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N552 Patho > Renal > Flashcards

Renal Flashcards

0
Q

Filtration: glomerulus to ______
Reabsorption: _____ to peritubular capillary
Secretion: peritubular capillary to _____
Excretion: to collecting duct, ureter

A

Filtration: glomerulus to prox. convoluted tubule
Reabsorption: lumen of tubule to peritubular capillary (vasa recta)
Secretion: peritubular capillary to tubule
Excretion: to collecting duct, ureter

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1
Q

What do the kidneys do?

A 
Remove waste/toxins from blood
Maintain proper water and electrolyte balance
Maintain proper pH of blood
Secrete EPO
Activate vitamin D
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2
Q

What is reabsorbed in the proximal tubule?

A

Mostly amino acids, protein, and glucose (that’s why hyperglycemia damages kidneys)
Also some bicarb

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3
Q

What is reabsorbed in the loop of henle?

A

Cl, K, Na and some bicarb

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4
Q

What is not reabsorbed in the proximal tubule, loop of henle, distal tubule, or collecting tubule, then excreted?

A

Urea and creatinine

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5
Q

What mechanisms are involved in tubuloglomerular feedback?

A

Baroreceptor mech: dec pressure promotes renin release, inc pressure inhibits renin
Sympathetic nerve mech: B1 stimulates renin
Macula densa mech: inc NaCl in distal renin inhibits renin, dec load promotes renin release

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6
Q

Normally, all filtered glucose is reabsorbed in the proximal tubule by ____ transporter

A

SGLT2

Can be overwhelmed by hyperglycemia

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7
Q

Bicarb is not directly reabsorbed across the renal epithelium, it combines with H in the tubule to form H2CO3, which dissociates to CO2 and water. What catalyzes this reaction?

A

Carbonic anhydrase catalyzes this reaction.

Then it catalyzes the reverse reaction as well so that bicarb can be transported out through the basolateral membrane

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8
Q

How do the kidneys compensate for high/low PaCO2?

A

When PaCO2 is high (acidosis), kidneys excrete more H (with NH3 and HPO4) and create new HCO3 by glutamine metabolism
When PaCO2 is low (alkalosis), kidneys compensate by excreting HCO3

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9
Q

Na-K pump is regulated by ____

A

Aldosterone. The more aldosterone, the more it can pump.

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10
Q

Acidosis can lead to _____kalemia, what exchanger contributes to this?

A

HYPERkalemia

H-K exchanger contributes (as it slows, we hold on to less H, but then the K isn’t being dumped in the urine either)

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11
Q

Insufficiency of ADH can be secondary to ____ damage, resulting in diabetes insipidus

A

Pituitary damage

Large volumes of dilute urine excreted leading to severe fluid and electrolyte imbalance

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12
Q

What 3 factors can cause renin release?

A

Decreased blood flow to kidneys
Reduced serum Na
Activation of sympathetic nerves to juxtaglomerular cells

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13
Q

What causes natriuretic peptide to be released and what does this result in?

A

Atrial cells in the heart are overstretched by excessive blood volume
Inhibits angiotensin II action and results in loss of Na and water in the urine

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14
Q

What causes urodilatin to be released and what does this result in?

A

Distal and collecting tubule cells identify increased volume (similar to natriuretic peptide)
Inhibits Na and water reabsorbtion

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15
Q

How do osmotic diuretics work?

A

Increase osmolality of the filtrate causing more water to remain in the tubule, which is excreted
K wasting

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16
Q

How do loop diuretics work?

A

Blocks the Na-K-Cl pumps in the ascending loop of henle

K wasting

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17
Q

What do thiazide diuretics block?

A

Na reabsorption

K wasting

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18
Q

Which diuretics are K sparing?

A

Aldosterone-blocking agents

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19
Q

Casts aggregate and form in the nephron and get excreted in the urine.
WBC casts are associated with ___ infection
RBC casts indicate _____
Epithelial cell casts indicate _____

A

WBC casts associated with renal infection (pyelonephritis)
RBC casts indicate inflammation of glomerulus (glomerulonephritis)
Epithelial cell casts indicate sloughing of tubular cells (acute tubular necrosis)

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20
Q

What two factors affect creatinine level?

A

Rate of creatinine produced from muscle (constant in absence of muscle breakdown)
Rate of creatinine excreted by kidney, determined by GFR

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21
Q

Elevated BUN indicates what?

A

Decrease in renal function/fluid volume

Increase in catabolism and dietary protein intake

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22
Q

What is more accurate for determining GFR, creatinine clearance or inulin clearance?

A

Inulin clearance is a more accurate measurement of GFR

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23
Q

Azotemia vs. Uremia?

A

Azotemia: elevated BUN and creatinine, decreased GFR
Uremia: elevated urea in blood
Azotemia can progres to uremia

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24
Where do people feel pain with internal disorders?
T10-L1 dermatomes, usually felt at costovertebral angle, CVA tenderness/ flank pain Dull, constant pain due to inflammation of kidneys
25
Congenital Renal abnormality: Agenesis
Kidneys don't develop in fetus | If bilateral, not compatible with life
26
Congenital Renal abnormality: Hypoplasia
Some fetal kidney development, can lead to pediatric ESRF
28
Congenital Renal abnormality: Cystic kidney disease. How is it transmitted? What is it? What is the treatment?
``` Genetically transmitted (autosomal dominant/adult and recessive/kid types), results in fluid-filled renal cysts that can disrupt urine formation/flow. Reduced Ca and excessive cAMP. Dec GFR Can lead to renal failure, requiring dialysis or transplantation ```
29
PKD1 (chromosome 16) vs. PKD2 (chromosome 4)
PKD1 supports Ca channels, lets Ca do its job, when damaged, dec calcium and ability to concentrate urine (85% cystic kidney disease affects this) PKD2 codes for Ca channel itself
30
Congenital Renal abnormality: Cystic kidney disease. What are clinical manifestations? How is it diagnosed?
Hypertension Pain Concomitant cystic liver involvement Diagnosed with genetic history and ultrasound
31
Renal cell carcinoma: what is it, what are symptoms?
Metastatic disease (clear cell) of the cortex, PCT Asymptomatic until advanced then symptoms are CVA tenderness, hematuria, palpable mass Hard to treat, resistant to radiation/chemo
32
What protects infection of the kidney?
``` Acidic pH Urea in urine Men: bacteriostatic prostate secretions Women: glands in urethra secrete mucus Micturition (washes out pathogens, prevents reflux) ```
33
Acute pyelonephritis? Diagnosis?
Infection of renal pelvis/parenchyma usually from UTI Can cause urosepsis (UTI organisms getting to the bloodstream) Diagnose with WBC casts
34
Chronic pyelonephritis: what is it?
Can result in chronic kidney disease, usually associated with reflux/obstructive process causing urine stasis Chronic inflammation leads to scarring and loss of functional nephrons
35
Chronic pyelonephritis: symptoms, diagnosis?
Symptoms: abdominal/flank pain, fever, malaise, anorexia | Diagnose with renal imaging
36
What can cause obstruction?
Stones Tumors Prostatic hypertrophy Stricture of ureters or urethra
37
What can the obstructive process cause?
Urine stasis leading to infection and structural damage Dilation of the tract proximally Complete obstruction results in hydronephrosis, dec GFR, ischemic kidney damage because of inc intraluminal pressure, ATN, CKD
38
What can renal calculi be made of?
Usually composed of Ca crystals, can also be uric acid, struvite, or cystine
39
Primary vs. secondary glomerular disorder?
Primary: only the kidney is involved Secondary: results from other diseases/meds. Ex: Goodpasture, SLE, diabetic nephropathy
40
What part of the glomerulus does SLE affect? Goodpasture syndrome?
SLE affects mesangial cells (antigen-antibody complex deposits here, our body attacks it) Goodpasture affects the basement membrane (antibody binds and releases inflammatory signals, leads to fibrosis)
41
What is the classic clinical manifestation of glomerular disorders? What else can occur?
Classic sign: proteinuria | Others: abnormal casts, dec GFR, edema, HTN
42
Nephrotic syndrome vs. nephritic syndrome?
Nephrotic: protein loss over 3g/24h, due to inc glomerular permeability to proteins, edema, associated with minimal change disease, SLE, DM, treat with diuretics, lipid-lowering ages, antiHTN meds, immunosuppressants Nephritic: mild-moderate proteinuria with hematuria and RBC casts present
43
What is minimal change disease? Symptoms? Treatment?
Lipoid nephrosis, alteration in glomerular podocytes, dec production of anions in GBM, occurs in children, initiated by immune condition, dec GFR Sudden onset of edema, protein loss, hypoalbuminemia, responds to corticosteroids
44
Acute glomerulonephritis: patho, s/s, treatment?
Immune cells attracted to inflamed area, results in degradation of basement membrane, GFR dec due to contraction of mesangial cells S/S: proteinuria, oliguria, azotemia, edema, HTN Treatment: steroids, plasmapheresis, fluids, manage HTN
45
How does post-infectious acute glomerulonephritis work?
Antigen binds to antibody-antigen disposition (IgG), mesangial cells proliferate, autoimmune reaction Impetigo (skin), throat infections, due to group A beta-hemolytic streptococci Smoky/coffee-colored urine More common in children
46
What is Berger disease/ IgA nephropathy (acute glomerulonephritis)
``` More common in adults Upper respiratory or GI virus, complex leads to mesangial injury Hematuria in 1-2 days NO proteinuria, edema, or HTN May progress to ESRD ```
47
Chronic glomerulonephritis: what is it? S/S? Treatment?
Progressive course developing into ESRD, causes sclerosis and fibrosis of kidney S/S: proteinuria with/without hematuria, slow declining renal function Tx: dialysis or kidney transplant
48
ARF is not a disease, but a final pathway of different disease processes, what can it cause? It can be pre-renal, intra-renal, or post-renal
Disruption in fluid, electrolyte, acid-base balance Retention of nitrogenous waste product Inc serum creatinine Dec GFR
49
How does BUN: creatinine ratio tell us if there is a problem pre-renal, intra-renal, or post-renal?
Over 20: pre-renal ARF, dec filtration Under 10: intra-renal ARF, tubules fail to reabsorb less urea 10-20: post-renal ARF, urea and creatinine are BOTH effected
50
What are causes of pre-renal? Symptoms?
Causes: diminished perfusion (hypovolemia, hypotension, HF, renal artery obstruction, fever, vomiting, diarrhea, burns, overuse of diuretics, edema, ascites, drugs: ACEI, ARB, NSAIDs) S/S: low GFR causes oliguria, high urine sp gravity, low urine Na, azotemia Treat with volume replacement, dialysis
51
Prolong pre/post/intra-renal ARF can lead to what?
ATN
52
What happens in the early phase (12-24 hours) of post-renal ARF?
Reflex adaptation to maintain GFR, despite rising tubular hydrostatic pressure Afferent arteriolar dilation to enhance glomerular perfusion
53
What happens in the late phase (after the 12-24 hours) of post-renal ARF?
Afferent vasodilation ceases Progressive fall in renal perfusion: glomerular blood flow and GFR drop which may result in anuria, ischemia, and nephron loss
54
What happens in the recovery phase (after relief of the urinary obstruction) of post-renal ARF?
Pre-renal vessels relax, perfusion is restored GFR increases in the nephrons that survived Tubular pressure returns to normal Dilation of calyces and collecting system may be permanent
55
What are the two ATN causes in intra-renal ARF?
1. Nephrotoxic insult (contrast) | 2. Ischemic insults (sepsis)
56
What are the 2 pathophysiological processes of intrarenal ARF?
Vascular: renal blood flow decreased; hypoxia; vasoconstriction Tubular: inflammation and reperfusion injury, causes casts, obstructs urine flow, tubular backleak
57
What happens in the ATN prodromal phase?
Insult to kidney has occurred (ramping up phase) | Inc BUN and creatinine
58
What happens in the ATN oliguric phase? (what happens to K levels)
1-8 weeks with adequate UO followed by oliguria and progressive uremia; decreased GFR; hypervolemia S/S of fluid excess, hyperkalemia, uremic syndrome, metabolic acidosis Pt may need dialysis
59
What happens in the ATN post-oliguric phase?
Diuresis, hypovolemia; tubular function impaired, azotemia Fluid volume deficit until kidneys recover, creatinine is normal in 1-3 weeks, full recovery takes a year (usually renal insufficiency persists)
60
What is chronic renal failure? Is it reversible?
Decreased kidney function/ kidney damage of 3 months based on blood tests, UA, and imaging, also low GFR for 3 months Progression is CKD to CRF to ESRD CRF is IRREVERSIBLE
61
Kidneys can compensate until ____% of nephrons are damaged/nonfunctional
75-80% | BFR reduction occurs with nephron loss
62
What electrolytes are off in CRF?
Retained potassium, phosphorus, and mag | Metabolic acidosis
63
What occurs in CRF?
Anemia: lack of erythropoietin Hypertension, hypervolemia Uremic syndrome: retention of metabolic waste, impaired healing Malnutrition, pain, bone/mineral disorders (kidney can't reabsorb calcium)
64
List extrarenal manifestations of renal failure
``` HTN Chronic pulmonary edema Depressed immune response N/V/D Anemia Sensory/motor neuropathy, disturbed mentation ```
65
What mediates micturition?
Pons Gravity Peristalsis Nervous system
66
The pons _____ (relax/contrax) the internal sphincter and _____ the bladder to enable urination
RELAX internal sphincter CONTRACTS bladder To enable urination
67
What do the sympathetic and parasympathetic nerves do for micturition?
Sympathetic nerves allow relaxation and filling | PSNS result in blade contraction and relaxation of internal sphincter to initiate bladder emptying
68
When voiding, the ____ muscle contracts and the _____ relax
Detrusor muscle contracts | Urethral sphincters relax
69
True/false: Incontinence is a normal part of aging
FALSE
70
What is urge incontinence?
Involuntary sudden leakage of urine with urge to void Overactive detrusor muscle Due to idiopathic, bladder infection, radiation, turmors/stones, or CNS damage
71
What is stress incontinence?
Occurs when urine is involuntary lost with increases in intra-abdominal pressure Precipitated by effort/exertion Due to weakening of pelvic muscles or intrinsic urethral sphincter deficiency
72
What is overflow incontinence?
Bladder becomes so full that it leaks urine | Due to obstruction, underactive/inactive detrusor muscle
73
Enuresis: what is it? What is the pathogenesis?
Intermittent incontinence while asleep, inappropriate, typically children having nighttime incontinence Deficiency is vasopressin (ADH), nocturnal overactive detrusor muscle
74
What is vesicoureteral reflux? What are the clinical manifestations?
Reflux of urine from ureter-bladder junction (overfilling leak) Clinical manifestations may include recurrent UTI, voiding dysfunction, renal insufficiency, or HTN in children May resolve or require surgery
75
What is ureteral ectopy?
Single ureter implanted in an abnormal location or a duplicate ureter Can increase risk of infection and reduce renal function
76
What is ureterocele? How does it effect kidney function and overall health? Clinical manifestations and treatment?
Congenital disorder of cystic dilation at distal end of the ureter Results in ureteral and renal calyx dilation, reflux, and infection Clinical manifestations: hydronephrosis, UTIs, voiding dysfunction, hematuria, urosepsis, or failure to thrive Surgery is necessary: endoscopic decompression or surgical reconstruction
77
Types of ureterocele: intravesical/orthotopic vs. extravesical/ectopic vs. single system vs. duplex?
Intravesical/orthotopic: within the bladder only Extravesical/ectopic: in neck of bladder or urethra Single system: ureterocele with a kidney that has just one ureter Duplex system: ureteroceles found with a kidney possessing 2 ureters
78
What prevents kidney stones and how?
Dietary calcium prevents kidney stones by binding oxalate and preventing absorption
79
What is acute hydronephrosis?
Hydronephrosis is distention/dilation of the kidney with urine, dilation of pelvis and calyces with thinning of renal parenchyma due to inflammation and damage Acute hydronephrosis is usually partial obstruction, oliguria
80
Chronic hydronephrosis?
Oliguria, anuria; elevated pressure from obstruction may damage the kidney leading to ARF; associated with vague intestinal symptoms like N/V and abdominal pain

N552 Patho (13 decks)

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