Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Patho test IV
study questions
| Question | Answer |
|---|---|
| 1. 2 Theories about Chronic Renal Failure | Traditional and Intact |
| 1. Traditional all nephron hypothesis | Nephrons are delicate and vulnerable; some insult= All nephrons affected. |
| 1. Intact Nephron Hypothesis | Diseased nephrons= completely destroyed. Others intact; killed or not killed; Intact nephrons may hypertrophy to compensate for the diseased nephrons. |
| 2. Define Glomerular Filtration Rate; GFR | HOW LONG IT TAKES BLOOD TO BE FILTERED THROUGH THE KIDNEYS; Filtration of plasma/min in kidneys(p.1285);Note: if lose 75% of nephrons- GFR becomes a problem; GFR= ↓'d |
| 3. Define Cystitis (p.1311) | BLADDER INFECTION; Inflammation of the bladder; infection up the urethra to the bladder. |
| 3. Define PYELONEPHRITIS | KIDNEY INFECTION; infection ↑ urethra; ↑ bladder, ↑ ureters, to renal pelvic part of the kidney; very unusual, b/c such a long trip up to the kidney. |
| 4. Most common organisms causing UTI's | 90%= Gram (-) rods; 70% E.coli; 20%Proteus (Notes) |
| 5. Explain why pregnancy increases the incidence of UTIs | progesterone relaxes sm. muscle around the urethra; Relaxed sm. muscles=larger urethra= ↑ infection |
| 6. Explain role of leukocidins in acute Glomerulonephritis (GN) | Antigen-Antibody Mistake (LEUKOCIDINS & KINASE); attack heart= Rheumatic Fever & kidney= GN.•In children 3 – 7 years old with h/o chronic strep infections |
| 7. Define Rapidly progressive GN | •Very Acute •Azotemia •Rapid accumulation of nitrogenous subs.•Rapid loss of nephrons •↑ retention and ↑ BP |
| 8. Define Azotemia | "Big Time" retention of nitrogenous substances, more severe than uremia •Deaminatin of protein results in productin of ammonia. NH₃-COOH (protein structure) → nitrogen breaks apart from protein (deamination) → Ammonia → urea → urea is excreted via urine |
| 9. Explain Chronic GN | •Very slow, insidious, gradual destruction of glomeruli •Kidney= 1/2 the size of your fist & weighs as little as 50g; Complete Atrophy of the kidney; Tubules have thickened; a non-functional mass of atrophied tissue. |
| 10. Explain the relationship b/w HTN & CRF | •↑ BP=constrict afferent/dilate efferent; presses against macula densa cells; activates renin-angiotensin aldosterone system. |
| 10. (cont.) renin-angiotensin aldosterone system | renin= activate Angio I→lungs convert Angio I→ Angio II → Constrict vessels systemically; release aldosterone get NA & H₂O retention= ↑ BP; ↑ blood vol •renal artery fills w/ plaque, ↓ kidney perfusion= repeats. Compensation → more plaque → higher BP. |
| 11. Explain malignant HTN | •Severe HTN with Diastolic BP >120 – 130 mmHg, grade 4 retinopathy, and renal excretory dysfunction, ranging from protenuria to hematuria to Azotemia•Occurs for many years |
| 12. Give most likely cause of renal artery stenosis | HTN/PLACQUE/ATHEROSCLEROSIS•KIDNEY COMPENSATORY MECHANISM•Plaque= ↓kidney perfusion →renin-angiotensin aldosterone system. Compensation → more plaque → higher BP (Bad Cycle!!!) |
| 13. Explain renal tubular acidosis in terms of H+ and HCO₃⁻ | •Problem with H+ and HCO₃ion excretion•GFR= Normal• Either can’t excrete H+ or reabsorb HCO₃⁻ |
| 14. ID the differences and pathology of distal RTA (Type I) and proximal RTA (Type II) | BOTH CAUSE ACIDOSIS... either b/c you can't pee out the H+ ions (Distal RTA)or b/c can't reabsorb HCO3 (Proximal RTA)back into the vascular system to buffer the H+ ions |
| 14. Distal RTA (Classic/Type I) | Can't acidify urine; Unable to excrete H+ into blood/urine= acidemia/acidotic (to excrete H+ into kidneys); More common in females (analgesic abuse) & children; in the distal tubule where transport H+ ions back/forth b/w vascular system & kidneys |
| 14. Proximal RTA (Type II) | Can’t reabsorb HCO₃⁻ to buffer H+=acidosis; Alkaline urine/acidotic blood; Problem is in the proximal tubule, unable to reabsorb HCO₃⁻;Pee out all bi-carb. |
| Urinary Tract Infections; (UTI's) | Not usually a kidney infection. Probably have an infected urethra. |
| Normal GFR | amt of plasma/min filtered thru glomerulus; every 20 mins filters entire blood volume in your body. |
| Nephron= | functioning unit of the kidney |
| Components of a Nephron | Afferent arteriole, glomerulus, efferent arteriole, Bowman's Capsule, proximal convoluted tubule, loop of Henle, distal convoluted tubule, collecting ducts. |
| Chronic Renal Failure (CRF) | lose one whole kidney (1/2 of your nephrons)and be o.k; lose 75% of nephrons= lose one whole kidney and 1/4th of the other kidney before Uremia is going to be a problem. |
| Uremia= | retention of nitrogenous substances; > 75% of your nephrons are gone= CRF |
| URETHRITIS | infected urethra; a.k.a. UTI |
| 15. Explain how chronic renal failure may lead to secondary gout | •CRF = ↓ uric acid excretion•Secondary gout is secondary to the loss of renal function•Leading cause of gout in children |
| 16. Explain toxic nephropathy | •Chemicals/toxins concentrated in kidneys; analgesic abuse= 1–2% of ESRD; females w/ hx of chronic back pn or HA's; ASA a combo med. w/ AA and Phenacetin; OTC (10 Yrs ago) damaged distal tubules; Acetaminophen = metabolite of phenacetin (liver damage) |
| 17. Explain the effects of lead on the kidneys | lead is incorporated into the bone, and over the years slowly leeks out; causes inflammation to renal tubules = nephritis. |
| 18. Explain Uremic Syndrome in terms of GFR | ↓ GFR = 5–10 % of normal cells remaining; Or loss of 90–95% of kidney’s ability to filter (GFR); Kidneys can’t filter = metabolic acidosis; basically means End Stage Renal Disease (ESRD) |
| 19. Explain how renal failure leads to metabolic acidosis | •H+ ↓ ability to excrete H+ ions (loss of 90 – 95% of ability to pee out H+) → remain in vasc. sys. → acidosis = uses HCO3 to buffer= ↓ pH = continuing acidosis; H+ attaches to → RBC → kicks out K+ → increased K+ → cardiac problems (K+ approx. 78 mEq/L) |
| 20. Explain the effects of sodium imbalance in uremic syndrome | •Decreased sodium output•Kidneys have a greater ability to handle Na+ than K+ (can pee out up to 20 gms/day of Na+), great flexibility to handle Na+•↓ Na+ output = ↑ BP with edema, circulatory overload, HTN and CHF! |
| 21. Explain the hematologic problems associated with uremic syndrome | •Normochromic, Normocytic anemias•Not enough RBCs being produced; No kidney production= ↓ RBC= ↓ erythropoetein= slow BM production; If produce RBCs w/o stimulation of erythropoetein, they don't last as long; & the toxic environment doesn’t help |
| 22. Explain the skin discoloration associated with uremic syndrome | •Increased urochrome D/T anemia and the retention of urochromans•Urochromans= pigments that give urine its color•Pasty, waxy, yellowish colored skin |
| 23. Explain the reasons for CNS disturbances in uremic syndrome | S/S's correl. w/ Azotemia; predict w/↑'ing BUN/Creatinine; Irritable, insomnia, lethargy, coma, seizures; BUN= best indicator; CC= measurement of blood vs. urine Creatinine |
| 24. Explain the reasons of skeletal disorders in uremic syndrome | Osteodystrophy disorders; Osteomalacia (most common)= softening of bones; Need Ca+ and vit D to keep bones calcified; kidneys activate Vit. D from sunlight, pts. don't have this step = ↓ Vit D → Ca+ is not utilized = ↓ mineralization of bones = softening |
| 25. Explain the causes of ARF in terms of prerenal, post renal, and renal causes | Pre-renal= vascular system prob; Renal= damaged kidneys; Post-Renal= prob w/urine excretion |
| 25. Pre-renal Acute Renal Failure | Caused from circulatory system failures (MI, PE, burns, severe hemorrhage, etc.); ↓ blood flow to the kidneys = ↓ urine output; Nothing wrong with the kidneys |
| 25. Renal causes of Acute Renal Failure | Intrinsic problem; Damage to kidneys (radiological dyes, ETOH, ethylene glycol-antifreeze), other toxic chemicals |
| 25. Post-Renal Acute Renal Failure | Filtration took place, but something is preventing excretion; Primarily past kidneys (ureters bladder, urethra, etc.); Possible causes: clot, trauma, CA, obstruction |
| 26. Define the following types of fractures | Transverse: Straight across; Oblique: Angle; Spiral: Spiral up bone(CHILD ABUSE); Impaction:Compression(jump off roof); Stress:↑ activity(runners); Avulsion: Separation of fragment of bone at the site of tendon/ligament insertion (a chip) |
| 27. Explain the four R’s of Fractures: | •Recognition: Probability of fx; X-Ray, to confirm•Reduction: Manipulating bones pieces back into alignment (closed fx)•Retention: Holding in place (cast, splint, traction), always cast above and below the joints.• Rehabilitation: Recovery |
| 28. Explain the difference between dislocation and subluxation: | •Dislocation: no connection b/w articular and mating cartilage(not touching); shoulder–classic location, ulnar nerve torn if can’t abduct/adduct fingers. If can’t tighten deltoid= axillary nerve torn; Subluxation: Slight Deviation from normal |
| 29. Explain Scoliosis | • Excessive curvature of the spine in a lateral fashion• May include rotation of the spine• Most common in pre-teens• Severe cases with curvature and rotation = brace• Brace is worn until rotation stops @ puberty = Risser’s sign |
| 30. Explain Risser’s sign: | • At puberty a small bone develops at the base of the spine & stops rotation |
| 31. Explain basic pathology of Multiple Myeloma | Malignancy in plasma cells; More common in males 2:1; Precursors of B-Lymphocytes; Leukemia of B-Lymphocytes(WBC, RBC, Bone)↓ production; bone lesions; soft/Weak bone(osteoporosis) |
| 31. Explain basic pathology of Giant Cell Tumor | Benign/Not malignant; Usually in young adults, more common in females; Usually occurs at end of long bones; 50% ↑ incidence of reoccurance after removal; Unknown etiology; Similar to osteogenic sarcoma |
| 31. Explain basic pathology of Osteogenic Sarcoma | Malignant in young adults; Usually occurs at end of long bones; looks like a bone infection; Bx to confirm; amputation; Radiation/Chemotherapy |
| 32. Explain the pathology of Osteoarthritis | aka (Degenerative Joint Disease); more common in females 10:1; Correlated w/ age & repetitive motion; finger joints swollen; almost never the knuckles; synovial fluid dries up; symmetry of joints= poss. SLE |
| 33. Explain the pathology of Rheumatoid Arthritis: | Multisys. Dx; More severe form; More common in females; ↑ with age; autoimmune?; hydrolytic enzymes directed at collagen; collagenase, proteinase; synovial fl components destroyed; pannus tissue develops; grainy tissue, burlap; WBC ↑'s 15–25,000 high; IgM |
| 34. Explain the pathology of SLE discussing arthritis, butterfly rash, Raynaud’s syndrome, and antinuclear antibody: | • 10:1 females to males• Multisystem, chronic, autoimmune disease• Correlated with arthritis• 40% have butterfly rash• 40% have Raynaud’s syndrome• 95% = ANA• pain is often symmetrical (both wrists, etc) |
| 35. Explain Scleroderma | Hardening of skin; Fibrosis; more common in females 3:1; Raynaud's very common; face taut |
| 36. Explain the basic pathology of gout | ↑ uric acid;↓ excretion uric acid; 95% males; Pain big toe d/t gravity; May get kidney stones; ETOH exacerbates contains urate= precursor of uric acid; also in lunch meat; ETOH= ↑ blood lactate levels= ↓kidneys ability to filter uric acid; sharp razr-like |
| 37. Explain the reasons for giantism and acromegaly | •Anterior pituitary oversecretes growth hormone•Excessive longitudinal growth; Giantism= kids; Acromegaly= adults b/c bones can only grow so long, after that they just get thicker. |
| 38. Explain Graves disease | Hyperthyroidism;More common in females; Characterized by fatigue, heat intolerance, increased sweating, increased appetite, muscle pain; Bulging eyes are due to lymphocytes forming around intraocular tissue; Autoimmune??? |
| 38. Explaing Toxic Nodular Goiter | Typically in older population; exclusive in those without medical preventative care; Big goiter on neck; Characterized the same as Grave’s disease |
| 39. Explain the differences between primary and secondary hyperthyroidism: | •Primary: Thyroid itself is hypofunctioning; ↓ T₃& T₄ & ↑TSH; •Secondary:Pituitary is the problem; ↓T₃& ↓T₄, ↓TSH |
| 40. Explain the differences between papillary, follicular, and medullary thyroid carcinoma: | •Neoplasms of the thyroid•Malignant nodule is approximately 50% with children < 15 yrs/old•Development of growth on thyroid after radiation to head/neck → malignant•Increased incidence in males (CA of thyroid) |
| 40. Explain papillary thyroid carcinoma: | most common; 75% of all malignancies; In epithelial tissue on boarders of thyroid, similar to follicular CA; Grows slowly, not invasive, stays outside of gland; Treatment = thyroidectomy with radiation. |
| 40. Explain follicular thyroid carcinoma: | 15% of all malignancies; Slow, growing outside of gland; Treatment is the same as papillary |
| 40. Explain medullary thyroid carcinoma: | uncommon;worst kind/prognosis; middle of the thyroid gland; secreting section; metastasizes quickly |
| 41. Explain the role of parathyroid hormone in hypercalcemia | Ca+ > 10.5; Cause = ↑ Parathyroid ↑, probably due to benign adenoma of parathyroid; ↑ Ca+ = ↓ Phosphorus; EKG changes, Bone cysts |
| 42. Define the clinical signs of hypocalcemia | Ca+ < 9.0; ↓ parathyroidism; ↑ neuromuscular irritability, Tetany; seizures; osteomalacia; hypotension; |
| 43. Explain the role of ACTH in Cushing’s Syndrome: | ↑ ACTH= stimulates adrenal glands to secrete hormones: ↑ cortisol; ↑ aldosterone, ↑ androgen, ↑ estrogen= ↑ Blood sugar,↑ Na+, ↑ facial hair, estrogen counteracts androgen; |
| 43. 2 causes of ACTH (adrenal corticotropic hormone) | dependent (Cushing's Disease): excessive excretion of ACTH from pituitary(adenoma)ACTH independent= Cushing's Syndrome, ↑ ACTH from over secretion of adrenal glands (pituitary= fine) |
| 43. Adrenal- Located superior to the kidneys | Hormones that affect the three S’s: •Sugar= glucocorticoid=cortisol •Sex= androgens and estrogens •Salt= mineralcorticoid= aldosterone Hyperglycemia, Hypernatremia, Hypertension, HYPO-IMMUNE (decreased thymus function) |
| 43. Effects of increased cortisol | Hyperglycemia, Hypernatremia, Hypertension, **HYPO-IMMUNE (decreased thymus function) |
| 44. Define the clinical consequences of aldosteronism: | •↑ aldosterone; •↑ reabsorbtion of Na++ in renal tubules; retain sodium; •↑ kidneys ability to pee out H+ & K+ •Clinical consequences: Na+ and H₂O retention, expansion of the extracellular fluid volume & HTN •↑ Na+, ↓ K+, ↑pH (Metabolic Alkalosis!!!!) |
| 45. Explain Hirsutism in terms of androgen excess: | •Hirsutism= excess body hair in male pattern•Pronounced in females after menopause D/T estrogen inhibits Androgens ("Bearded Lady"); |
| 46. Define Addison’s disease and explain the effects of cortisol, aldosterone, and androgen deficiency in this disease | •↓ cortisol production = ↑ cell sensitivity to insulin= ↓ Blood sugars; •↓Aldosterone production= ↓ Na+ & ↓H₂O = ↓blood volume= ↓ BP & ↑K+; •Males don’t lose a lot of hair b/c testes secrete androgens; •Females lose lots of hair |
| 47. Explain the difference between IDDM and Non-insulin Dependent DM | Insulin dependent Diabetes Mellitus (IDDM) •90% beta cells destroyed before symptomatic •Require daily insulin •More likely to have complications of DKA & microangiopathy |
| 47. Explain the difference between IDDM & Non-Insulin Dependent DM | •Defect insulin secretion and action •Defect in insulin receptors •80% =obese |
| 48. Explain the criteria for diagnosis of Non- PG diabetes: | •DX= hyperglycemia, Fasting BS= greater than 126mg; on more than one occasion •GTT = greater 180mg at 2hrs and at least one other time |
| 49. Explain why ketoacidosis is a complication of DM: | Ketones= fat converted to sugar, cells think starving; lack of insulin; convert ketones into Na+ salts, excreted from kidneys w/extra H₂O; ↓ pH, ↑ RR (Kussmauls) b/c lungs thing prob w/ CO2; metabolic acidosis; Kussmaul's breathing can't fix the acidosis |
| 50. Explain the vascular complications of DM: | Vascular lesions, retinal lesions, peripheral nerves & glomerulus (don't need insulin); Glomeruli, retinas, & peripheral nn. get big, fat, sluggish & nonfunctioning; More immediate prob. in IDDM, may happen in NIDDM pts that have continual hyperglycemia |
Created by:
jn study stop
Popular Nursing sets