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BIOL 171 Lecture Notes - Lecture 22: Calcinosis, Hydronephrosis, Connective Tissue

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School
UC Riverside
Department
Biology
Course
BIOL 171
Professor
Chappell

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Document Summary

Acute tubular necrosis: calcinosis in the pyramid no shadowing. Infarction: not enough blood supply: thus, will be seen as anechoic! If there is an obstruction it can cause back log: reason causing it fluid, mass, stroke, sometimes severe chronic hydronephrosis can be confused on us as cysts. You can see that there is communication between the cysts. If there is a little room in between or there are interconnected by doppler, you can tell that there is communication between cysts thus it is hydronephrosis! Demonstrates connection between the cysts: calcinosis calcification; located in the renal parenchyma. Lithiasis stones; located tubules of the urinary bladder. Nephrolithiasis: white area lithiasis! (right side - mri image, fusion imaging! Twinkle artifacts: on us, decrease the gain in order to see this, also, use color doppler to, to see turbulent flow (multiple colors) Renal artery stenosis (ras: blood vessel has 3 layers, media. Inertia: adventitia, most common causes of the ras, atherosclerosis, fibromuscular dysplasia.

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Related Questions

Case-3: Patient History

P.W. is 23 years old. He was the victim of a hit-and-run auto-pedestrian accident and suffered multiple abrasions, a concussion, and a deep laceration of his left thigh. He was discovered approximately 2 hours after the incident and is now in the emergency department. P.W.’s vital signs and hematocrit suggest that he has had a blood loss of about 2500 ml. A urinary catheter is inserted to monitor urine output, and fluid resuscitation is initiated while his wounds are cleaned and sutured. The urine output is averaging 15 ml/hr, with a high urine osmolality and low urine sodium.

What type of renal failure is P.W. likely developing? (select all that apply)

Intrarenal acute renal failure
Prerenal acute renal failure
Postrenal acute renal failure

Chronic renal failure

Based on your answer for the previous question, what is the best therapy for preventing this from occurring? (select all that apply)

Adequate extracellular volume replacement with blood or isotonic fluids to ensure adequate circulating blood volume and perfusion pressure to the kidney is essential.
Antibiotic therapy should be administered immediately.
Restriction of fluid intake to prevent increase in circulating blood volume and perfusion pressure to the kidney is essential.
Dialysis should be initiated immediately.

In addition to urine output, what laboratory data should be monitored to assess changes in P.W.’s renal function? (select all that apply)

Serum BUN, creatinine, and potassium should be monitored. A decrease indicates decreased renal function.
Creatinine clearance can be measured to more accurately assess glomerular filtration rate.
Serum BUN, creatinine, and potassium should be monitored. An increase indicates decreased renal function.

Serum sodium may be useful in determining the correct IV fluid composition to administer.

If P.W.’s renal function does not return to normal, but continues to be diminished, what renal disorder might develop? (select all that apply)

He may progress to acute tubular necrosis.
He may develop renal calculi.
He may develop pyelonephritis
He may develop nephrotic syndrome

P.W. is 23 years old. He was the victim of a hit-and-run auto-pedestrian accident and suffered multiple abrasions, a concussion, and a deep laceration of his left thigh. He was discovered approximately 2 hours after the incident and is now in the emergency department. P.W.’s vital signs and hematocrit suggest that he has had a blood loss of about 2500 ml. A urinary catheter is inserted to monitor urine output, and fluid resuscitation is initiated while his wounds are cleaned and sutured. The urine output is averaging 15 ml/hr, with a high urine osmolality and low urine sodium.

Analyze this case study and answer the next four questions that follow.

Case-3: Question-4

If P.W.’s renal function does not return to normal, but continues to be diminished, what renal disorder might develop? (select all that apply)

A) He may develop nephrotic syndrome
B) He may develop renal calculi.
C) He may progress to acute tubular necrosis.
D) He may develop pyelonephritis



1. Martha’s first patient on the pediatric floor is a 12-year oldboy named Sam who is undergoing kidney dialysis treatment. Sam hasbeen on dialysis for the last week, and the treatments willprobably be discontinued because his kidneys are becoming fullyfunctional again. Martha questions Sam’s mother concerning hisillness. Three weeks ago, Sam had a sore throat, which kept himhome from school for two days but was not medically treated. Oneweek ago, Sam told his mother his urine looked red-brown and foamy.He was admitted to the hospital. Physical exam revealedcostovertebral tenderness and blood pressure of 135/90. Theurinalysis and other studies revealed the following:

Color: red-brown tinged
Specific gravity: 1.030
RBC’s: numerous RBC’s per high powered field
Protein: > 1g/24 hr
Casts: epithelial cells and RBC’s
BUN: 90 mg/dl
Creatinine: 4mg/dl
Creatine Clearance Test: 50 ml/min


a. What is your diagnosis?
i. Glomerulonephritis
ii. Cystitis
iii. Urinary obstruction
iv. Pyelitis

b. The etiology would be a(n):
i. Virus
ii. Bacteria
iii. Genetic or developmental anomaly
iv. Anatomic malfunction after birth


2. Fred suffers from chronic emphysema. His arterial blood gasresults are as follows: pH 7.30; bicarbonate 32 mEq/l; PCO2 50 mmHg. Which of the following best describe Fred’s condition?
a. Metabolic acidosis with respiratory compensation
b. Respiratory acidosis with metabolic compensation
c. Metabolic alkalosis with respiratory compensation
d. Respiratory alkalosis with metabolic compensation

3. Hypocalcaemia may develop in a patient with which of thefollowing conditions?
a. Chronic renal failure
b. Hyperparathyroidism
c. Thiazide therapy
d. Vitamin D overdose

4. Which of the following conditions would cause prerenalfailure?
a. Nephrotoxicity
b. Glomerulonephritis
c. Acute tubular necrosis
d. Hypovolemia

5. Abnormal serum laboratory findings common to patients with acuterenal failure are:
a. Increased potassium and BUN; decreased creatinine
b. Increased potassium and creatinine; decreased BUN
c. Decreased potassium; increased BUN and creatinine
d. Increased potassium, BUN and creatinine

6. In the diuretic phase of acute tubular necrosis (ATN), theclinician must be alert for which of the followingcomplications?
a. Fluid overload
b. Hypokalemia
c. Hypertension
d. Hypernatremia

7. The primary acid-base disorder associated with renal failureis:
a. Respiratory acidosis
b. Metabolic acidosis
c. Respiratory alkalosis
d. Metabolic alkalosis

8. Patients with acute renal failure may have all of the followingcomplications EXCEPT:
a. Peaked T wave EKG and pericarditis
b. Sinus tachycardia and ST elevation
c. Heart failure and Friction rub
d. Mitral insufficiency and Mobitz type II heart block

9. A patient’s glomerular filtration rate can be measure byevaluating:
a. Serum creatinine
b. Blood urea nitrogen
c. Serum osmolarity
d. Creatinine clearance

10. A patient taking medication that acts to block or inhibit theaction of aldosterone would:
a. Have high blood potassium levels
b. Have high blood sodium levels
c. Have high levels of circulating aldosterone
d. A, B, and C
e. A and C only

11. A patient exhibits the following signs and symptoms: Elevatedblood pressure, elevated blood glucose, muscle weakness, poor woundhealing, red cheeks, thin arms and legs with fat deposits in thetrunk, neck and face. The patient findings are consistentwith:
a. Addison’s Disease
b. Myxedema
c. Cushing’s disease or long-term high dose steroid use
d. Grave’s disease
e. Pheochoromocytoma

12. The MOST dramatic functional change that occurs in theendocrine system due to aging is
a. A decrease in blood and tissue concentrations of ADH andTSH
b. And overall decrease in circulating levels of mosthormones.
c. A decline in the concentration of reproductive hormones
d. And increase in the secretion of glucocortioids