell crisis? 23 24 Inflammatory Response 1 ►2nd line of defense Neutrophils, macrophages, dendritic cells, mast cells, etc. showing up to a threat –Histamine –Pro-inflammatory cytokines –Other chemical messengers Clotting cascade Bradykinin Complement ► 25 26 27 Endotoxic Shock 28 25 26 27 Endotoxic Shock 28 Viral Infections Need host cell DNA to replicate Must invade the cell HIV –Infects CD4+ lymphocytes –AIDS diagnosis at CD4+ count < 200 cells/mm3 Anorexia, weight loss, Kaposi sarcoma, herpes lesions, cytomegalovirus retinitis, thrush (candida albicans), etc. – 29 Hypersensitivity Reactions Auto-immune conditions Antibody-mediated (humoral) –Type I: allergies, anaphylactic reactions –Type II: tissue-specific reactions of antigens binding to antibodies –Type III: antigen-antibody complexes deposit in vessel walls or extra-vascular tissues Type IV: cell-mediated reactions 30 Type I Hypersensitivity Reaction: Anaphylaxis Mediated by IgE Allergy reaction à Anaphylactic reaction Antigen from allergen causes either Mast cell or eosinophils to “de- granulate” –Immediate response: 5-30 minutes after exposure IgE released by B cells Release of histamine from mast cells Eosinophil recruitment, release of granules/mediator, epithelial damage, –Delayed response: 2-8 hours after exposure Leukocyte infiltration, edema, mucus secretion, epithelial damage Prostaglandin Results in –Decreased blood pressure (vasodilation), increased heart rate –Swelling, redness, itching, rash (mast cells and other inflammatory responses) 31  –Swelling, redness, itching, rash (mast cells and other inflammatory responses) –Bronchospasms (bronchoconstriction) and upper airway swelling 31 Other HSR’s Myasthenia gravis (Type II) –Antibodies attack acetylcholine receptors –Muscle weakness Goodpasture’s (Type II) –Antibodies attack basement membrane of lungs and kidney –Dyspnea, renal issues including hematuria Reynaud’s (Type III) –Antibody/antigen complexes in blood vessels of hands in response to cold –Lack of blood flow resolves with warmth SLE (Type III) –Antibody/antigen complexes in health tissue throughout body (esp. face, kidneys) –Butterfly rash, aches, pains, renal failure Type IV HSR –Delayed response –Cell-mediated NOT antibody mediated – 32 Cardiac Terms 1 ►Preload: the filling pressure during diastole (filling): affected by blood volume and blood pressure (can also think of it as how much blood is being presented to the heart during diastole and making it stretch) ►Contractility: how well the heart can contract ►Afterload: the pressure the heart needs to push against to get blood out of the heart during systole, for our purposes…SVR Left ventricle = highest pressure as blood is going to the whole body ►Cardiac output = Stroke volume x heart rate (CO = SV x HR) Stroke volume is impacted by preload, contractility and afterload 33 Coronary Artery Disease 1 ►Any vascular disorder that narrows or occludes the coronary arteries. ►An imbalance between coronary supply of blood and myocardial 33 1 arteries. ►An imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients ►Reversible myocardial ischemia or irreversible infarction may result. ►Most common cause: Atherosclerosis ►Atherosclerosis: cholesterol engulfed by macrophages causing plaque formation in blood vessel walls ► 34 35 Heart Failure 36 Atelectasis 37 38 39 40 41 42 43 Acute Kidney Injuries Decrease in GFR and urine output with accumulation of nitrogenous wastes in the blood Measure kidney function with BUN (blood urea nitrogen) and creatinine Pre-renal: inadequate perfusion such as hypovolemia, sepsis, low cardiac output, etc. Intra-renal/Intrinsic: kidney/nephrons themselves are injured/not working properly such as glomerulonephritis Post-renal: obstructions, stenosis 44 45 46 Thyroid and Parathryoid Conditions Hypothyroidism –Primary vs. secondary – interpret labs 44 45 46 Hypothyroidism –Primary vs. secondary – interpret labs –Know: Hashimoto’s; endemic goiter Hyperthyroidism –Primary vs. secondary – interpret labs –Know: Grave’s; thyroid crisis/storm Hypoparathryoidism –What does parathyroid hormone do? –What are you going to monitor? 47 Adrenal Crisis ►Life-threatening condition ►Severe acute adrenal insufficiency of cortisol (and sometimes aldosterone due to: Trauma Addison’s disease Pituitary injury Severe dehydration Physiological stress (e.g. infection), emotional stress, or strenuous physical activity Sudden discontinuation from glucocorticoids – most common cause 48 Adrenal Crisis: Signs and Symptoms ►Acute Shock that doesn’t respond to fluids or medications Hypotension Tachycardia ►Weakness ►Fatigue ►Decreased appetite/weight ►Orthostatic hypotension ►Electrolyte imbalances 49 Diabetes Mellitus Type I: autoimmune destruction of beta cells in pancreas due to some trigger (possibly viral) –Cannot make insulin –Need exogenous insulin to get glucose into cells –DKA is always a concern Type II: insulin resistance –PANCREAS IS FINE – can still make insulin, but cells are resistant  Type II: insulin resistance –PANCREAS IS FINE – can still make insulin, but cells are resistant to insulin’s attempts to get glucose into cells (target cell receptor dysfunction) –Develops due to chronically high levels of blood glucose and circulating triglycerides – causes damage and down-regulation of insulin receptors –Over time, beta cells will wear out and may cause individual to become dependent on exogenous insulin (when this occurs, and only when this occurs, DKA is a concern) 50 Complications from Diabetes: DKA Diabetic Ketoacidosis Lack of insulin à glucose can’t enter the cell à starving cells + high BG Fat gets broken down for fuel à ketone production (acid) à ketones in urine S/S: Fruity-scented breath, N/V, polyuria/polydipsia, fatigue, confusion à coma/death At risk: –Type 1 or insulin-dependent diabetes (missed insulin dose, clog in pump, etc.) –BG > 250 mg/dl x 2 –Ketones in urine –Infection, stress, etc. What does an acid/base balance look like? 51 52 GI Mallory-Weiss tears – vertical, shallow tears in esophagus causing bleeding; typically from vomiting GERD and Barrett’s esophagus – cause, mechanism, and cellular adaptations Mechanical obstructions –Intussusception: telescoping bowel obstruction –Volvulus: twisted intestine –Herniation: piece of bowel slips in between a tear in a muscle –Adhesions: scar tissue formation 53  –Adhesions: scar tissue formation 53 Crohn’s vs UC Crohn’s –Skip lesions –Transmural inflammation can lead to fissures –Small and large intestine affected Ulcerative colitis –Pseudopolyps –Mucosal/submucosal ulcerations –Large intestine continuously affected 54 Portal Hypertension and Ascites 55 Esophageal varices and liver disease 56 Types of Jaundice 57 Cerebral Vascular Disease 1 ►Most frequently occurring neurologic disorder ►Any abnormality of the brain caused by a pathologic process in the blood vessels Vessel wall- ex: aneurysm Vessel occlusion- ex: thrombus, embolism Vessel rupture Blood abnormality- ex: increased viscosity, clotting ► ► 58 TIA’s vs. Strokes Transient Ischemic Attack (TIA): episodes of neurologic dysfunction lasting no more than 1 hour. –Results from focal ischemia. –Up to 17% of people with TIA will have a true stroke within 90 days; higher percentage within 1 year CVA (Cerebral vascular accident) (aka Stroke) –Ischemic stroke –Hemorrhagic stroke –Hypertension is biggest risk factor –Neurons undergo changes that disrupt plasma membranes, cellular edema causes compression of capillaries, contralateral weakness in  –Neurons undergo changes that disrupt plasma membranes, cellular edema causes compression of capillaries, contralateral weakness in arms, legs, and/or face, possible motor, speech, and/or swallowing problems – – 59 Other Neuro Conditions Seizures –Generalized vs. focal –Triggers Hematomas –What is the significance of intracranial pressures? –What is a brain herniation? Parkinson’s –Patho: dopamine deficiency –Cardinal signs: tremor, bradykinesia, cogwheel rigidity, postural instability TBI’s: know in general S/S of mild, moderate, severe 60