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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
epithelial cells cast indicated what
sloughing of tubular cells, ATN
26
Creatinine and BUN: which one more reliable for what
Creatinine more reliable for renal function. | monitor progression of renal disease
27
Creatinine is what
the end product of muscle metabolism, excreted EXCLUSIVELY by kidney
28
Creatinine is affected by 2 factors
1 rate muscle produces it 2 rate kidney (GFR) excretes it if no muscle breakdown, then creatinine is a constant. increase- decreased function
29
BUN is what
urea, the end product of protein metabolism excreted PRIMARILY by the kidneys Increase- decrease function, increase in dietary protein intake
30
As GFR decreased creatinine does what
increases
31
most accurate why to measure GFR and what does it measure
creatinine clearance, most accurate is insulin clearance | GFR is estimated by measuring the clearance of a filterable substance.
32
Azotemia
increase BUN and creatinine | related to decreased in GFR
33
uremia
increased urea in blood, sign of failing excretory system and metabolic/endocrine problem.
34
proteinuria/albuminuria
increased [protein] in urine, due to leakiness of glomerular barrier
35
pyuria
leukocytes in urine
36
Glomerulonephritis in 2 words!
glomeruli inflam
37
urine of a UTI
bacteriuria, pyuria, cloudy
38
nephrolithiasis
kidney stone! | renal colic, hematuria, and recurrent stone formation
39
what are the intrarenal disorders 5
``` results in renal insufficiency/failure congenital neoplastic infectious obstructions glomerular ```
40
s/s of intrarenal disorders
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
agenesis
kidneys do not develop in fetus | bilateral not compatible with life.
42
hypoplasia what is is, what can it lead to and what must be done with it?
some kidney development in fetus can lead to pediatric ESRD 1 normal kidney can maintain normal renal function. life long kidney monitoring
43
polycystic kidney disease is what and causes what?
genetic: fluid filled cysts | can restrict kidney filtration/urine formation
44
2 types of polycystic kidney disease who gets which
autosomal recessive-kids ESRD by age 15 | autosomal dominant-adults (cyst else where too)
45
polycystic kidney disease autosomal dominant different chromosomes
Chromosome 16- PKD1 | Chromosome 4 PKD2
46
whats happening in polycystic disease and it causes
decrease in intracellular Ca increase in cAMP causes decreased GFR and ability of concentrate urine
47
polycystic kidney disease s/s 2, tx
hypertension and pain | tx: supportive, controlling BP. may initiate dialysis
48
neoplasms, whats it called, where is it, s/s and tx
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
Acute pyelonephritis what where dx, tx
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
Chronic pyelonephritis can do what, why
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
obstruction causes what
urine stasis--infx and structural damage, dilation in tract proximally
52
complete obstruction causes what
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
how do kidney stone form?
crystal aggregates composed of organic and inorganic materials form from: solute supersaturation!!, low urine volume and abnormal pH.
54
most kidney stones are made of what?
Ca crystals , some uric acid
55
what causes pain with kidney stones? dx, tx
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
primary vs secondary glomerulopathies
P: only in kidney S: result from other disease
57
2nd glomerulopathies 3
1goodpasture syndrome: specific to basement membrane 2Systemic lupus erythematosus: antigen antibody complex 3Diabetic nephropathy
58
Glomerulonephritis main s/s and then the others
Proteinuria | oliguria, azotemia, edema, HTN
59
Nephritic syndrome
mild to moderate proteinurea | hematuria and RBC cast present.
60
Glomerulonephritis is what
inflam of glomerulus immune from something more common in men
61
patho definition of acute glomerulonephritis
attraction of immune cells to the area of inflamm causes lysosomal degradation of basement membrane
62
why does GFR fall in Glomerulonephritis
bc of the contraction of mesangial cell resulting in a decreased surface area for filtration
63
Glomerulonephritis tx
steroids, plasmapheresis, fluid mgmt | mgmt of renal and systemic HTN
64
postinfx Glomerulonephritis is from what, causes what, happens after what and s/s
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
IgA nephropathy Berger disease, where, who, s/s, can end in?
``` 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
Chronic Glomerulonephritis has what, s/s, tx
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
Nephrotic Syndrome what is it, s/s, leads to, causes an increase in what which does what AND tx
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
what causes nephrotic syndrome?
minimal change disease Systemic lupus DM increased glomerular permeability to proteins
69
Nephrotic syndrom and nephritic syndrome are what
glomerulopathies
70
minimal change disease is what, problems with what, initiated by what, s/s, tx
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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