MARYVILLE NURS 611 ADVANCED PATHO FINAL EXAM 2025

MARYVILLE NURS 611 ADVANCED PATHO FINAL EXAM 2025 Pituitary adenomas are usual - -benign slow-growing tumors that arise From cells of the anterior pituitary Hypersecretion of growth hormone/acromegaly - -patient will report gradual increase in their shoe size, facial bones, hands (rings no longer fit). Increased body odor, coarse skin. Diabetes insipidus (DI) - -ADH=water. In Diabetes insipidus, there is insufficient ADH. Can be neurogenic or nephrogenic DI can be... - -neurogenic or nephrogenic WBCs: - -Netrophils are the first to the scene of an inflammatory response. They eat up bacteria/viruses and move on. When the body is overcome with infection, the bone marrow begins releasing numerous immature neutrophils. This is when we see a "shift to the left" of all those immature neutrophils in response to infection. (bands, segs.) Modifiable risk factors for CAD - -Modifiable are dyslipidemia, sedentary lifestyle, diet, hypertension, smoking, diabetes, obesity Non-modifiable risks for CAD - -non-modifiable risk factors are age, gender, post menopausal women, family history. Non-STEMI: - -Non-STEMI: There is a thrombus but it's not causing complete occlusion of the coronary artery. Resulting damage of a non-stemi is: - -The resulting infarction is sub-endocardial. Right sided heart failure - -ascites, hepatosplenomegaly, secondary to pulmonary issues, anorexia/GI distress, dependent edema Types of aneurysms - -true=involves all three layers. saccular-bulge, fusiform abdominal usually, false-little tear in artery wall. Most common causes of aneurysms - -Risk with chronic hypertension, atherosclerosis. Hypothyroidism - -sluggish, slow causes of hypothyroidism - -Can be related to autoimmune causes such as Hashimoto disease. Surgical removal of the thyroid as in thyroid cancer, radiation treatment. Nurs 611 Nurs 611 Clinical manifestations of hypothyroidism - -Symptoms: bradycardia for no known reason, boggy non-pitting edema under the eyes, thinning hair, thickening/swelling of the neck. dyspnea related to hypoventilation=increased PaC02. Hyperthyroidism - -everything speeds up... causes graves disease What causes graves disease? - -type II hypersensitivity antibodies are directed against the TSH receptors and cause increased secretion of TH. Symptoms of hyperthyroidism - -increased weight loss, fine/soft hair, tachycardia, restlessness, insomnia, dyspnea, but related to a hypermetabolic state. Hyperparathyroidism - -Calcium-phosphate balance is a reciprocal relationship. Decrease in calcium and the parathyroid puts out PTH. Increased calcium levels, PTH is prevented from being released because calcitonin is secreted and stops osteoclastic activity. What usually precipitates DKA? - -infection, . Inflammatory process creates glucose to fight infection, resulting in hyperglycemia. DKA is most commonly associated with ______________ - -type 1 diabetes What type of respirations are associated with DKA and explain reason - -Body begins depleting fat and muscle stores. Kussmaul respirations are a compensatory mechanism for metabolic acidosis(ridding body of CO2/acid). Nauseated, vomiting as body's way to release acid from GI tract. Hyperglycemic Hyperosmolar Syndrome is usually related to - -type 2 DM Hyperglycemic Hyperosmolar Syndrome - -Typically not spilling ketones in urine because they have some intrinsic insulin. Otherwise, very high sugars and presentation otherwise similar to DKA. Hypoglycemia - -Pallor, arousal, anxiety. Need 15 grams of carbs Microvascular complications - -disease that effects the little capillaries Microvascular complications can lead to: - -Blindness, ESRD Microvascular complications and hyperglycemia - -High glucose levels cause thickening of the capillary basement membrane. This results in decreased tissue perfusion, and the cells become hyperplastic. Horrible vicious cycle where tissue perfusion and hyperplasia feed off each other. This highlights the need to screen and treat pre diabetics also Nurs 611 Nurs 611 Hemoglobin A1C - -Reflects the glucose coating on the RBC. Lifespan of an RBC is about 120 days, so it's giving us an average glucose over that time period. Microvascular complications - -Large and medium sized arteries. There is an increased risk or atherosclerosis. Plaque development is accelerated. There is an increased risk of ______ and _______ with microvascular complications - stroke, heart attack, and PVD SIADH - -cancers such as those from the lung start pumping out ADH and the body has a hemodilutional state. High water/low sodium. Headache can result, confusion. Addison's disease - -Need to add something" Not enough cortisol or aldosterone . S/s of addison's disease - -Weakness, fatigue, nausea, vomiting, anorexia. Hypoglyemic, bronze skin from hyperpigmentation, hyperkalemia, vitiligo Severe hypotension can result with Addison's crisis. Cushing disease - -"cushy=too much cortisol." Lack of ACTH, so the adrenals pump out cortisol. s/s of cushing disease - -This results in glucose intolerance, moon face, truncal obesity, buffalo hump, easy bruising. Erythrocytes - -RBCs are able to be reversibly deformed by bending to go through capillaries. Anemias result from a variety of dietary insufficiencies and several diseases. What causes aplastic anemia? - -caused by an autoimmune disease activated by cytotoxic T cells. What does aplastic anemia cause? - -It effects all types of blood cells including leukocytes and thrombocytes. Aplastic anemia is also known as - -pancytopenia Sideroblastic anemia - -iron overload state resulting from acquired or hereditary state. Sideroblastic anemia s/s - -bronze tinge to skin What can cause iron deficiency anemia? - -heavy menses, pregnancy, S/s of iron deficiency anemia - -fatigue, weakness, SOB Iron deficiency anemia - -Defect is occuring in the mitochondria At what point will s/s be seen of iron deficiency anemia? - -hemoglobin below 9 Nurs 611 Nurs 611 Vitamin B12 deficiency (pernicious anemia) - -More common in the elderly as the intrinsic factor in the gut diminishes and the body cannot process B-12 S/s of vitamin B12 deficiency (pernicious anemia) - -Can cause confusion and other symptoms that mimic neuropsychiatric disorders in the elderly. What will be seen in labs for acute blood loss anemia? - -increase in reticulocytes as body attempts to replace what is lost Hodgkin lymphoma - -enlarged painless lymph nodes What is often seen on slide for hodgkin-lymphoma - -reed-sternberg cells What are reed-sternberg cells - -large abnormal lymphocytes with more than one nucleus Heparin induced thrombocytopenia (HIT) - -auto-immune reaction by IgG antibodies. Platelets begin decreasing, can be down to 50%. Destruction of thrombosis results. PF4 antibodies attack the platelets. These patients cannot have heparin products for 3-4 months, if ever. Disseminated intravascular coagulation (DIC) - -You will see all the platelets used up in inappropriate ways so excess bleeding will result S/s of DIC - -bleeding from central line, IV, blood in urine DIC and organs - -bood clots can block the organs, resulting in failure Electrical activity of the heart - -SA-AV-bundle of HIS-purkinje fibers What will an increase and decrease of catecholamines do to the heart - -increase: increase heart rate decrease: decrease heart rate LVEDP - -Preload. Remember Starlings law where stretch increases the strength of contraction. However, too much stretch reduces contractility, like an overstretched rubber band. effect of angiotensin II on the heart - -When there is decreased tissue perfusion or decreased cardiac output, the kidneys are not getting an adequate amount, so renin starts pumping out, which activates angiotensin. angiotensin I converts to angiotensin II, which results in vasoconstriction. Result is hypertensive hypertrophy. Unstable angina - -inadequate oxygen to the cardiac tissues, so pain signals are sent out. Potential for non-stemi or STEMI. Nurs 611 Nurs 611 STEMI - -necrosis, or death, is occuring. STEMI is also known as - -transmural MI STEMI damage to heart - -This is a transmural MI, going through all the layers of the myocardium. Post MI - -the heart remains weak and vulnerable to re-injury. Acute pericarditis can occur post-MI, as can pericardial effusion (tamponade in severe cases). Cardiac tamponade - -Compression of the heart caused by fluid collecting in the sac surrounding the heart. S/s of left sided heart failure - -SOB at night, exertional dyspnea, cyanosis, pulmonary conestion, confusion, cough/wheeze Two types of cardiomyopathy - -dilated and hypertrophic obstructive cardiomypathy Dilated cardiomyopathy - -dimished myocardial contractility = diminished systolic performance increases in intracardiac volume biventricle dilation systolic heart failure Hypertrophic obstructive cardiomyopathy- cause - -commonly inherited to autosomal dominatnt inheritance Hypertrophic obstructive cardiomyopathy - -thickening of the septum results in a hyperdynamic state, esp with exercise diastolic relaxation also is impaired and ventricular compliance is decreased: significant risk for serious ventricular arrhythmias and sudden death Hypertension - -also causes tubular ischemia, which can result in renal failure. Watch for microalbuminemia. Heart valve dysfunction - -atrial valve stenosis more common with aging Heart valve dysfunction: regurgitation - -valve doesn't close all the way, so blood leaks backwards. Heart valve dysfunction: stenosis - -valve doesn't open enough and not enough blood passes through PVD - -atherosclerotic disease of the arteries that perfuse the limbs. Intermittent claudication and pain at rest. Hyperpigmentation of feet and ankles, swelling will be seen. Nurs 611 Nurs 611 Hyper pituitary and hormones - -the adenoma that is usually the cause can secrete hormones randomly and cause hyposecretion of APH Respiratory effects of hypothyroidism - -dyspnea due to not breathing well-- decreased PACO2 Renal effects of hypothyroidism - -decreased blood flow to the kidneys Erythrocytes and hypothyroidism - -decreased erythropoeisis = anemia = decreased hemoglobin and hematocrit Parathyroid hormone with calcium and phosphorus - -PTH responds to decreased calcium in the blood and starts osteoclastic activity to get the calcium out of the bones into circulation because more its more important roles are related to nerve impulses and contractility of the heart PTH and increased calcium levels - -then the thyroid will release calcitonin which will decrease PTH release- osteoblastic activity- building up the bones Diabetes Insipidus - -not enough ADH Hormones that cause an increase in glucose - -growth hormone, steroids, catecholamine’s (epi & norepi), glucagon Hormone to decrease glucose levels - -insulin DKA and blood glucose levels - -if above 100 glucose starts spilling into the urine and takes fluid with it causing a hypovolemic state Kentonuria - -body does not recognize the sugar that is building up in the blood so it begins to break down proteins and fat which release ketones creating metabolic acidosis- body will do what it can to get rid of acid to bring body back into balance-- n/v, hypervent (kussmaul) labs and DKA - -first obtain an ABG then venous- anion gap will be wide then continued labs will show the gap getting smaller if the treatment is effective hypoglycemia levels - -less than 45-60 DM and macrovascular problems - -large arteries- can lead to PVD, Atherosclerosis. can lead to stroke or MI. people with macrovascular problems often don't feel the MI as well and subsequently have greater complications due to not receiving treatment in a timely manner Nurs 611 Nurs 611 SIADH - -opposite of DI-- too much ADH; hemodilutional state, weight gain not associated with edema, LUNG CANCER TUMORS WILL OFTEN SECRETE ADH; may cause confusion and severe headaches What needs to be added for Addisons - -cortisol and aldosterone S/s of addisons - -hypoglycemia, hyperpigmentation-- a decrease in aldosterone leads to an increase in potassium-- leading to n/v/d and weight loss Cushing’s - -too much acth and cortisol Neutrophilia - -demand for neutrophils exceeds supply so there will be a release of premature WBC (bands) causing a SHIFT TO THE LEFT- pancreatitis Aplastic anemia - -autoimmune, cytotoxic t cells- AKA Pancytopenia Post hemorrhagic anemia - -there will be an increase in immature RBCs (reticulocytes) usually 10-15% from 1% HIT - -antibodies attack platelets- can result in DVT and PE- when platelets decrease by about 50% need to turn off Heparin DIC - -usually caused by Sepsis and gram negative inflammation response- causes little clots all over which decreases perfusion then there are no platelets when needed SNS and mechanical contraction of the heart - -increases heart rate = increase impulse though AV node PNS and mechanical contraction of the heart - -decreases heart rate = prolonged conduction through the heart Healing after MI - -acute pericarditis which is inflammation around pericardium S/s of cardiac tampinod - -dyspnea, tachycardia, JVD, and cardiomegaly Most common characteristic of pericarditis - -INTERMITTENT PAIN- will still treat as MI until dx testing complete and MI ruled out