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chronic disease process with abnormal thickening and stiffening of arterial system that decreases vessel's lumen size and ability to dilate and constrict to meet metabolic demands -Atherosclerosis- form of arteriosclerosis caused by accumulation of lipid-laden macrophages within the arterial wall that leads to plaque formation
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chronic disease process with abnormal thickening and stiffening of arterial system that decreases vessel's lumen size and ability to dilate and constrict to meet metabolic demands -Atherosclerosis- form of arteriosclerosis caused by accumulation of lipid-laden macrophages within the arterial wall that leads to plaque formation
-Disease process- injury to endothelial lining of vessel → endothelial inflammation → macrophage migration and adherence → macrophages release inflammatory cytokines → free radicals oxidize LDL cholesterol which recruits more monocytes that differentiate into macrophages → macrophages engulf oxidized LDL cholesterol and turn into foam cells → accumulation of foam cells induce fatty streaks in vessels → vicious cycle of more inflammation and autoimmune response induces plaque formation -Plaques can break off and damage vessel wall, causing formation of thrombi → tissue ischemia and necrosis -Fibrous caps- smooth muscle cells grow over lipid core, fibrous caps harden over time and encroach upon lumen of vessel -Risk factors- diabetes, smoking, hyperlipidemia or dyslipidemia, HT, autoimmunity -Complications- peripheral artery disease, coronary artery disease, cerebrovascular disease -S&S- intermediate claudication, acute occlusions
Intermittent claudication
pain affecting the calf, and less commonly the thigh and buttock, induced by exercise and relieved by rest, occurs as a result of muscle ischaemia during exercise caused by obstruction to arterial flow r/t peripheral arterial disease, symptom severity varies from mild to severe
acute occlusion
arterial blood clot or trauma cuts of blood perfusion to tissue- 6 Ps Pain is intense when the blockage is acute. Once the blockage is in an area of complete ischemia the pain may stop -Pulses- diminished or absent, present with chronic ischemia -Poikilothermia- perishing cold -Pallor with chronic ischemia -Paresthesias- sensation that occurs if muscle function is affected -Paralysis if muscle function is affected
consistent elevation of arterial BP, >130/80 mmHg -Primary HT= essential or idiopathic HT- most common primary diagnosis in US, more common than secondary HT in adults -Risk factors- family hx, environmental stress, high sodium low calcium, potassium, and magnesium diet, tobacco and alcohol, obesity, glucose intolerance -Secondary HT- caused by systemic disease that increases peripheral vascular resistance or cardiac output -Risk factors- renal vascular or parenchymal disease, adrenocortical tumors, adrenomedullary tumors, drugs -Complicated HT- chronic HT damages blood vessels and tissues leading to organ damage in heart, kidneys, brain, and eyes, can cause myocardial hypertrophy Increased risk for atherosclerosis, MI, HF, stroke, and renal disease -Hypertensive crisis- rapidly progressive HT > 180/120 mmHg, life threatening as it can cause heart attack or stroke
coronary artery disease
any disease that narrows or occludes the coronary arteries, leading to myocardial ischemia -Leading cause= atherosclerosis -Conventional risk factors- older age, family hx, male or female post-menopause, HT, smoking, diabetes, obesity, sedentary lifestyle, artherogenic diet (high in salt, fat, and carbs), dyslipidemia -Nontraditional risk factors- markers of inflammation (high density C-reactive proteins) and thrombosis (troponin I serum proteins), adipokines, chronic kidney disease, air pollution, ionizing radiation, poor microbiome health -complications- transient myocardial ischemia, heart attack, HF, arrythmias
transient myocardial ischemia
local, temporary deprivation of coronary blood supply -Stable angina- chest pain r/t myocardial ischemia, plaques occlude coronary vessels which increases stress on heart, pain goes away with nitrates and rest -Prinzmetal angina- less predictable angina that can occur during rest or even sleep, generally benign condition -Unstable angina- results from reversible myocardial ischemia, associated with atherosclerosis rupturing which can lead to MI, worsening angina is often accompanied with dyspnea, diaphoresis, and anxiety -Silent ischemia- no angina, myocardial ischemia can instead cause fatigue, SOB, or uneasy feeling -Acute coronary syndrome- onset of symptoms is different from the individual's stable angina symptoms (if they have stable angina) or the first time an individual has these symptoms
venous thrombosis
clot attached to vessel wall, causes obstruction of venous flow leading to increased venous pressure -Thromboembolism- clot that breaks off from vessel wall, can travel to lungs and cause pulmonary embolism -Risk factors- Triad of Virchow: venous stasis, venous endothelial damage, and hypercoagulable states, cancer, orthopedic surgery or trauma, heart failure, immobility -local S&S- pain in calf, heat in area, tenderness -PE S&S- chest pain, SOB, tachycardia, palpitations, dizziness, coughing
inflammation of the sac covering the heart manifestation of another disorder so diagnostics will be done to try to determine underlying cause S&S include a friction rub heard on auscultation, chest pain that is worse when lying down than sitting up (positional) which helps to distinguish from angina chest pain (not positional), ECG changes in all 12 leads, possibly a temp. Complications- pericardial effusion- fluid and exudate from inflamed pericardium accumulates in pericardial sac, if severe enough will decrease heart's CO
local dilation or ballooning/pouching of an artery or heart chamber -True aneurysm- weakening and out pouching of all 3 layers of arterial wall -False aneurysm- extravascular hematoma that connects with intravascular space -Dissecting aneurysm- aneurysm that is open or ruptured, will affect all tissues distal to dissected aneurysm
Acute Rheumatic Fever
systemic inflammatory disease, that results from a delayed response to a strep infection of group A beta-hemolytic strep, if it is left untreated it can cause scarring and deformity of cardiac structures. The acute rheumatic fever usually occurs in kids 5-15 years, rheumatic heart disease is diagnosed in adults around the ages of 25-34 -Common manifestations of the acute rheumatic disease (symptoms of joint inflammation, skin, nervous system and heart)- fever, lymphadenopathy, arthralgia, N/V and abdominal pain, tachycardia, epistaxis -Major clinical manifestations: carditis (murmur, chest pain, pericardial friction rub, ECG changes and heart valve dysfunction), polyarthritis: (heat, redness, swelling, andd pain in the large joints), chorea: (sudden aimless, irregular, involuntary movements), erythema marginatum (nonpruritic, erythematous macules on the trunk that may fade in the center), subcutaneous nodules (palpable nodules over bony prominences and extensor tendons)
infective endocarditis
general term used to describe infection and inflammation of the endocardium especially the cardiac valves -Risk Factors: Acquired valvular disease, implantation of prosthetic heart valves, congenital lesions associated with highly turbulent flow (ie ventricular septal defect), previous endocarditis, IV drug use, long-term indwelling IV catheterization ( pressure monitoring, feeding, hemodialysis), heart transplant with defective valve -Manifestations: fever, new or changed cardiac murmur, petechial lesions on skin, conjunctiva, or mucosa, Osler nodes: painful erythematous nodules on the pads of the fingers and toes, Janeway lesions: nonpainful hemorrhagic lesions on the palms and soles, weight loss, back pain, night sweats, HF -Pathogenesis requires at least 3 critical elements: Endocardial damage (trauma, congenital heart disease etc), adherence of blood-borne microorganisms at the damaged surface, formation of infective endocardial vegetations, the pathogens can arrive from dental, GU, or cardiac procedures, skin/wound/lung/GU infection, indwelling catheters or IV drug use -diagnosis: positive blood cultures & echocardiography -Treatment: support for acute valvular and organ dysfunction & administration of IV antibiotic combinations for several weeks -Complications: stroke, CNS abscesses, and meningitis
heart failure
heart is unable to generate adequate CO causing inadequate perfusion of tissues, increased diastolic filling P in L ventricle, and increased P in pulmonary capillaries -L sided has increased pulmonary P and congestion- systolic HF: decreased ejection fraction, diastolic HF: preserved ejection fraction -R sided: cor pulmonale, arterial HT
systolic HF
type of L sided HF ejection fraction< 40%, decreasing CO progressively worsens HF -Manifestations: dyspnea, orthopnea, coughing foamy sputum, fatigue, decreased urine output, decreased CO, pulmonary edema/lung crackles, hypotension or HT, S3 gallop -Preload will be increased, afterload will be increased, contractility will be decreased
diastolic HF
type of L sided HF preserved ejection fraction- pulmonary congestion despite normal stroke V and CO, abnormal diastolic relaxation -Manifestations- dyspnea on exertion, fatigue, pleural effusions, pulmonary edema develops with time, S4 gallop -Causes- HT-induced myocardial hypertrophy, myocardial ischemia-induced ventricular remodeling
congenital heart defects
structural abnormalities caused by the failure of the heart to develop normally before birth -Acyanotic defects- L to R shunting of blood- generally change circulation in a way that increases the return of blood to the lungs, so the blood gets enough oxygen to prevent cyanosis, includes VSD and PDA -Cyanotic defects- R to L shunting of blood- are defects that result in less blood going to the lungs. The blood doesn't get oxygenated and cyanosis results as the tissues do not get enough oxygen, includes tricuspid atresia and Tetralogy of Fallot
ventricular septal defect Acyanotic defect with L to R shunting of blood pressures in the left side of the heart are higher than the pressures on the right, so blood flows through a septal wall defect to the right side of the heart and enters pulmonic valve to return to lungs, can contribute to pulmonary hypertension -Most common type of congenital heart defect -Manifestations: dyspnea, tachypnea, loud and harsh pansystolic murmur and systolic thrill/tremor
patent ductus arteriosus Acyanotic defect with L to R shunting of blood Normally the ductus arteriosus closes after birth, but when pressures in the system are abnormal, that artery may remain patent. With increased pressure in the aorta after birth, the blood flows back to the pulmonary artery rather than heading out to oxygenate the body's tissues -Manifestations- may be asymptomatic- dyspnea, fatigue, poor feeding, continuous machinery-like murmur in both systole and diastole -Complications- risk for bacterial endocarditis, pulmonary HT later in life
Tricuspid Atresia
Absence of tricuspid valve between R atrium and ventricle and hypoplastic R ventricle -requires both ASD and VSD for viability -cyanotic defect with R to L shunting of blood
Tetralogy of Fallot
4 defects: large ventricular septal defect (VSD), overriding aorta that straddles the VSD, pulmonary valve stenosis, and right ventricle hypertrophy -cyanotic defect with R to L shunting of blood -Manifestations: acute cyanosis at birth or gradual cyanosis over first year of life, acute episodes of cyanosis and hypoxia: "tet" spells, difficulty feeding and poor growth -Pressures in the right ventricle are higher than the pressures in the left ventricle so some blood bypasses circulation to the lungs by going through a defect in the septal wall -During hypoxic episodes use knee to chest position in infants to increase P in L side of heart or squatting in children
Kawasaki disease
vasculitis of medium-sized vessels, most common cause of acquired childhood heart disease, caused by abnormal response to viral or bacterial infection with autoimmune component -Diagnosis- fever lasting more than 5 days with at least 4 of CREAM criteria: Conjunctivitis, Rash on trunk or genitals, Erythema of palms or soles of feet, Adenopathy or unilaterally swollen lymph nodes, Mucosal involvement: red, cracked dry lips and strawberry tongue
not having enough ventilation to meet the body's metabolic needs -Hypercapnia-increased amounts of carbon dioxide in the arterial blood -Clubbing- bulbous enlargement of distal ends of fingers due to chronic hypoxemia
flail chest
instability of a portion of the chest wall due to broken ribs, lung tissue may blow out during exhalation, mediastinum moves toward opposite lung during inhalation
air enters into pleural cavity and causes separation of the pleural membranes and preventing the expansion of the lung tissue leading to lung collapse/atelectasis -Tension pneumothorax- most serious form of pneumothorax. It may result from either open or closed pneumothorax. With inspiration air enters but is then trapped because the pleural rupture is a one-way valve. Increased pressure pushes internal organs aside, which compresses the other lung and heart vessels and causes tracheal deviation. -Severe hypoxia and respiratory distress develop quickly. can be life threatening. There isn't time to confirm diagnosis with ultrasound, CT or chest x-ray. Based on tracheal deviation and auscultation, treatment must occur immediately
restrictive lung disease
characterized by decreased compliance (stiffness) of the lung tissue, increases effort needed to breathe, includes: atelectasis, pulmonary fibrosis, pulmonary edema, and ARDS
lung collapse and incomplete expansion of alveoli -S&S- dyspnea, cough, fever, leukocytosis -Compression atelectasis- tumor or abdominal distention increases P on lung tissue causing collapse -Obstructive (absorption) atelectasis- develops when the air is taken out of the alveoli and isn't replaced because the air doesn't have a way in -Surfactant impairment (adhesive) atelectasis- occurs when there isn't enough surfactant or there is a problem with the surfactant being able to keep the alveoli inflated
pulmonary edema
excess water in lungs, usually the result of L sided HF -S&S- coughing up blood or bloody froth, difficulty breathing when lying down (orthopnea), lung crackles with auscultation
acute respiratory distress syndrome rapidly progressive type of acute respiratory failure that results in damage to the alveolar-capillary membrane. These resulting acute inflammatory changes cause pulmonary edema, atelectasis, and severely impaired gas exchange and can lead to death if not quickly identified and treated -Direct factors- aspiration of gastric contents, pneumonia, chest trauma, cardiopulmonary bypass, embolism, toxic substance inhalation, oxygen toxicity and radiation pneumonitis. -Indirect factors- sepsis, massive trauma, pancreatitis, DIC, opiate drug overdose, severe head injury, multiple blood transfusion and shock. Three phases: -Phase 1- Exudative: occurs 24 to 48 hours after insult- Interstitial edema develops. Fluid enters the alveolar space. Blood cannot be oxygenated= pulmonary shunt -Phase 2- Proliferative: 1 to 2 weeks after the initial lung insult. Neutrophils 1st then monocytes, lymphocytes, and fibroblasts. They destroy pulmonary vascular system→ pulmonary vascular resistance & pulmonary hypertension. Lung compliance continues to decrease as a result of interstitial scarring from the destroyed cells. Hypoxemia worsens because of the alveolar scarring, and oxygen diffusion across the capillary membrane is unable to occur. The proliferative phase is complete when the diseased lung contains widespread scar tissue. This is a combination of diffusion limitation and shunting -Phase 3 Fibrotic phase: Occurs approximately 2 to 3 weeks after the initial lung insult. This phase is a chronic or late phase of ARDS. By this time, the lung is completely remodeled by scar tissue. The diffuse scarring results in decreased lung compliance. The surface area for gas exchange is significantly reduced because the tissue between the alveoli and the capillary membrane is fibrotic, leading to continued hypoxemia. Pulmonary HT develops from pulmonary vascular destruction and scarring -Manifestations: Dyspnea and hypoxemia despite supplemental oxygen, hyperventilation, respiratory alkalosis, decreased tissue perfusion, metabolic acidosis, organ dysfunction, increased work of breathing, decreased tidal volume, hypercapnia, respiratory failure, decreased CO, hypotension, and death
pulmonary fibrosis
excessive amount of fibrous connective tissue in lung causing loss of lung compliance and increased lung stiffness -Idiopathic or caused by scar tissue -Inflammation induces fibrosis Causes: ARDS, inhalation injury, several autoimmune disorders including rheumatoid arthritis
obstructive lung disease
narrowing of airways results in obstruction that is worse with exhalation, increases work of breathing and requires accessory muscles to exhale -includes asthma, COPD, emphysema, bronchitis
chronic inflammation of airways with bronchial type I hypersensitivity that reversibly constricts airways in presence of allergens or irritants -Process: Inhalation of an allergen or irritant → response by immune cells of alveoli → activation of mast cells with release of inflammatory mediators → overproduction of mucus by goblet cells and bronchoconstriction -S&S: bronchospasm, vascular congestion, mucus secretion, thickening of airway walls, increased contraction of bronchial smooth muscle, dyspnea, tachypnea, expiratory wheezing -Status asthmaticus- severe asthma attack that doesn't respond to treatment
chronic obstructive pulmonary disease progressive, chronic disease with persistent limited airflow, most common chronic lung disease in world, due to chronic bronchitis and/or emphysema -Risk factors: smoking, occupational dusts and chemicals, air pollution, factors affecting lung growth during gestation or childhood
chronic bronchitis
hypersecretion of mucous and chronic productive cough that lasts at least 3 months of the year for 2 consecutive years -pathophys: begins with the inspiration of irritants which lead to airway inflammation. Neutrophils, macrophages, and lymphocytes infiltrate the bronchial wall. There will be bronchial edema. That continued irritation leads to increased size and number mucous glands and goblet cells. The smooth muscle hypertrophies and there is fibrosis and airway narrowing. The mucus becomes thick which further obstructs the airways
Abnormal permanent enlargement of the gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis, loss of elastic recoil with collapse of the airways with expiration, air trapping causes hyper-expansion of the chest -S&S- dyspnea, wheezing, barrel chest, prolonged expiration, cough with lung infections, weight loss, increased risk of infection -Late stage: chronic HT, polycythemia, cor pulmonale/R sided HF, hypoventilation, hypercapnia
pulmonary embolism
thrombi lodging in the pulmonary arteries and blocking blood flow to the lungs (blood clot, tissue fragment, lipids, foreign body, air bubble, amniotic fluid) -pulmonary emboli commonly arise from the deep veins in the lower leg -Most common cause of death in hospitals -Associated with impaired quality of life, impaired mobility, infection, surgery, and cancer -Risk factors- venous stasis: restricted blood flow due to immobility, obesity, surgery, paralysis, etc., genetics, hemolytic and coagulative disorders, endothelial injuries and inflammation, hypercoagulability, medications, African American, older than 45 -S&S- compensatory hyperventilation and tachycardia, diaphoresis, hypoxia -Massive emboli: sever crushing chest pain, hypotension, weak and rapid pulse, loss of consciousness, leads to shock and cardiac arrest -Large emboli: Sudden onset of chest pain that is exacerbated with cough and deep breathing, tachycardia, tachypnea, and dyspnea due to decreased cardiac output occurs (Many small emboli can act as a larger embolus blocking circulation through the lungs) -Moderate-sized embolus can cause respiratory distress and cardiac infarction -Single emboli- May be considered "silent" with chest pain, cough, and possible dyspnea. Symptoms may be discreet or unnoticed but should be considered important since emboli may be developing
deep vein thrombosis blood clots forms in deep veins of lower leg → breaks off and travels to heart and passing through A atrium and ventricle → lodges in shrinking pulmonary arteries, blocking blood flow into the lungs thus preventing gas exchange -S&S- pain and tenderness in calf, heat and edema in affected area, positive Hohman's sign: pain in calf while foot is dorsiflexed -Systemic S&S- fever, diaphoresis, high WBC count, tachycardia, hypoxia post-thrombotic syndrome- occurs in 50% of individuals with DVT, a long-term complication manifesting as symptoms such as swelling, pain, discoloration, and scaling in the affected limb
cor pulmonale
hypertrophy and dilation of the right ventricle in response to chronic pulmonary hypertension. It results in R HF -pulmonary artery hypertension/constricted vessels cause the right ventricle to work harder. The cells of the right ventricle may hypertrophy. The cavity of the right ventricle may also enlarge -S&S- cardiovascular and pulmonary disease with many S&S- murmurs may be auscultated, certain heart sounds may be accentuated, increased BP may also cause jugular distention, hepatosplenomegaly, and peripheral edema
cystic fibrosis
Autosomal recessive, thick mucous production, causes bulky, fatty stool, wheezing, coughing, dyspnea, clubbing, high sodium concentration in sweat and tears, increased susceptibility to infection, increased risk for GERD, poor absorption of nutrients Affects exocrine glands through impaired epithelial chloride ion transport -Leads to GI obstruction, infection, and inflammation Maldigestion of proteins, carbs, fats, and at-soluble vitamins -Manifestations: pancreatic insufficiency (mucous clogs ducts so pancreatic enzymes aren't released), steatorrhea/fatty stools, abdominal distention, gastroesophageal reflux, intestinal obstructions
upper urinary tract obstruction
-Causes: kidney stones, tumor in the kidney, strictures in the ureters, other tumors pressing on the ureters or ureter-bladder junction -Manifestations: impaired ability to concentrate urine, increased urine V, decrease in GFR, impaired ability to reabsorb bicarbonate and metabolic acidosis, impaired ability to excrete ammonia, alteration in mental status, compensatory hypertrophy in other kidney -Expected response to upper urinary tract obstruction: Dilation of tissue in response to P: Ureter = hydroureter, renal pelvis, calyces, parenchyma = hydronephrosis, ureterohydronephrosis -Tubulointerstitial fibrosis: within 7 days fibrotic changes begin in the tubules with collagens and other proteins getting deposited along the tubules -Irreversible glomerular damage- will begin within approx. 4 weeks, medulla and cortex of the kidney will begin to shrink as cells undergo apoptosis, decreased ability of the kidneys to concentrate the urine -Post-obstruction diuresis- If the obstruction is relieved body may produce as much as 10+ liter of urine/day causing dehydration which will again threaten renal function
kidney stones
Solid crystalline masses formed in the kidney, resulting from an excess of insoluble salts or uric acid crystallizing in the urine; may become trapped anywhere along the urinary tract. Calcium stones = most common -Risk factors: age> 50 yrs, male, caucasian, low fluid intake/chronic dehydration, excessive vitamin D and calcium ingestion, vitamin A deficiency, sedentary lifestyle -S&S- renal colic, dull, aching flank pain, N&V, pallor, cool, clammy skin -renal colic- pain related to dilation and spasms of smooth muscle related to ureteral obstruction. Pain starts in the flank and radiates to the groin. N&V comes from the pain -Assessment: UA for blood, protein, and bacteria, 24 hr urine analysis and watch for stones, KUB, IVP, US, CT, cystoscopy -Stones less than 5 mm is size have a 50% chance of passing through ureter. -If the stone is > 1 cm in size- it will not be passed on its own -ESLW- extracorporeal shock wave lithotripsy- Ultrasonic waves passed through the body until they strike the stones, sonic waves pulverize the stones to be passed through ureter & out of body in urine
Wilms tumor- rare embryonal tumor of the kidney usually diagnosed between ages 2-3, parents tend to notice asymptomatic, unilateral abdominal mass -Autosomal dominant pattern -20% of diagnoses children have other congenital abnormalities or syndromes -S&S- Vague abdominal pain, hematuria, fever, excess renin secretion, HT (r/t excess renin) -Uses national Wilms Tumor Staging instead of TNM: I: Tumor limited to the kidney II: Tumor ascending beyond the kidney but can be totally resected III: Residual non-hematogenous tumor confined to the abdomen IV: Hematogenous metastases to organs such as lungs, liver, bone, or brain V: Bilateral disease either at diagnosis or later, then staged for each kidney
end stage renal failure
more than 90% nephron loss and uremia, increased serum BUN and creatinine levels -Uremia S&S- uric acid excreted through skin à "uremic frost", breath smells like urine, abnormal yellow pigmentation, encephalopathy, peripheral neuropathy, loss of motor coordination, twitching, coma
Acute poststreptococcal glomerulonephritis
most commonly a type III hypersensitivity/immune complex mediated reaction where immune complexes lodge in glomeruli and complement activation destroys membrane -Sudden onset caused by group A hemolytic strep bacteria 7-10 days after infection -manifestations- decreased GFR, increased capillary permeability with blood and protein in urine, acute renal failure, HT, edema, fever and chills, pallor, increased serum BUN and creatinine, azotemia/abnormally high levels of nitrogenous compounds -Hematuria with RBC casts, proteinuria>3-5 g/day (primarily albumin) -Complications- severe, prolonged inflammation can cause kidney scarring
Hemolytic Uremic Syndrome
acute disorder characterized by hemolytic anemia, thrombocytopenia, and acute renal failure -Associated with viral or bacterial illness- upper respiratory infection or GI illness 1-2 weeks before -Associated with bloody diarrhea due to E coli bacteria that produce shiga toxin -Most common cause of acute renal failure in children -Occurs most often in children and infants younger than 4 years -90% survival rate, most children regain normal renal function -With the E coli infection, the Shiga toxin, moves from the intestines to the blood and binds to WBCs. The blood makes its way to the kidneys where the WBCs and the toxins cause damage. Platelets gather and the clotting cascade is activated. Endothelial lining of the glomerular arterioles becomes swollen and occluded by the clots and RBCs get damaged in the area. Because they are damaged, when they make it over to the spleen, the spleen pulls them out of circulation leading to acute hemolytic anemia. Because of the clotting cascade, platelets get used up in clots leading to thrombocytopenia. The vascular occlusion causes decreased renal perfusion and renal insufficiency leading to renal failure
Prerenal acute kidney injury
most common cause of acute kidney injury caused by impaired renal blood flow -Leads to decreased GFR due to decreased filtration P -Causes: hypovolemia, renal hypoperfusion, systemic vasodilation, afferent arterial vasoconstriction, decreased arterial blood V -Continued low pressure will causes ischemic cell injury and acute tubular necrosis or acute interstitial necrosis -S&S- oliguria/decreased urine output, metabolic acidosis, urinary tract infection, increased BUN and creatinine, electrolyte imbalances, anorexia, vomiting, fatigue, stupor, difficulty concentrating -Plase 1- kidney injury is evolving, prevention possible -Phase 2- oliguric phase- established kidney injury with oliguria and increase in serum BUN and creatinine -Phase 3- recovery- renal function stabilizes to normal or impaired level, diuresis common, decline in serum BUN and creatinine
nephrotic syndrome
syndrome due to glomerular injury that affects podocytes, allowing passage of proteins into urine (no hematuria) (more sever than nephritic syndrome) -severe proteinuria, periorbital edema, hypoalbuminemia, hyperlipidemia and fat in urine -Pediatric- likely idiopathic with systemic immune mechanism, usually between ages 2-3, more often affects boys -Secondary- more common in adults, r/t drugs like NSAIDs or systemic diseases like diabetes or malignancies -Treatment- normal protein diet, low fat diet, salt restriction, diuretics, immunosuppression, corticosteroids
Nephritic syndrome
syndrome due to glomerular injury (less severe than nephrotic syndrome) -RBCs are able to pass through pores in the podocytes within the kidneys - will see hematuria and mild proteinuria
Lower UTI/bladder infection Affects 50% of women at some point in their lives, especially when they become sexually active -S&S- suprapubic pain, dysuria, urinary frequency, urinary urgency, backache -can progress upwards into pyelonephritis

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