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Patho test 3 > Renal > Flashcards

Renal Flashcards

1
Q

renal basic function is to do 5

A 
filter
maintain proper H2O and elyte balance 
maintain proper pH of blood
secrete EPO
activate vit D
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2
Q

filtrate proximal tubule: what should be completely removed?

A

Glucose, protein, amino acids

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3
Q

Proximal tubule what declines?

A

HCO3

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4
Q

Proximal tubule what increases?

A

Creatinine and urea

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5
Q

filtrate loop of henle what do the elytes do?

A

all (HCO3, Cl, Na, K) all go up then down

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6
Q

Filtrate of distal tubule: what happens here?

A

fine tune, end with (most)Creatinine, Urea, K, Cl, Na, HCO3(least)

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7
Q

Baroreceptor mechanism where, does what

A

in afferent arterole
tells JG cell whether to release renin or not
increase PRESSURE- inhibit renin release

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8
Q

tubuoglomerular feedback SNS what receptor stimulates release of what?

A

B1 stimulation, renin release

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9
Q

macula densa mechanism

A

in distal Nephron

increase NaCl- inhibits renin release

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10
Q

reabsorption of glucose where and by what

A

proximal tubule by SGLT2

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11
Q

SGLT2 transporter does what

A

Na and glucose (apical)

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12
Q

GLUT2 transporter does what

A

gradient glucose transporter (basallateral)

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13
Q

Acid base

A

LOOK in your damn notes

bottom line kidneys either reabsorb HCO3 through that dumb equation or make a new one with glutamine metabolism

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14
Q

hypochloremic metabolic alkalosis how get to alk and tx

A

vomiting loss of Cl- so kidney increased the reabsorption of HCO3 to compensate for the loss of neg end up with Alkalosis
**give NaCl and K to stop HCO3 reabsorption.

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15
Q

K in the distal tubule how does it get places

A

Basolateral membrane: Na-K pump, reabsorb Na, kicks out K

Apical membrane: H and K exchanger: K in to lumen (pee out) if acidic won’t reabsorb H there for won’t kick out K

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16
Q

DI, have a problem with not enough what bc of what

A

not enough ADH 2nd to pituitary damamge

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17
Q

who responds to ADH and what happens when they don’t?

A

the collecting tubules, and if unresponsive then get neurogenic DI

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18
Q

renin is released when?

A

decreased blood flow to kidneys, decreased Na, activation of SNS to JG cells

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19
Q

Natriuretic peptides release when, causes what

A

atrial cell in heart are over stretched.

Results in loss of Na, H2O

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20
Q

Urodilation released when does what

A

when the distal and collecting tubule cells identify increased volume.
Results in loss of Na, H2O

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21
Q

24 hr helpful for what

A

varying concentrations

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22
Q

urine color: cloudy, brown

A

cloudy WBC

brown: RBC

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23
Q

WBC cast associated with

A

pyelonephritis

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24
Q

RBC cast associated with

A

glomerulonephritis

*in RBC think bigger injury bc RBCs are big

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25
Q

epithelial cells cast indicated what

A

sloughing of tubular cells, ATN

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26
Q

Creatinine and BUN: which one more reliable for what

A

Creatinine more reliable for renal function.

monitor progression of renal disease

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27
Q

Creatinine is what

A

the end product of muscle metabolism, excreted EXCLUSIVELY by kidney

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28
Q

Creatinine is affected by 2 factors

A

1 rate muscle produces it
2 rate kidney (GFR) excretes it
if no muscle breakdown, then creatinine is a constant.
increase- decreased function

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29
Q

BUN is what

A

urea, the end product of protein metabolism excreted PRIMARILY by the kidneys
Increase- decrease function, increase in dietary protein intake

30
Q

As GFR decreased creatinine does what

A

increases

31
Q

most accurate why to measure GFR and what does it measure

A

creatinine clearance, most accurate is insulin clearance

GFR is estimated by measuring the clearance of a filterable substance.

32
Q

Azotemia

A

increase BUN and creatinine

related to decreased in GFR

33
Q

uremia

A

increased urea in blood, sign of failing excretory system and metabolic/endocrine problem.

34
Q

proteinuria/albuminuria

A

increased [protein] in urine, due to leakiness of glomerular barrier

35
Q

pyuria

A

leukocytes in urine

36
Q

Glomerulonephritis in 2 words!

A

glomeruli inflam

37
Q

urine of a UTI

A

bacteriuria, pyuria, cloudy

38
Q

nephrolithiasis

A

kidney stone!

renal colic, hematuria, and recurrent stone formation

39
Q

what are the intrarenal disorders 5

A 
results in renal insufficiency/failure
congenital 
neoplastic
infectious
obstructions
glomerular
40
Q

s/s of intrarenal disorders

A

Pain- renal/kidney pain called nephralgia, CVA tenderness, flank pain. DULL constant character, T10-L1 SNS afferent neurons
Urinalysis: FOUNDATION of Dx dark and smelly(decreased renal function), cloudy

41
Q

agenesis

A

kidneys do not develop in fetus

bilateral not compatible with life.

42
Q

hypoplasia what is is, what can it lead to and what must be done with it?

A

some kidney development in fetus
can lead to pediatric ESRD
1 normal kidney can maintain normal renal function.
life long kidney monitoring

43
Q

polycystic kidney disease is what and causes what?

A

genetic: fluid filled cysts

can restrict kidney filtration/urine formation

44
Q

2 types of polycystic kidney disease who gets which

A

autosomal recessive-kids ESRD by age 15

autosomal dominant-adults (cyst else where too)

45
Q

polycystic kidney disease autosomal dominant different chromosomes

A

Chromosome 16- PKD1

Chromosome 4 PKD2

46
Q

whats happening in polycystic disease and it causes

A

decrease in intracellular Ca
increase in cAMP
causes decreased GFR and ability of concentrate urine

47
Q

polycystic kidney disease s/s 2, tx

A

hypertension and pain

tx: supportive, controlling BP. may initiate dialysis

48
Q

neoplasms, whats it called, where is it, s/s and tx

A

Renal cell carcinoma, metastatic disease (clear cell)
in the cortex, proximal collecting tubule
familial pattern, risk: smoking, obesity, HTN
aysmptomatic until advanced: pain, CVA tenderness, hematuria, palpable mass

49
Q

Acute pyelonephritis what where dx, tx

A

most common infection. infx of renal pelvis(pyleo), parenchyma(nephro) from lower (ascending) tract UTI

dx: WBC cast in urine (upper UTI)
tx: antimicrobials

50
Q

Chronic pyelonephritis can do what, why

A

can result in chronic kidney disease
associated with reflux/obstruction- chronic urine stasis
s/s: abd/flank, fever, malaise, anorexia
tx: correct underlying problem- extended Abx

51
Q

obstruction causes what

A

urine stasis–infx and structural damage, dilation in tract proximally

52
Q

complete obstruction causes what

A

hydronephrosis(“water in kidney” dilation and distention of renal pelvis and calyces), decreased GFR, Chronic kidney disease, Ischemic kidney disease (bc of increased intraluminal pressure) and Acute tubular necrosis (intrarenal ARF)

53
Q

how do kidney stone form?

A

crystal aggregates composed of organic and inorganic materials
form from: solute supersaturation!!, low urine volume and abnormal pH.

54
Q

most kidney stones are made of what?

A

Ca crystals , some uric acid

55
Q

what causes pain with kidney stones? dx, tx

A

them moving- renal colic pain, acute onset, N/V, diaphoresis, hematuria
dx CT scan
tx: pass spontaneously or Fluids 2L/day, lithotripsy, endoscopic approaches, stents, PAIN MEDS

56
Q

primary vs secondary glomerulopathies

A

P: only in kidney
S: result from other disease

57
Q

2nd glomerulopathies 3

A

1goodpasture syndrome: specific to basement membrane
2Systemic lupus erythematosus: antigen antibody complex
3Diabetic nephropathy

58
Q

Glomerulonephritis main s/s and then the others

A

Proteinuria

oliguria, azotemia, edema, HTN

59
Q

Nephritic syndrome

A

mild to moderate proteinurea

hematuria and RBC cast present.

60
Q

Glomerulonephritis is what

A

inflam of glomerulus
immune from something
more common in men

61
Q

patho definition of acute glomerulonephritis

A

attraction of immune cells to the area of inflamm causes lysosomal degradation of basement membrane

62
Q

why does GFR fall in Glomerulonephritis

A

bc of the contraction of mesangial cell resulting in a decreased surface area for filtration

63
Q

Glomerulonephritis tx

A

steroids, plasmapheresis, fluid mgmt

mgmt of renal and systemic HTN

64
Q

postinfx Glomerulonephritis is from what, causes what, happens after what and s/s

A

from infectious agent Ag to Ab-Ag deposition IgG which causes proliferation of mesangial cells (lesions) scaring Autoimmune
Glomerular hypercellularity is caused by intracapillary leukocytes
happens after impetigo, throat infx (group A beta hemolytic strep)
s/s smoky(WBC) or coffee (extra damage RBC cast) colored urine
Usually in kids and developing countries

65
Q

IgA nephropathy Berger disease, where, who, s/s, can end in?

A 
ducts and tracts
most commonly dx, common in adults 
from upper resp or GI viral infx 
hematuria present in 1-2 days other usual Glomerulonephritis s/s not evident 
can lead to ESRD
66
Q

Chronic Glomerulonephritis has what, s/s, tx

A

progressive course: proliferative, membranous lesion
leads to ESRD
*Sclerosis and Fibrosis of kidney
present with porteinuria, may or may not have hematuria
Slow decline in renal function
dialysis or transplant

67
Q

Nephrotic Syndrome what is it, s/s, leads to, causes an increase in what which does what AND tx

A

increase glomerular permeability to proteins
protein loss >3-3.5gm/24h reflects glomerular inflamm.
leads to hypoalbuminemia and generalized edema
decrease blood colloid osmotic pressure
increased liver activity–hyperlipidemia and hyper coag
***characterized by hypoalbuminemia, edema, hyperlipidemia and lipiduria
tx: conservative symptom mgmt: diuretics, lipid lowering, HTN meds, immunosuppressents

68
Q

what causes nephrotic syndrome?

A

minimal change disease
Systemic lupus
DM
increased glomerular permeability to proteins

69
Q

Nephrotic syndrom and nephritic syndrome are what

A

glomerulopathies

70
Q

minimal change disease is what, problems with what, initiated by what, s/s, tx

A

lipoid nephrosis,
**alteration in glomerular podocytes–foot processes fuse together which decreased production of anions of basement membrane
Kids
initiated by allergic/immune
sudden onset of edema, decreased protein and hypoalbumineia
Tx: cortiocsteroids

Patho test 3 (4 decks)

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