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ADVANCED PATHOPHYSIOLOGY Midterm REVIEW NR507, Exams of Nursing

Valdosta State University (VSU)Nursing

ADVANCED PATHOPHYSIOLOGY Midterm REVIEW NR507

Typology: Exams

2024/2025

Available from 02/06/2025

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ADVANCED PATHOPHYSIOLOGY
Midterm REVIEW NR507 QUESTIONS &
ANSWERS
Glomerulonephritis - ANSWERSThe glomerular-capillaries can trap blood-borne Ab &
Ag-Ab complexes
- Causes: PRIMARY: infection, drugs, toxins, vascular disorders, ischemia, immunologic
responses, free radicals. SECONDARY: DM, CHF, HIV, Lupus
Triggering event (infection)- Ag-Ab complex formation & deposition in glomerulus-
Activation of complement system & WBC infiltration- Glomerular injury & leakage-
Proteinuria/hematuria- edema, increase creat, azotemia, oliguria
OR
after glomerular injury & leakage- Coagulation cascade activation & FIbrin deposition-
Decreased capillary perfusion- decreased GFR- edema, increase creat, azotemia,
oliguria
S1 - ANSWERS-Closing of mitral and tricuspid valve
- Beginning of systole
S2 - ANSWERS- Closure of the aortic and pulmonic valve
- End of systole
Valvular stenosis - ANSWERSthe valve orifice is constricted and narrowed, impeding
the forward flow of blood and increasing the workload of the cardiac chamber proximal
to the diseased valve. Intraventricular or atrial pressure increases in the chamber to
overcome resistance to flow through the valve. Increased pressure causes the
myocardium to work harder, causing myocardial hypertrophy.
Aortic stenosis - ANSWERS- LV hypertrophy
- L heart failure
- Pulmonary edema
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ADVANCED PATHOPHYSIOLOGY

Midterm REVIEW NR507 QUESTIONS &

ANSWERS

Glomerulonephritis - ANSWERSThe glomerular-capillaries can trap blood-borne Ab & Ag-Ab complexes

  • Causes: PRIMARY: infection, drugs, toxins, vascular disorders, ischemia, immunologic responses, free radicals. SECONDARY: DM, CHF, HIV, Lupus Triggering event (infection)- Ag-Ab complex formation & deposition in glomerulus- Activation of complement system & WBC infiltration- Glomerular injury & leakage- Proteinuria/hematuria- edema, increase creat, azotemia, oliguria OR after glomerular injury & leakage- Coagulation cascade activation & FIbrin deposition- Decreased capillary perfusion- decreased GFR- edema, increase creat, azotemia, oliguria S1 - ANSWERS-Closing of mitral and tricuspid valve
  • Beginning of systole S2 - ANSWERS- Closure of the aortic and pulmonic valve
  • End of systole Valvular stenosis - ANSWERSthe valve orifice is constricted and narrowed, impeding the forward flow of blood and increasing the workload of the cardiac chamber proximal to the diseased valve. Intraventricular or atrial pressure increases in the chamber to overcome resistance to flow through the valve. Increased pressure causes the myocardium to work harder, causing myocardial hypertrophy. Aortic stenosis - ANSWERS- LV hypertrophy
  • L heart failure
  • Pulmonary edema
  • Exertional dyspnea -Syncope -Angina pectoris
  • Systolic murmur Mitral Stenosis - ANSWERS- LA hypertrophy -R ventricular failure
  • Pulmonary edema
  • Orthopnea
  • Respiratory infections
  • PH -Edema -Atypical chest pain
  • Diastolic murmur Stroke volume - ANSWERSThe volume of blood ejected per bear during systole Cor Pulmonale - ANSWERSright ventricular hypertrophy and heart failure due to pulmonary hypertension Cardiac output - ANSWERSHR x SV -Normal= 5Lpm -Preload, afterload, contractility, heart rate Preload - ANSWERSThe volume inside the ventricle at the end of diastole Determined by:
  • Amount of venous blood returning to the ventricle during diastole
  • The amount of blood in the ventricle after systole Afterload - ANSWERSThe resistance to ejection of blood from the ventricle total peripheral resistance (TPR) Systemic vascular resistance (SVR) Contractility - ANSWERSsympathetic nervous system, epi and norepi) + inotropes Acetylcholine released from vagus nerve - inotrope Cytokines released during sepsis impair contractility O2 < 50% decreased contractility Troponin - ANSWERSRelaxing protein

-Symptoms: chest constriction, exp wheezing, dyspnea, coughing, tachycardia, tachypnea -Beta-agonist inhaler, inhaled corticosteroids, -Anticholinergic drugs:Block acetylcholine binding in the lung. Promotes bronchodilation through decrease parasympathetic response (tiotropium, ipratropium) Polycythemia vera - ANSWERSchronic, progressive disease that is characterized by overgrowth of the bone marrow, excessive red blood cell production, and an enlarged spleen and causes headache, inability to concentrate, and pain in the fingers and toes -increased viscosity, platelet dysfunction, hypercoagulable, Bronchitis - ANSWERS-Bronchial wall inflammation

  • Hypersecretion of mucus
  • Chronic productive cough (3 consecutive months for at least 2 successive years) -release of inflammatory mediators( histamine, prostaglandins, leukotrienes, interleukins) -smooth muscle constriction, hypertrophy
  • Airflow obstruction ( SOB, wheezing, cyanosis)
  • Peripheral edema
  • alveolar hyperinflation
  • CO2 retention
  • Irreversible Caused by: -Long-term exposure to environmental irritants
  • Repeated episodes of acute bronchitis
  • Factor(s) affecting gestational or childhood lung development - the most common being pre-term birth and/or RSV infection in early infancy nephron anatomy - ANSWERS kidney anatomy - ANSWERS
    • ANSWERS Nephron - ANSWERSMulticellular structure
  • Bowman's capsule
  • Tubule system (PCT, Loop of henle, DCT, and collecting duct)
  • Glomerular & Peritubular capillaries surround each nephron -Cannot regenerate
  • GFR decreased by 1 ml/min/year after 30
  • Filtration -Reabsorption
  • Secretion
  • Excretion Glomerular filtration - ANSWERS- Blood pressure forces water and dissolved plasma components ( Glucose, ions, amino acids, urea, and creatinine) through glomerulus & Bowman's capsule into the renal tubule system Tubular reabsorption - ANSWERSSelective return of water and solutes ( glucose, ions, amino acids, urea) FROM the filtrate of the nephron tubule system INTO the bloodstream of the peritubular capillaries -65% of salt, water and most organic substances are reabsorbed in the PCT
  • Remainder of water and ions are reabsorbed throughout the tubule system; ADH & Aldosterone influence amounts Tubular Secretion - ANSWERS- Movement of material (Urea, NH3, H, K, some Rx, Misc chem) FROM the bloodstream of the peritubular capillaries INTO the filtrate of the nephron tubule system proximal tubule - ANSWERSReabsorption -Na, Glucose, K, Amino acids, Hco3, Po4, Urea, H2o (ADH not required) Secretion -H, Foreign substances Isotonic Loop of Henle - ANSWERSDesc loop -Water reabsorption, NA diffuses in Asc loop -Na reabsorbed (active transport), water stays in Urea secretion in thin segment Isotonic, Hyper and hypotonic Distal tubule - ANSWERSReabsorption -Na, H2o (ADH required), Hco Secretion -K, Urea, H, Nh3, some drugs Hypotonic
  • increased proximal tubule NA and H2O reabsorption- Increased aldosterone and ADH secretion- Increased distal tubule NA and H2O reabsorption -Most common cause of AKI Intrarenal - ANSWERS-Caused by ATN, acute glomerulonephritis, and other glomerulopathies -Cast formation- Increased intratubular obstruction, Increased intratubular pressure- tubular backleak Postrenal - ANSWERS- Caused by UT obstruction (BPH, Calculi, Inflammation, tumor)
  • Increased intraluminal pressure- release of inflammatory mediators and vascular endothelial cell injury- renal vasoconstriction- cellular/interstitial edema- decreased glomerular filtration pressure Causes of renal failure - ANSWERS- AKI
  • HTN -DM -Lupus Treatment of renal failure - ANSWERS- Dietary control (protein intake, Vitamin D replacement, K restriction, Iron, Low phos)
  • Control of chronic conditions
  • treat anemia
  • lower cholesterol
  • Dialysis Renal Calculi - ANSWERS- Crystals, protein and other substances (Calcium/phosphate/Uric acid/cystine/struvite) -Influenced by: HTN, fluid intake, obesity, DM, metabolic syndromes, Alkaline urine

  • 1cm almost never pass on their own -Colic to lateral flank of abd = midureter obstruction - Urgency, frequency, incontinence= obstruction of lower ureter or ureterovesical junction. may have blood -High PH: CA -Low PH:uric acid Role of angiotensin converting enzyme (ACE) - ANSWERSWhen renin is released, it cleaves an α-globulin (angiotensinogen produced by liver hepatocytes) in the plasma to form angiotensin I, which is physiologically inactive. In the presence of ACE produced from the pulmonary and renal endothelium, angiotensin I is converted to angiotensin II. Angiotensin II stimulates secretion of aldosterone by the adrenal cortex, is a potent vasoconstrictor, and stimulates antidiuretic hormone secretion and thirst

Conditions associated with renal failure - ANSWERS-malnutrition-inflammation complex syndrome or protein-energy wasting Leads to atherosclerosis, CV disease -Insulin resistance

  • bone fractures (vitamin d/ calcium deficiency) -pulmonary edema (fluid overload) -Encephalopathy/neuro (accumulation of uremic toxins)
  • Stroke associated with dialysis
  • Goiter/Restricted growth in kids (elevated parathyroid hormone/decreased thyroid hormone)
  • Anemia ( reduced erythropoietin/ RBC production) -GI (n/v, ulcers, bleeding) ( retention of metabolic acids)
  • Skin (retention of urochromes, high CA in plasma)
  • immune/infection ( suppression of cell-mediated immunity, decreased lymphocytes/phagocytosis) Erythrocyte (RBC) - ANSWERSFunction: gas transport to and from tissue cells and lungs Lifespan: 80-120 days -48% of blood volume -Contains Hgb, has no nucleus and cytoplasm, cannot synthesize protein
  • Removed by the spleen Anemia risk factors/causes - ANSWERS- Blood loss -Impaired erythrocyte production -Increased erythrocyte destruction -COmbination a-Thalassemia - ANSWERS-Chinese, Vietnamese, Cambodians, and Laotians -Microcytic-hypochromic -high serum iron, splenomegaly
  • Deletion involving HBA1 or HBA2 genes (involved in hemoglobin production) -Hb bart syndrome- most severe, loss of all 4 a-globin alleles. -HbH- loss of 3 a-globin alleles -a-thalassemia trait- loss of 2 a-globin alleles. mild anemia, small, pale erythrocytes -a-thalassemia carrier- loss of 1 a-globin allele and not clinical symptoms
  • most fetuses develop intrauterine heart failure and are stillborn or die shortly after birth

B-thalassemia - ANSWERS-Greeks, Italians, and some Arabs and Sephardic Jews. -More common than A -Erythrocytes have decreased hemoglobin, and accumulations of free a chains

  • Mild to mod. microcytic-hypochromic anemia