Patho Final Study Guide PDF

Patho Final Study Guide **Importance of ATP and Oxidative Phosphorylation** **Oxidative metabolism:** - 95% of ATP production - 20 times more ATP produced compared to anaerobic metabolism - No oxygen=less energy, more waste in the form of lactic acid **Metabolic Acidosis** - Excessive...

Patho Final Study Guide **Importance of ATP and Oxidative Phosphorylation** **Oxidative metabolism:** - 95% of ATP production - 20 times more ATP produced compared to anaerobic metabolism - No oxygen=less energy, more waste in the form of lactic acid **Metabolic Acidosis** - Excessive buildup of acid OE excessive loss of bicarb - Look at ANION GAP to help determine underlying cause LOW pH OK CO2 LOW HCO3 **Anion Gap** - Difference in cation and anion ratios in plasma - Tells us if metabolic acidosis is acid build-up (H+) or loss of bicarb (HCO3) - Normal anion gap is \~12 mmol/L **Metabolic Alkalosis** - Loss of acid from blood resulting in an excess of bicard - Excessive vomiting - Hyperaldosteronism - Meds: diuretics HIGH pH OK CO2 HIGH HCO3 **Respiratory Acidosis** - Excessive build-up of carbon dioxide - Hypoventilation: drugs , meds, CNS depression - Diffusion issues - Obstructive disease LOW pH HIGH CO2 OK HCO3 **Respiratory Alkalosis** - Excessive loss of CO2 - Hyperventilation is most common cause - Altitude - Panic attacks HIGH pH LOW CO2 OK HCO3 **O2 Carrying** [PaO2 = partial pressure of oxygen ] - Oxygen content dissolved in arterial blood - Measures how well O2 is able to move from the lungs into the bloodstream to be transported to the rest of the body [Oxygen saturation] - \% of hemoglobin sites in the blood that carry oxygen to all hgb [O2 affinity] - How much hemoglobin wants to bind oxygen to itself - Higher affinity = more binding of O2, less letting it go into tissues **Oxygen-Hgb Dissociation Curve** [Right Shift]: oxygen leaves hemoglobin and goes to the tissues in cases of lactic acid production, DKA or loss of bicarb (diarrhea), or CO is being retained in lungs. It wants oxygen to leave it and go to the tissues where its needed but also makes it less likely to pick up oxygen in the lungs where and take it to where it is needed = hypoxia - Reduced Hb-O2 affinity - Lower pH (Acidosis) - Higher CO2 - Higher temp [Left Shift] : oxygen will stay or go with or go to hemoglobin in cases of alkalosis (vomiting), low temperature, and low partial pressure of CO2. Hemoglobin 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 - Higher Hb-O2 affinity - Higher pH (Alkalosis) - Lower Co2 - Lower Temperature **Hypoxemia**=low blood oxygen Causes - Hypoventilation - Diffusion impairment - Ventilation/perfusion mismatch - Shunt **Filtration and Reabsorption** - [Filtration]: movement of fluid OUT OF vascular space (capillaries) - Major force is capillary hydrostatic pressure pushing fluid out of capillary - [Reabsorption]: movement of fluid moving BACK INTO vascular space (capillaries) - Major force is capillary oncotic pressure pulling fluid back into the capillary - Albumin, made in liver is the protein responsible for this force **RAAS**: a mechanism that maintains balanced BP and tissue perfusion - People with HTN can have an OVERACTIVE RAAS, which leads to salt and water retention and increase blood vessel tone Diagram of a diagram of the human body Description automatically generated **ADH**:  **RBC's and EPO** - RBC are more in bone marrow - EPO is made in the kidneys - EPO stimulates the production of RBCs **What are some reasons Anemia can develop?** - Iron deficiency, B-12 deficiency, hemolysis, cancers, SCD, bleeds, renal disease, liver disease, etc. **Signs and symptoms of anemia include:** - Fatigue, tachycardia, DOE, Diaphoresis, leg cramps, insomnia **What lab values can help with the Diagnosis of Anemia?** - CBC, Hgb, Hct, MCH, MCV, RBCC, Iron levels **Types of Anemia** - [Microcytic hypochromic] = small cell size, low color - Caused by iron deficiencies and small, chronic bleeds - [Macrocytic normochromic] = large cell size, normal color - Caused by nutritional deficiencies such as B12 - [Normocytic normochromic] = normal cell size, normal color - Caused by blood loss Plasma Protein System: clotting **Clotting Factors** - All factors are made in the liver EXCEPT factor 8 which is made by the endothelium - Low or missing clotting factors = increased risk for bleeding **How to measure clotting factors** - [PT/INR]: measures EXTRINSIC pathway - Helpful to determine effectiveness of WARFARIN - [PTT]: measures INTRINSIC pathway - Helpful to determine the effectiveness of HEPARIN **Sickle Cell Disease** - Autosomal recessive disease (inherited) - Proteins undergo polymerization, this leads to sickling of RBC's - S/S: bilateral pain, extremity edema, acute chest syndrome, glomerular disease, infection - Situations that can cause a sickle cell crisis: **Inflammatory Response**  **2^nd^ 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, complementA diagram of a pain and redness Description automatically generated **Functions of Antibodies** - [Direct protection] - Neutralize - Secreted into blood and mucosa - Bind to and thus, inactivate pathogen - Agglutinate - Cause pathogens to clump together - Makes removal by phagocytosis more efficient - Precipitation: makes a soluble antigen into an insoluble precipitate - [Indirect protection] - Complement activation bacterial destruction by lysis - Opsonization: help phagocytes recognize what needs to be eaten **Mechanisms of Immune evasion**  **Endotoxic shock** A close-up of a list of diseases Description automatically generated **Viral Infections** - Need host cell DNA to replicate - Must invade the cell - HIV - Infects CD4+ lymphocytes - AIDS diagnoses at CD4+ count \< 200 cells/mm3 - Anorexia, weight loss, Kaposi sarcoma, herpes, cytomegalovirus, retinitis, thrush, etc. **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 **Type I Hypersensitivity Reactions: Anaphylaxis** - Mediated by IgE - Antigen from allergen causes mast cell or eosinophils to "de-granulate" - Immediate response: 5-30 mins 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), increase heart rate - Swelling, redness, itchy, rash (from mast cells) - Bronchospasms (bronchoconstriction) and upper airway swelling **HSR Diagnoses** - [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 in 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 **Cardiac Terms** - [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]: SV x HR - Stroke volume is impacted by preload, contractility, and afterload **Coronary Artery Disease** - Any vascular disorder that narrows or occludes the coronary arteries. - An imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients - Reversible myocardial ischemia or irreversible infarction may result. - Most commonly caused by atherosclerosis - [Atherosclerosis:] cholesterol engulfed by macrophages causing plaque formation in blood vessel walls  Left Sided Heart Failure vs. Right Sided Heart Failure Pin on NCLEX Mastery **Atelectasis**: collapse of alveoli - Reduced alveolar ventilation **OR** air inside a plugged alveolus gets absorbed the alveolus collapses - [Risk factors]: confinement to bed, infections, disease, foreign body - [Leads to]: hypoxia, **pneumonia,** respiratory failure - [Symptoms]: dyspnea, tachycardia, cough, pain, cyanosis, wheezing - What are some in-hospital nursing interventions we do to help prevent this and pneumonia development? INCENTIVE SPIROMETER  Pulmoary Embolism Risk: Virchow's Triad Pneumonia - Infections of the lungs - Viral, Bacterial or Fungal - Causes purulent fluid in alveoli - Can occur as - Lobar: one or more whole sections of the lungs - Bronchial: patches throughout both lungs - Risks: \>65 years, \35% d/t sepsis, respiratory failure Asthma - Chronic inflammatory obstructive lung disease - Periods of no symptoms with "attacks" caused by allergen/irritant - Causes bronchospasms, airway inflammation, mucous production = narrowed airway - Symptoms: wheezing, dyspnea, anxiety, coughing, chest tightness/pain, decreased FEV1 that can be revered with bronchodilators COPD: Chronic Obstructive Pulmonary Disease - Umbrella term for progressive obstructive lung diseases - Chronic bronchitis - Emphysema - Refractory asthma-non reversible with bronchodilators - Associated with long term exposure/risks: smoking, environmental exposures, obesity, \>40 years old, family history - Rare "genetic COPD": alpha1-antitrysin deficiency - Cause permanent functional impairent of lungs - 4^th^ leading cause of death in U.S. A pink sea creature with a list of words Description automatically generated with medium confidence Acute Kidney Injuries - Dec in GFR and urine output with accumulation of nitrogenous wastes in the blood - Measure kidney function with BUN (blood urea nitrogen) and creatine - Pre-renal: inadequate perfusion such as hypovalemia, sepsis, low cardiac output, etc. - Intra-renal/Intrinsic: kidney/nephrons themselves are injured/not working properly such as glomerulonephritis - Post-renal: obstructions, stenosis Chronic Kidney Disease - Progressive loss of renal function associated with systemic diseases such as HTN, DM - Symptomatic changes result from increased levels of creatinine, urea, potassium - Alterations in salt and water balance usually do not become apparent until renal function declines to less than 25% of normal when adaptive renal reserves have been exhausted - Clinical manifestations - Azotemia: inc levels of serum urea, serum creatinine, and other nitrogenous compounds related to decreasing kidney function - Uremia: pro-inflammatory state with many systemic effects and is associated with accumulation of urea and other nitrogenous compouds and toxins - S/S: HTN, anorexia, nausea, vomiting, diarrhea or constipation, malnutrition and weight loss, pruritis, edema, anemia, neurologic, CVD and skeletal changed Thyroid and Parathyroid Conditions - Hypothyroidism - Primary - Secondary - Interpreting labs - Hashimoto's - Endemic goiter - Hyperthyroidism - Primary - Secondary - Interpreting labs - Grave;s - Thyroid crisis/storm - Hypoparathyroidism - What does parathyroid hormone do? - What are you going to monitor? Adrenal Crisis - Life-threatening condition - Severe acute arenal insufficiency of cortisol (sometimes aldosterone) due to: - Trauma, Addison's Disease, pituitary injury, severe dehydration, physiological stress, emotional stress, strenuous physical activity, sudden discontinuation from glucocorticoids - Does not respond to fluids or meds - HTN - Tachycardia - Weakness, fatigue, decreased appetite or weight, ortho, electrolyte imbalances Diabetes Mellitus - Type I: autoimmune destruction of beta cells in pancreas due to some trigger (viral) - Cannot make insulin - Need exogenous insulin to get glucose into - DKA is always a concern - Type II: insulin resistance - Pancrease 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 down-regulation of insulin receptors - Overtime, 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) - DKA - Lack of insulin glucose can't enter the cell starving cells + high BG - Fat gets broken down for fuel ketone production (acid) ketones in urine - S/S: Fruity-scented breath, N/V, polyuria/polydipsia, fatigue, confusion coma/death - Who's 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. Where is the Bleed? - Upper GI Tract - Proximal to ligament of trietz - Hematemesis: upper GI - Frank blood-active bleed - Coffee grounds-mixed with gastrin - Melena: upper and lower - Black or maroon tarry stools - Hematochezia - BRBPR - Lower GI or massive upper GI - Occult - Typically asymptomatic - Normal stools/gastric secretions - Found often in older adults who are anemic GI - Mallory-weiss tears- vertical, shallow tears in esophagus causing bleeding; usually from vomiting - GERD and Barrett's esophagus- cause, mechanism, and cellular adaptions - Mechanical obstructions - Intussussception: telescoping bowel obstruction - Volvulus: twisted intestine - Herniation: piece of bowel slips in between a tear in a muscle - Adhesions: scar tissue formation Crohn's UC vs. Ulcerative Colitis - Crohn's - Skip lesions - Transmural inflammation can lead to fissures - Small and large intestine affected - Ulcerative Collitis - Pseudopolyps - Mucosal/submucosal ulcerations - Large intestine continuously affective Portal HTN and Ascites Image result for pathogenesis of ascites  Portal HTN and Varices - Dilated submucosal veins in lower 1/3 esophagus, secondary to portal HTN - Most common cause is cirrhosis - Asymptomatic unless a vessel ruptures - Hematemesis, melena, shock, death Types of Jaundice Y:\\ELS-IW26-SRC\\Course-N\\Graphics\\Frames\\McCance\\output\\ppt\\\\041019.jpg Cerebral Vascular Disease - Most frequently ocurring neurologic disorder - Any abnormalilty of the brain caused by a pathologic procress in the blood vessels - Vessel wall- ex: aneurysm - Vessel occlusion- ex: thrombus, embolism - Vessel rupture - Blood abnormality- ex: increased viscosity, clotting 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 - Stroke (Cerebral vascular accident) (CVA) - Ischemic stroke - Hemorrhagic stroke - HTN is biggest risk factor - 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 Other Neuro Conditions - Seizures - Generalized vs. focal - Triggers - Hematomas - What is the significance of of intracranial pressures? - What is a brain herniation? - Parkinson's - Patho: dopamine deficiency - Cardinal signs: tremor, bradykinesia, cogwheel rigidity, postural instability - TBI's