Systemic Disease Midterm 2

Front 1

The juxtaglomerular cells are part of which: the afferent or efferent arteriole of the glomerulus?

Back 1

Afferent - the arteriole that supplies the glomerulus.

Front 2

List the key anatomical distinctions of the nephron in the direction of filtrate flow.

Back 2

Glomerulus, Proximal Tubule, Loop of Henle, Distal Tubule, Collecting Duct

Front 3

What are the 2 main mechanisms that maintain water balance?

Back 3

1)Structure/transport properties of nephron 2)Anti-Diuretic Hormone

Front 4

What 3 major factors control passage through the glomerulus?

Back 4

Size, Charge, and Configuration of substance. Negatively charged substances are repelled and stay in the blood.

Front 5

What should not be in the filtrate? (only looking for 1 word)

Back 5

Protein

Front 6

What makes up the filtrate? (looking for 5 things)

Back 6

Water, ions, glucose, amino acids, sodium bicarbonate

Front 7

There are cells that sample the osmolarity of the filtrate and control the release of renin. Name them and what part of the nephron are they in?

Back 7

Macula Densa cells, Distal Convoluted Tubule

Front 8

What is the function of ADH and what secretes it?

Back 8

Anti-Diuretic Hormone increases water reabsorption, it is secreted by the pituitary.

Front 9

What are the 2 major stimuli to secretion of ADH? Explain each.

Back 9

1)Low BP. Body wants to retain water to increase BP, and ADH will cause body to retain water. 2)Incread blood osmolarity. Blood needs more water blah blah blah ADH.

Front 10

If the Macula Densa cells sense a decrease in filtrate osmolarity, do they want to increase or decrease the rate of filtration?

Back 10

Increase. If the filtrate is traveling too slowly, too many ions are re-absorbed in the Proximal Tubule and Ascending loop of Henle. This results in low osmolarity of the filtrate that passes by the MD cells.

Front 11

The reabsorption of salt in the proximal tubule is controlled by what hormone?

Back 11

Angiotensin II, a hormone that is created in response to renin release.

Front 12

What hormone lowers BP, and by what mechanisms?

Back 12

Prostaglandins. Mechanims: block ADH in collecting duct, prevents water and sodium reabsorption, and prevents potassium excretion.

Front 13

How do NSAIDS and steroids affect urine production?

Back 13

They interfere with PGs, which normally act as a diuretic. Thus they cause water retenion resulting in increased BP and edema. BAD

Front 14

How does an increase in renin affect blood pressure?

Back 14

Increases it. It starts a cascade that produces Angiotensin II causing more salt and water to be re-absorbed in the proximal tubule. It also stimulates THIRST.

Front 15

How does the kidney maintain the pH of the blood?

Back 15

Regeneration of bicarbonate, excretion of hydrogen ions when blood too acidic, exretion of bicarbonate ions when blood to alkaline.

Front 16

What does the kidney release in response to low oxygen levels, and what does it do?

Back 16

Erythropoietin, which stimulates bone marrow to produce RBCs.

Front 17

How do the kidneys affect blood calcium levels?

Back 17

They are where calcitriol is produced via conversion from calcidiol. Calcitriol increases absorption of calcium from the intestine.

Front 18

What is the normal glomerular filtration rate?

Back 18

125 mL/min. The test to measure this is complex and NOT routinely done. It involves patient consuming a substance (inulin) and then collecting timed urine samples.

Front 19

Talk to me about creatine clearance test.

Back 19

This is a urine test. Normal is about 100mL/minute. Less than 60mL/minute is a significant indicator of kidney disease. It is filtered by kidney but not reabsorbed by the tubules.

Front 20

Talk to me about serum creatine test.

Back 20

This is a blood test. Normal is 1mg/100mL of serum. If value doubles, kidney function is 50% of normal. If value triples, kidney function is 25% of normal.

Front 21

Talk to me about urea (BUN) test.

Back 21

Blood test. Normal levels are 7-20mg/dL. Levels increase with decreasing kidney function.

Front 22

Talk about ion levels and if they go up or down with kidney failure.

Back 22

With failure:
Up - potassium and phosphate
Down - bicarbonate, pH, calcium

Front 23

What percentage of US adults have some kind of chronic kidney disease?

Back 23

4-16%

Front 24

How does hypertension influence kidney failure?

Back 24

It can cause it, which in turn causes increased hypertension, etc...
The 2nd most common cause of chronic kidney failure.

Front 25

What percentage of kidney function must be lost before signs and symptoms present?

Back 25

80-90%. This indicates that the kidneys have a lot of reserve.

Front 26

What are some common symptoms of kidney disease?

Back 26

High BP, swelling of legs, pulmonary edema, fatigue, headaches, weight loss, itching, increased tendency to bleed.

Front 27

What systemic disease is most commonly diagnosed because of anyridia?

Back 27

Wilm's

Front 28

What are some ocular symptoms of renal disease?

Back 28

eyelid edema, calcium deposits on lids or conj, uveitis, macular drusen, retinal changes

Front 29

What distinguishes renal failure from renal disease?

Back 29

Patients with renal failure must have medical intervention to survive.

Front 30

What ethnic group is predisposed to renal disease?

Back 30

People of african descent are 8 times more likely to get it.

Front 31

What are some common sytemic diseases that can cause kidney disease?

Back 31

Diabetes, hypertension, glomerulonephritis, collagen vascular disease, systemic lupus.

Front 32

What systemic conditions have ocular and renal effects?

Back 32

Diabetes, hyptertension, TINU syndrome, MPGN, Von Hippel-Lindau, Wilm's.

Front 33

What is Azotemia?

Back 33

An abrupt decrease in renal function that leads to retention of nitrogenous waste products in the body over a few days.

Front 34

If a patient survives an acute episode of Azotemia, what is the percentage chance that full kidney function will be restored?

Back 34

90%

Front 35

What 3 kidney functions are lost in Azotemia?

Back 35

Regulatory, excretatory, and endocrine.

Front 36

What is the common mechanism in acute PRE-renal failure?

Back 36

Reduced blood flow to the kidneys. Examples include burns, hemorrhage, heart failure, diarrhea/vomiting, thromboemboli, etc...

Front 37

What are the three major components that are affected by Intrinsic Acute Renal failure?

Back 37

Vessels (malignant HTN, vasculitis), Glomerulus (infections, immune-mediated), Tubular (toxicity)

Front 38

What is the most likely form of acute renal failure to be caused by optometric drug Rx? (be specific)

Back 38

Intrinsic, specifically vasculitis.

Front 39

What is the most common cause of intrinsic acute renal failure, and what is the mechanism?

Back 39

Acute Tubular Necrosis. The epithelial cells in the tubules are destroyed, so ions are not reabsorbed. The macula densa cells then send the signal to slow the flow rate, and the problem is made worse. Urine volume decreases and waste products accumulate in blood.

Front 40

Define pre-, intrinsic, and post-renal kidney failure.

Back 40

Pre-renal is a result of decreased blood flow to the kidney. The kidney itself is fine. Intrinsic renal failure is a result of a problem with the kidney itself, and can be associated with the tubules, the glomerulus, or the vessels. Post-renal kidney failure is caused by an bladder outlet obstruction.

Front 41

What are the characteristics of the most common intrinsic cause of acute renal failure?

Back 41

(Acute Tubular Necrosis) It occurs as a result of acute ischemic or nephrotoxic insult. The tubular epithelial cells are destoyed, which release endothelin and cause vasocontriction of afferent arteriole. Thus blood flow into the kidney is reduced, urine volume is reduced, and waste products in blood increase.

Front 42

What conditions lead to Acute Tubular Necrosis?

Back 42

Acute ischemia or nephrotoxic insult.

Front 43

What are the mortality rates for the different causes of acute tubular necrosis?

Back 43

Surgery/Trauma - 60%
Medical Illness - 30%
Pregnancy - 10-15%

Front 44

What are the characteristics and pathophysiology of malignant HTN?

Back 44

Characteristics: Diastolic BP >120, optic nerve head edema, encephalopathy, CV abnormalities, renal failure.
Pathophysiology: vascular damage to kidneys, increased permeability of small vessels, which causes fibrosis and narrowing of vessel lumen, resulting in ischemia to the kidney, also causing the release of renin, causing further vasoconstriction.