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Physiology II Exam 1 > Renal Pathophysiology > Flashcards

Renal Pathophysiology Flashcards

1
Q

Acute Kidney Injury (aka Acute renal failure) results in a rapid…

A
  • reduction in GFR
  • increased retention of nitrogenous metabolic waste
  • low urine output
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2
Q

Causes of Acute Kidney Injury (Ischemia and Toxicity):
Pre-renal

A

Inadequate blood flow
- hemorrhage, heart failure, hypotension, renal atherosclerosis
- hepoxia
- necrosis

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3
Q

Causes of Acute Kidney Injury (Ischemia and Toxicity):
Intra-renal

A

Drug toxicity and infections
- aminoglycoside antibiotics –> PT –> necrosis
- tetracycline: breakdown products toxic –> liver and renal
- radiocontrast: osmotic stress, toxicity –> hypoperfusion
- sepsis: immune rx’s –> inflammation –> sclerosis or obstruction

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4
Q

tetracycline (function, damage)

A
  • breakdown products toxic
  • may lead to Fanconi syndrome (proximal tubule damage)
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5
Q

aminoglycoside antibiotics (affect, damage)

A
  • affect proximal tubules can cause necrosis
  • may lead to fanconi syndrome (proximal tubule damage)
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6
Q

Causes of Acute Kidney Injury (Ischemia and Toxicity):
Post-Renal

A

anything causing obstruction

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7
Q

Causes of Acute Kidney Injury (Ischemia and Toxicity):
Pre-renal Disease
Compensations for Renal stenosis

A

A. Baroreceptors release renin –> activate RAAS
B. Angiotension II: increase TPR and blood volume, increase BP, RBF and GFR; increase efferent arteriole resistance and GFR

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8
Q

Medications for Pre-renal disease

A

A. Medications (AngII blockers and NSAIDs)
i. ACE inhibition –> eliminates compensation for renal stenosis
ii. NSAIDs: inhibit afferent vasodilatory prostaglandins; limiting O2 delivery to nephrons; elderly are especially vulnerable

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9
Q

Intra-renal disease sources of damage

A

Extrinsic sources:
A. environmental toxins: lead and cadmium: proximal tubule toxicity
B. bacterial infections –> inflammation and sclerosis
Intrinsic sources:
A. high blood pressure –> glomerulosclerosis
B. hypercholesterolemia –> renal stenosis
C. auto-immune diseases attack portions of nephron

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10
Q

mechanism of lead and cadmium toxicity

A

ii. Pb decreases GFR and inhibits uric acid secretion which leads to gout
iii. Cd decreases ATP, Na/K/ATPase, endocytosis (small filter proteins end up in urine
iv. Pd and Cd cause tubular fibrosis

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11
Q

Post-renal diseases: obstructions
Concerns and causes

A

A. Volume and pressure overload may lead to hydronephrosis
Causes:
A. kidney stones
B. prostatic enlargement
C. cancer, stricture, incompetent valves

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12
Q

Pathophysiology of Acute Kidney Injury –> acute tubular necrosis (cell death)
Two causes

A
  1. inadequate perfusion/hypoxia –> death (necrosis) –> sloughing of renal tubular epithelial cells in proximal tubule and thick ascending limb LOH
  2. Occlusion of tubular lumen may occur due to dead cells clumping or sloughing off. leads to: a) reduced GFR due to intratubular obstruction and b) leakage of fluid back into interstitium
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13
Q

Recovery from Acute Kidney Injury and Acute Tubular Necrosis

A
  1. regeneration of tubular cells
  2. treatment is supportive i.e. dialysis
    a) is ischemic corrected, the return of GFR to normal can take 3-21 days
    b) recovery does not occur or is incomplete, resulting in chronic kidney disease
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14
Q

Diseases that may cause chronic kidney disease:

A
  1. diabetes mellitus
  2. hypertension
    presence of CKD in either disease greatly increases the risk of dying from ischemic cardiovascular disease
    dental patients with CKD are also at high risk for an acute cardiac event
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15
Q

CKD treatment: major renal protective strategy

A

rigorous blood pressure should be maintained with RAAS inhibitors

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16
Q

CKD treatment: patients without hypertension but have microalbuminuria

A

should be placed on anti-RAAS therapy to reduce proteinuria

17
Q

CKD treatment: if diabetes is present,

A

controlled blood glucose levels is renal-protective

18
Q

CKD treatment: other renal protective strategies include

A
  • statin therapy (control of dyslipidemia)
  • smoking cessation
  • reducing protein intake
19
Q

Clinical symptoms of severe chronic kidney disease

A

a. volume overload
b. hyperkalemia
c. metabolic acidosis
d. hyperphosphatemia
e. systemic hypertension
f. anemia
g. dyslipidemia
h. sexual dysfunction

20
Q

Contraindications in CKD patients

A

a. GFR is significantly reduced and tubular metabolism altered which reduces the rate of clearance for many drugs
1. drug types: avoid penicillin formulations with potassium salts to increase half-life of antibiotic
2. drug types: tetracycline antibiotics are nephrotoxic and are contraindicated

21
Q

Proteinuria (protein in urine)

A

small amounts of protein in healthy individual urine but a dipstick does not pick it up. however, if the protein can be detectable on dipstick, it is a sign of renal dysfunction

22
Q

Proteinuria promotes

A

tubular and interstitial inflammation leading to ischemia and fibrosis –> loss of function

23
Q

excessive loss of plasma protein in urine can lead to

A

hypoalbuminemia which can result in peripheral edema (Decreased oncotic pressure)

24
Q

Glomerular Proteinuria

A

appearance of excessive amounts of medium to large plasma proteins in urine is strongly suggestive of a change in function of glomerular barrier. change in fxn may be:
a. physiologic or pathologic
b. transient or permanent
c. if barrier compromised, it will result in loss of massive quantities of plasma protein

25
Q

Tubular Proteinuria

A

a. much of filtered proteins are reabsorbed in proximal tubule by endocytosis
b. if endocytotic process impaired, then lots of excretion of beta-2 microglobulin and albumin

26
Q

a small freely filtered plasma protein typically measured in urine is

A

beta-2 microglobulin

27
Q

overflow proteinuria

A

excessive excretion of proteins occur bc the production/filtration of protein exceeds the ability of the proximal tubule to reabsorb it.

28
Q

causes of overflow proteinuria

A

a. excessive production of immunoglobulin light chains in multiple myeloma can cause overflow proteinuria
b. rhabdomyolysis (myoglobin) and red cell lysis can cause overflow proteinuria
c. they all damage the renal tubule cells over time

29
Q

Exercise proteinuria

A

strenuous exercise leads to a transient increase in protein excretion. exercise proteinuria typically resolves within several hours
i. can be both tubular and glomerular, depending on intensity and duration of exercise

30
Q

Orthostatic proteinuria

A

assumption of an upright position increases protein excretion. nighttime or recumbent protein excretion is normal

31
Q

Microalbuminuria indicates

A

vascular dysfunction and is a risk factor for increased cardiovascular morbidity and mortality, especially in patients with pre-existing diabetes and hypertension

32
Q

non-nephrotic proteinuria

A

would be detected with the typical protein dipstick screening tool. an ACR > 30 mg/mmol is considered clinically significant proteinuria in adults without diabetes

33
Q

Urge incontinence

A

a condition of detrusor muscle over-activity (bladder contractions); muscarinic blockade (anticholinergic medications) are used to reduce detrusor over-activity

34
Q

Stress incontinence

A

happens with actions that increase intra-abdominal pressure such as sneezing, coughing, and physical activity. the sphincter has issue staying closed due to the pressure.

35
Q

Overflow incontinence

A

inability to completely empty bladder due to poor detrusor muscle constractility or underactivity. often associated with bladder outlet obstruction. could be a side effect of anti-muscarinic therapy

36
Q

Incontinence due to transient or reversible conditions

A
  • excessive urine production
  • urinary tract infection
  • impaired mobility or cognition
  • medication side effect
37
Q

diabetes insipidus

A

excessive thirst and urination caused by disorders in salt and water metabolism

38
Q

central diabetes insipidus

A

caused by decreased production or release of ADH from pituitary gland (stroke, tumor, drug-induced, genetic)
results in water loss and stimulates thirst and water intake

Physiology II Exam 1 (2 decks)

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