Translational Physiology Block 4

Question 1

What are lab tests to diagnose kidney diseases?

Answer 1

Clinician should estimate GFR by using the Modification of Diet in Renal Disease (MDRD) (serum creatinine, age, gender, and race taken into consideration); presences of abluminuria or proteinuria (damage to filtration barrier); finally renal ultrasound

Question 2

What is estimated GFR proportional to?

Answer 2

the number of functioning nephrons

Question 3

What of the stages of kidney disease?

Answer 3

Stage 1 GFR 90 mL/min/1.73 m2, with signs of kidney damage
Stage 2 GFR 60–89 mL/min/1.73 m2, with signs of kidney damage
Stage 3 GFR 30–59 mL/min/1.73 m2
Stage 4 GFR 15–29 mL/min/1.73 m2
Stage 5 GFR 15 mL/min/1.73 m2

Question 4

Do the kidneys appear abnormal on renal ultrasound following acute tubular necrosis or acute injury associated with hypovolemia? what about in chronic kidney disease?

Answer 4

No;yes: kidney is smaller, cortex is thinned, and hyperechoic (scar tissue; glomerular sclerosis); decreases glomerular capillary surface area

Question 5

What are the “consequences” of acute kidney injury?

Answer 5

Loss of kidney function in AKI results in accumulation of nitrogenous wastes in body fluids (azotemia) that would otherwise by excreted. The most commonly used markers of AKI are serum creatinine and blood urine nitrogen (BUN), which are both elevated; uremic toxins can cause multiple organ dysfunction (uremia)

Question 6

What is a patients’ prognosis following AKI?

Answer 6

rather poor (high mortality): some regain complete renal function; others develop chronic kidney disease; some patients may have progression of pre-existing CKD; some may evolve end-stage renal disease

Question 7

What is a pre-renal etiology of AKI?

Answer 7

hypovolemia, decreases cardiac output, and decreased effective circulating volume (pre-existing conditions: congestive heart failure or liver failure) impaired renal autoregulation (patients on NSAIDs or ACE inhibitors)

Question 8

What are intrinsic AKI etiologies?

Answer 8

acute glomerular nephritis and glomerular vasculitis (infection) or acute tubular necrosis (ischemia)

Question 9

What are postrenal AKI etiologies?

Answer 9

bladder obstruction

Question 10

What are signs and symptoms of acute tubular necrosis?

Answer 10

granular casts in urine and kidney biopsy; Oliguria (decreased urine flow; less than 400 mL) is a poor prognostic sign in acute kidney injury, correlating with high mortality or less recovery of renal function compared to nonoliguric patients.

Question 11

What is acute interstitial nephritis?

Answer 11

presence of inflammatory infiltrates and edema with the interstitium (Bowman’s space); commonly caused by antimicrobials and NSAIDs

Question 12

What are treatment options for acute kidney injury?

Answer 12

conservative- repletion of extracellular fluid volume, correction of heart failure
acute hemodialysis (unstable and needs to be applied intermittently)
continuous renal replacement therapy (precise control of volume, uremia, plus acid/base and electrolyte disorders)

Question 13

What are risk factors for CKD?

Answer 13

diabetes and hypertension

Question 14

Describe CKD progression.

Answer 14

Progressive proteinuria and damage to glomerular capillaries (increased glomerular capillary pressure increases ultrafiltration and GFR); increased glomerular capillary permeability destroys glomerular tissue

Question 15

In CKD, why does GFR fall?

Answer 15

loss of capillary surface area

Question 16

What are treatment options for CKD?

Answer 16

hemodialysis, peritoneal dialysis, and kidney transpant

Question 17

What are signs and symptoms of untreated hypertension?

Answer 17

systolic and diastolic dysfunction; decreases RPF and GFR

Question 18

What is anuria?

Answer 18

less than 50 ml of urine output in 24 hours

Question 19

What is hypovolemia? why does it occur?

Answer 19

isotonic fluid loss from ECF; lost from GI, kidney, skin, or through trauma (cholera)

Question 20

How do you treat hypovolemia?

Answer 20

IV isotonic saline

Question 21

How do you diagnose hypovolemia?

Answer 21

increased heart rate, dizziness (lack of perfusion to CNS); orthostatic hypotension (poor prognosis associates with hypotension at rest); anuria or oliguria; poor skin turgor

Question 22

describe volume contraction in diarrhea, water deprivation, and adrenal insufficiency.

Answer 22

diarrhea: loss of ECF (no osmolality change); water deprivation: decreased volume in ECF and ICF (increased osmolality in both); adrenal insufficiency: osmolality of both decreases and increased fluid in ICF

Question 23

describe volume expansion with infusion of NaCl, increased NaCl intake, and SIADH

Answer 23

infusion: increase ECF (no change in osmolality); NaCl intake: increased ECF fluid (increased osmolality); increased ICF and ECF (decreased osmolality)

Question 24

What is a cause of edema?

Answer 24

increased hydrostatic pressure (increased sodium content in blood)

Question 25

how do you treat edema?

Answer 25

diuretics and salt diet restriction

Question 26

How does hyponatremia affect the CNS? hypernatremia?

Answer 26

swelling; shrinking

Question 27

What is stage 1 hypertension? stage 2?

Answer 27

above 140; above 160

Question 28

What is the pathogenesis of hypertension?

Answer 28

increased afterload and arterial damage (blockage)

Question 29

How does the kidney modulate blood pressure?

Answer 29

excretion or reabsorption of sodium

Question 30

What is the suggested mechanism for primary hypertension?

Answer 30

increased total peripheral resistance with normal cardiac output

Question 31

Is hypertension influenced by genetic or environmental factors?

Answer 31

both

Question 32

What are causes of secondary hypertension?

Answer 32

pheochromocytoma, oral contraceptives, primary hyperaldosteronism (aberrant renin-angiotensin-aldosterone or RAAS)

Question 33

describe the pathogenesis of secondary hypertension with renal artery stenosis.

Answer 33

decrease renal perfusion and decreases GFR increase ang II which vasoconstricts (raises GFR) and increases production of aldosterone leading to hypertension

Question 34

Why can severe volume depletion cause hyponatremia?

Answer 34

non-osmotic release of AVP

Question 35

What do NSAIDs do?

Answer 35

Block Cox-1 and production of prostaglandins

Question 36

What is osmotic diuresis? how does it compare to water diuresis?

Answer 36

when poorly permeable substances are present in plasma (sucrose or mannitol) or with diabetes mellitus patientas (untreated); mechanism: mannitol holds water in the lumen producing diuresis; rich in solutes

Question 37

Why would a physician treat a patient with mannitol?

Answer 37

increased ICPs and reduces risk of radiocontrast-induced renal disease

Question 38

Describe micturition following combined afferent and efferent lesions.

Answer 38

bladder distended and flaccid (residual urine remains)

Question 39

Describe micturition following an afferent lesion.

Answer 39

less severe to combined lesions (still have distension and reduced tone and residual urine remains); however, some residual contractions

Question 40

Describe micturition following spinal cord lesion.

Answer 40

first, overfilling and sporadic voiding (must be catheterized); later decreased capacity and loss of voluntary control (increased incidence of UTIs)

Question 41

What are hyperaminoacidurias? what is the cause of hyperargininemia?

Answer 41

increased excretion of amino acids; metabolic defect that increases plasma arginine levels

Question 42

Do amino acids compete for transporters?

Answer 42

Yes

Question 43

What are renal aminoacidurias? Hartnup disease? cystinuria? lysinic protein intolerance? Fanconi syndrome? kidney stones?

Answer 43

defective transporters; neutral amino acids (alanine serine, phenylalanine, tryptophan, and tyrosine); defect in transporter for cysteine, arginine, lysine, and ornithine); lysine and arginine (impairs urea cycle); loss of proximal tubule function; cystine excretion

Question 44

How does hyperkalemia effect ECG? hypokalamia?

Answer 44

t wave tented and PR interval prolonged (further hyperkalamia: P wave indiscernible and QRS complex prolonged; possible ventricular fibrillation) hypo: flatten T wave merges with a U wave

Question 45

What is central diabetes insipidus? nephrogenic? treatment for central DI? nephrogenic? signs?

Answer 45

failure of AVP secretion; poor kidney response to AVP (electrolyte abnormalities, familial, or idiopathic); desmopressin acetate (AVP analogue); diuretic; polydipsia and polyuria

Question 46

Where are AQP2 channels? are they subject to AVP? AQP3 and 4?

Answer 46

apical collecting duct (yes); basolateral (no)

Question 47

What is SIADH? causes? treatment?

Answer 47

high secretion of AVP; tumor, cranial disorders, pulmonary disorders, and drugs (phenothiazines, chlorpropamide, and carbamezepine); fluid restriction (sometimes infusion of hypertonic saline)

Question 48

Does sodium excretion increase or decrease in renal failure?

Answer 48

decreases

Question 49

Where does fluid accumulate in situations of edema?

Answer 49

liver (ascites) and lungs (pleural effusion); may be local malfunction of veins

Question 50

What are causes of excessive sodium excretion?

Answer 50

diuretics, proximal tubular acidosis and recovery from AKI

Question 51

Describe renal hypertension. what causes it?

Answer 51

Clipping the renal artery (reducing perfusion pressure distally) increases the synthesis and secretion of renin; angiotensin II and ACE in the general circulation decreases within a few days but stays elevated in the kidney and aldosterone (systemic arterial pressure remains high); cause: renal hypertension results from stenosis of the renal artery (arteriosclerotic thickening of the vessel wall), constriction of the aorta below the head and upper extremities, and from inflammatory or fibrotic lesions which stenose the preglomerular arteries or arterioles (most common)