Download NURS 5315: Advanced Patho Exam 5 Questions with Simplified Solution and more Exams Pathophysiology in PDF only on Docsity!
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NURS 5315: Advanced Patho Exam 5
Questions with Simplified Solution
1. What are the key functions of the kidneys?: Excretion of metabolic waste.
Regulation of water and electrolyte balance Regulation of arterial BP Erythrocyte production 1, 25 -dihyydroxy vitamin production (calcitriol) Gluconeogenesis
2. What metabolic waste do the kidneys excrete?: Urea
Creatinine Bilirubin Drugs Hormone metabolites
3. How do the kidneys regulate arterial blood pressure?: RAAS
The renin-angiotensin-aldosterone system (RAAS) is a critical regulator of blood volume, electrolyte balance, and systemic vascular resistance.
4. How do the kidneys regulate acid base balance?: Exertion of H+ ions and reabsorption of
sodium bicarb.
5. How does blood flow into and out of the kidneys?: In through the renal artery.
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i. Interlobal artery.
ii. Arcuate arteries.
iii. Capillary beds
Out through the renal vein
6. Renal capillary beds.: 1. Atterent (glomerular capillaries)
a. filtration
2. Etterent (peritubal capillaries)
a. Water, electrolytes, substances exchanged between blood and filtrate making urine.
b. Vasa recta (long etterent arterioles-extend through medullar glomerulus to form the juxtaglomerular cells)
i. Regulate urine and serum concentration and volume.
ii. Reabsorb filtrate to return to systemic circulation.
7. How does filtrate and urine move through the kidney?: 1. Bowmans capsule
2. Proximal tubule
3. Loop of Henle
a. Descending (thin)
b. Ascending (thick)
4. Macula densa
5. Distal tubule
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c. Excretion of substances from the blood into the renal tubules.
12. What are the structures of the glomerular membrane?:
Endothelium Basement membrane Podocyte
13. What is the structure of the endothelium (fenestrae)?
(Glomerular membrane): Regulates vasomotor tone, homeostasis and traflcking of leukocytes.
14. What is the function of the basement membrane (collagen & proteoglycan)
(Glomerular membrane): Scattold supporting the function of the endothelium and podocytes (problems with the basement membrane result in albumin leaking into filtrate)
15. What is the function of the Podocyte (filtration slits/slit membranes)?
(Glomerular membrane): The slits serve as a barrier between the foot process to prevent leaking of albumin into the filtrate.
16. How can GFR be manipulated?: Increase or decrease GFR.
17. What is the big idea and mechanism for increasing GFR?: Big idea:
Hormones and autocoids: local angiotension II. Mechanism: Constricts etterent arterioles; increased blood flow; increased GFR. Big idea: Nitric oxide, prostaglandins. bradykinin Mechanism: Dilate atterent artioarterioles; increased blood flow; increased GFR.
18. What is the big idea and mechanism for decreasing GFR?: Big idea: SNS:
5 / 37 Norepi-nephrine and Epinephrine (adrenal medulla) Mechanism: Constricts atterent arterioles, decreases blood flow, decreased GFR. Big idea: Hormones: endo-thelin (vascular endothelium) Mechanism: Constricts atterent arterioles, decreased blood flow, decreased GFR.
19. What happens in the proximal tubule?: Sodium, Chloride, Phosphourous, sodium bicarbon-
ate, glucose, amino acids, are reabsorbed. Very water permeable. Hydrogen, organic acids, organic bases (metabolic by products, bile salts, uric acid, catecholamines) are secreted. Controlled by: Angiotensin II (increased sodium and H20 absorption) PTH (decreased Phosphorous reabsorption).
20. What happens in the thin descending loop of Henle?: Small amounts of sodium are
reabsorbed. Highly water permeable.
21. What happens in the thin ascending loop of Henle?: Dilutes filtrate. Highly
water permeable.
22. What happens in the thick ascending loop of Henle?: Sodium, chloride, potassium,
calcium, magnesium, bicarb, are reabsorbed. Impermeable to water; dilutes filtrate. Hydrogen ions are secreted here. Controlled by angiotensin II (NaCl reabsorption/H+ secretion) Parathyroid hormone (calcium reabsorption)
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a. Elevated level correlates with decreased GFR.
b. Not attected by infection, diet, inflammation, gender, age, or race.
28. What do cells in the urine measure?: 1. RBCs.
a. Glomerular nephritis.
b. Trauma.
c. Kidney stones.
2. WBC
a. Ingection
3. Casts
a. Coagulated portiens.
i. Cellular debris
1. Acute kidney injury
b. RBC
i. Tubular or glomerular injury.
c. WBC
i. Inflammation
d. Epithelial
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i. Tubular injury.
e. Broad waxy
i. Stasis and tubular injury
a. Not a good sign.
29. What do biomarkers in the urine measure?: a.) NGAL
- Neutrophil gelatinase-associated lipcalin (plasma, urine)
b.) KIM 1
1. Kidney injury molecule 1 (urine)
c.)IL- 18
1. Interleukin -18 (urine)
d.) IDF BIP
1. Insulin like growth factor binding protein (urine)
e.) TIMP- 2
1. Tissue inhibitor of metallopretinases-2 (urine)
f.) Urokinase-type plasminogen activator receptor.
30. What changes occur in the kidney with aging?: a.) May hypertrophy as compensatory
mechanism
i. Kidney donation, trauma, disease
10 / 37 Manifestations: pH of urine (>-7-Calcium, Ph, struvite; <5 uric acid-related to movement (pain) or obstruction.
32. Evaluate the etiology, pathophysiology, and manifestations of nephrotic: -
Etiology: Glomerulonephritis, drugs, infections, thrombo-embolism. Pathophysiology: Increased permeability through damaged basement membrane. Manifestations: Proteinuria; hypoalbuminemia, edema, hyperlipidemia, lipiduria
33. Evaluate the etiology, pathophysiology, and manifestations of nephritic
syndrome: Etiology: Infection related and rapidly progressive glomerulonephritis Pathophysiology: Inflammation of the glomerulus Manifestations: Hematuria and RBC casts (proteinuria less significant); HPTN, oliguria.
34. Explain the etiology, pathophysiology, and manifestations of acute
glomerular nephritis: Etiology:
1. Post-infectious
2. Auto-ummune0antibodies formed in-situ;
3. Rapidly progressive glomerulonephritis
Pathophysiology:
1. Deposits of IgG and complement complexes. Kids: Group A beta-hemolytic strep; adults post staphylococcus; IgA
nephropathy deposits of IgA (lupus/early diabetic nephropathy)
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2. Membranous glomerulonephritis
3. Accumulation of macrophages and proliferation of epithelial cells in Bowmans space form crescents and occludes capillary
flow. Manifestations: Fatigue, HTN, edema/ascites, proteinuria/hematuria, decreased urine output
35. Explain the etiology, pathophysiology, and manifestations of chronic
glomerular nephritis: Etiology: Chronic inflammation (slow to develop): diabetic nephropathy; lupus nephritis. Pathophysiology: Podocyte injury, thickening of basement membrane and glomerulosclerosis. Manifestations: Nausea, vomiting, hematuria, proteinuria, HTN, edema, decreased urine output.
36. List the definition, onset, and common etiologies of acute kidney injury.: Def-
inition: Decline in GFR (not enough blood at suflcient pressure for perfusion) urine output and clearance of waste products and electrolytes Stage 1: Baseline creatinine 1.5-1.9 or = 0.3mg/dl increased. Stage 2: Creatinine 2-2.9 x baseline Stage 3: Creatinine 3x baseline or use of renal replacement therapy Onset: Sudden Manifestations: Elevated creatinine, oliguria Electrolytes: K, Ph, BUN, metabolic acidosis, edema, dysnpea, fatigue, AMS, muddy urine. Common etiologies: Pre, intrinsic, post-renal
13 / 37 Edema, dyspnea (fluid overload), fatigue, altered mental status, muddy brown urine.
42. Explain the severity, GFR, progression, and symptoms of CKD Stage I: Severity:
GFR: >
Progression: mild damage Symptoms: asymptomatic
43. Explain the severity, GFR, progression, and symptoms of CKD Stage II:
Severity: 60-89% GFR: 60- 89 Progression: mild damage Symptoms: asymptomatic
44. Explain the severity, GFR, progression, and symptoms of CKD Stage IIIa and
IIIb: Severity: 30-59% GFR: 45- 59 30- 44
14 / 37 Progression: mild to moderate damage, some decrease in functional unit Symptoms: asymptomatic
45. Explain the severity, GFR, progression, and symptoms of CKD Stage IV: Sever-
ity: 15-29% GFR: 15- 29 Progression: Severe damage-prepare for replacement Symptoms:
46. Explain the severity, GFR, progression, and symptoms of CKD Stage V: Severity:
GFR: <
Progression: ESRD Symptoms: Kidneys not able to keep up with filtration demands and removal of excess fluid
47. What are the effects of CKD on the skeletal system?: Osteodystrophy, decreased vitamin
D production
16 / 37 pertrophy: Etiology: Obstruction of the urethra Pathophysiology: Overdistention of the bladder-hydronephrosis Manifestations: Overflow incontinence, frequency, UTI. Rare AKI or CKD
55. What organs make up the upper GI tract?: Mouth/oral cavity, pharynx, esophagus, stomach,
duodenum.
56. What organs make up the lower GI tract?: Small intestines, large intestine, colon
57. What are the four basic actions of the GI system?: Digestion, absorption, motility, and
secretion.
58. What is a sphincter?: Muscle that aids in closing ott the ditterent compartments and helps promote
absorption of nutrients and motility of food.
59. What sphincters are found in the GI tract?: Esophageal sphincter: separates esophageal and
stomach. Pyloric sphincter: separates the stomach and small intestine. Ileocecal sphincter: separates small intestines and large intestines; people with large intestine resections lose this valve and lose ability to properly absorb nutrients and fluid.
60. Where does most digestion and absorption take place?: Small intestine
61. What enzymes are contained in saliva?: Amylase and lysosome
62. What does gastric inhibitory peptide (GIP) do?: Stimulates the release of insulin from beta
cells in the pancreas, maintains blood sugar after eating.
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63. What does glucagon -like peptide 1 (GLP1) do?: Stimulates pancreatic glucose-dependent
insulin secretion.
64. Explain the GI circulation anatomy and
physiology. (ARTERIAL): Arterial blood supply: Celiac artery supplies Hepatic artery (Liver) Stomach Spleen Pancreas Superior mesenteric artery supplies Pancreas Small intestine Colon Inferior mesenteric artery supplies Colon
65. Explain the GI circulation anatomy and physiology. (VENOUS): Blood flows
thru gut to hepatic circulation via the Hepatic Portal Vein to the liver to the hepatic veins to the inferior vena cava Liver: Majority of blood from abdomen runts thru 3 veins (hepatic portal vein, splenic vein, and mesenteric veins)
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72. Describe the etiologies of constipation.: Primary (chronic idiopathic):
i. Functional: normal motility rate but diflculty passing stool.
ii. Slow transit: slow, infrequent/straining defecation, and accumulation of stool in sigmoid colon.
iii. Constipation - predominant irritable bowel syndrome (IBS-C): chronic constipation with abdominal pain.
1. Pathology: diet, genetics, motility, absorption, daily behaviors, medication use.
iv. Other causes: lack of toilet access, suppression of urge, pelvic floor dyssynergia, dehydration.
Secondary: Diet, medications (antiacids, anticholinergics, iron, bismuth), neurogenic disorders (stroke, Parkinsons, spinal cord lesions, multiple sclerosis, Hirschsprung), rectal fissures, strictures, hemorrhoids, opioid-induced constipation, en- docrine/metabolic disorders (hypothyroidism, DM, hypokalemia, hypercalcemia), pelvic hiatal hernia, diverticula, IBS, pregnancy, aging.
73. What is the etiology and clinical manifestations of osmotic diarrhea?: Etiology:
Large PO doses of poorly absorbed ions (magnesium sulfate, phosphate, synthetic and non-absorbable sugars (ie sorbitol), once ingestion stops, diarrhea stops. Malabsorption related to lactase/pancreatic enzyme/bile salt deficients, small intestine bacterial overgrowth, celiac disease. Clinical manifestations: Non-absorbable substance (ie miralax, lactulose, mag citrate) in intestine draws excess water into intestinal lumen by osmosis and increases stool weight and volume, producing large volume diarrhea.
74. What is the etiology and clinical manifestations of secretory diarrhea?:
20 / 37 Etiol-ogy: Large-volume: infection: viruses (rotavirus), bacterial enterotoxins (E. Coli, vibrio cholera, shiga toxin), exotoxins (C. ditt, post antibiotics), small bowel bacterial overgrowth. Increased Cl- or HCO3- secretion of decreased Na+ absorption Small-volume: Inflammatory bowel disorder (ulcerative colitis or Crohn's disease) or impaction. Clinical manifestations: Large-volume: excessive mucosal secretions of chloride or bicarbonate-rich fluid or overall inhibition of net sodium absorption causing decreased water absorption. Small volume: Inflammation of colon causes smooth muscle contraction, cramping pain, bowel urgency, frequency; fecal impaction causes mucous and fluid secretion to lubricate and move stool that flow around impaction.
75. What is the etiology and clinical manifestations of motility diarrhea?: Etiology:
Resection of small intestine (small bowel syndrome), surgical bypass of an area of intestine, fistula formation between loops of intestine, IBS-diarrhea, diabetic neuropathy, hyperthyroidism, laxative abuse. Clinical manifestations: Excessive motility decrease transit time and opportunity for fluid absorption; negative ettects on fluid, electrolyte, acid-base balance.
76. What are the manifestations and common complications associated with
diarrhea?: Acute or chronic; systemic ettects of prolonged: dehydration, electrolyte imbalance (hyponatremia, hypokalemia), metabolic acidosis, weight lossl fever with bacterial/viral infection, vomiting, pain, usually lasting <2 weeks; IBD or dysentry: fever, pain, bloody stools, chronic diarrhea; malabsorption syndrome: steatorrhea (fatty stool), bloating, and diarrhea.
