Translational Physiology Block 4 Flashcards Preview

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Flashcards in Translational Physiology Block 4 Deck (51):
1

What are lab tests to diagnose kidney diseases?

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

2

What is estimated GFR proportional to?

the number of functioning nephrons

3

What of the stages of kidney disease?

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

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?

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

5

What are the "consequences" of acute kidney injury?

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)

6

What is a patients' prognosis following AKI?

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

7

What is a pre-renal etiology of AKI?

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)

8

What are intrinsic AKI etiologies?

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

9

What are postrenal AKI etiologies?

bladder obstruction

10

What are signs and symptoms of acute tubular necrosis?

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.

11

What is acute interstitial nephritis?

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

12

What are treatment options for acute kidney injury?

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)

13

What are risk factors for CKD?

diabetes and hypertension

14

Describe CKD progression.

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

15

In CKD, why does GFR fall?

loss of capillary surface area

16

What are treatment options for CKD?

hemodialysis, peritoneal dialysis, and kidney transpant

17

What are signs and symptoms of untreated hypertension?

systolic and diastolic dysfunction; decreases RPF and GFR

18

What is anuria?

less than 50 ml of urine output in 24 hours

19

What is hypovolemia? why does it occur?

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

20

How do you treat hypovolemia?

IV isotonic saline

21

How do you diagnose hypovolemia?

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

22

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

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

23

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

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

24

What is a cause of edema?

increased hydrostatic pressure (increased sodium content in blood)

25

how do you treat edema?

diuretics and salt diet restriction

26

How does hyponatremia affect the CNS? hypernatremia?

swelling; shrinking

27

What is stage 1 hypertension? stage 2?

above 140; above 160

28

What is the pathogenesis of hypertension?

increased afterload and arterial damage (blockage)

29

How does the kidney modulate blood pressure?

excretion or reabsorption of sodium

30

What is the suggested mechanism for primary hypertension?

increased total peripheral resistance with normal cardiac output

31

Is hypertension influenced by genetic or environmental factors?

both

32

What are causes of secondary hypertension?

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

33

describe the pathogenesis of secondary hypertension with renal artery stenosis.

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

34

Why can severe volume depletion cause hyponatremia?

non-osmotic release of AVP

35

What do NSAIDs do?

Block Cox-1 and production of prostaglandins

36

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

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

37

Why would a physician treat a patient with mannitol?

increased ICPs and reduces risk of radiocontrast-induced renal disease

38

Describe micturition following combined afferent and efferent lesions.

bladder distended and flaccid (residual urine remains)

39

Describe micturition following an afferent lesion.

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

40

Describe micturition following spinal cord lesion.

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

41

What are hyperaminoacidurias? what is the cause of hyperargininemia?

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

42

Do amino acids compete for transporters?

Yes

43

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

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

44

How does hyperkalemia effect ECG? hypokalamia?

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

45

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

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

46

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

apical collecting duct (yes); basolateral (no)

47

What is SIADH? causes? treatment?

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

48

Does sodium excretion increase or decrease in renal failure?

decreases

49

Where does fluid accumulate in situations of edema?

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

50

What are causes of excessive sodium excretion?

diuretics, proximal tubular acidosis and recovery from AKI

51

Describe renal hypertension. what causes it?

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)