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ABSN > renal - patho - Exam 2 > Flashcards

renal - patho - Exam 2 Flashcards

1
Q

pyelonephritis etiology

A

inflammation of the kidneys caused by infection ascending up the urinary tract or from a bloodstream infection

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2
Q

risk factors of pyelonephritis

A

pregnancy, recurrent lower UTIs, or develop a abx resistant strain

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3
Q

what is the most common pathogen of pyelonephritis

A

E.coli

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4
Q

chronic pyelonephritis can lead to what if severe enough

A

chronic kidney disease or sepsis

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5
Q

pyelonephritis characteristics of the kidney

A

swollen, abscesses can form and necrosis can develop which impairs renal function

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6
Q

clinical manifestations of pyelonephritis

A

sudden onset of fever, chills, CVA tenderness + lower UTI symptoms and possible hematuria (if systemic then also N/V & anorexia)

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7
Q

treatments for pyelonephritis

A

ABX -> bactrim (trimeth + sulfa), ciproflozacin, nitrofurantoin

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8
Q

bactrim

A

-class: sulfonamides
-inhibits bacterial growth by stopping synthesis of folic acid
-1st choice for UTIs
-sulfa allergies start w/ a fever then rash
-do not use during pregnancy

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9
Q

ciprofloxacin

A

-class: Fluoroquinolones
-alters bacterial DNA
-UTIs & STIs
-arthropathy (non reversible joint point) do not give <18 or >60
-do not use during pregnancy

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10
Q

complications of pyelonephritis

A

urosepsis -> more likely in elderly w/ high mortality rates

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11
Q

locations for urinary obstruction + most likely cause

A

-renal pelvis; renal calculi
-ureter; renal calculi, pregnancy, tumors
-bladder or urethra; bladder cancer, neurogenic bladder, prostate cancer, urethral strictures

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12
Q

what is the potential complication of urine stasis

A

infection

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13
Q

what does back up pressure cause

A

when the kidneys are still making urine but there is a blockage -> hydroureter, hydronephrosis, or postrenal acute kidney injury

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14
Q

hydronephrosis & hydroureter

A

enlarged areas d/t urine back up -> fix the blockage to treat
emergency & usually needs surgical intervention

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15
Q

what does manifestation of an obstruction depend on

A

-site
-cause
-speed of onset

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16
Q

which factor of obstruction determines severity of pain

A

speed of onset

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17
Q

what is nephrolithiasis

A

renal calculi / kidney stones
clumps of crystals in the urinary tract

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18
Q

nephrolithiasis pathogenesis

A

urine is a solution of solvent (water) and solutes (particles) -> w/ stones we get super saturation w/ a solute and we begin to form crystals in the nephron

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19
Q

what enhances formation of crystals

A

-pH changes (UTI)
-excessive concentration of insoluble salts in the urine (dehy, bone disease, gout, renal disase)
-urinary stasis (immobility)

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20
Q

nephrolithiasis risk factors (7)

A

-male
-ages 20-30s
-white
-family history
-congenital defect (kidneys or urinary sys)
-weather (hot)
-obesity

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21
Q

what are the 3 types of stones

A

1) calcium (oxalate or phosphate); 70-80%
2) struvite; 15%
3) uric acid: 7%

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22
Q

causes of/risks calcium stones (4)

A

family hx, idiopathic, increased calcemia, increased oxaluria

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23
Q

what diet is a risk factor for calcium stones

A

high Na
high oxalate (beets, strawberries, carrots, caffeine, chocolate, oats)
high protein

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24
Q

causes of/risks struvite stones

A

urinary tract infections

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25
Q

causes of/risks of uric acid stones

A

gout

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26
Q

clinical manifestations of nephrolithiasis (+describe pain felt)

A

pain / acute renal colic
- flank region that radiates to the lower abd & groin
- spasms, lasts 20-60 min
- intermittent
- sharp
+ N/v, dysuria, chills & fever w/ infection, hematuria, foul smelling urine, diaphoresis

27
Q

what is the treatment goal of nephrolithiasis

A

treat pain

28
Q

nephrolithiasis treatment

A

acute pain: morphine, NSAIDs, IV fluids

29
Q

preventive meds for nephrolithiasis

A

-thiazide diuretics for calcium stones
-abx for struvite
-allopurinol for urate

30
Q

urologic cancer

A

kidney cancer , rare
-renal cell carcinoma (85%)
-usually not caught before it metastasizes & if not caught in early stages 5 yr survival rate is <10%

31
Q

renal cell carcinoma risk factors (5)

A

-smoking (#1 reason)
-obesity
-age
-male
-genetics hx

32
Q

clinical manifestations of renal cell carcinoma

A

early: none
late: CVA tenderness, hematuria (cola colored), possible palpable abdominal mass

33
Q

renal cell carcinoma signs of metastasis

A

usually will spread to bones or lungs so bone pain or dyspnea/difficult breathing

34
Q

renal cell carcinoma treatment

A

resistant to chemo -> surgery to remove kidney

35
Q

bladder cancer

A

-fourth most common cancer in med
-urothelial carcinoma (within bladder lining)

36
Q

risk factors for bladder cancer (4)

A

-smoking (#1 cause)
-male
-occupations w/ exposure to toxins (rubber or paint factories)
-low fluid intake (toxins sit in low concentration of urine & sit longer)

37
Q

bladder cancer clinical manifestations

A

early: hematuria
later: frequency, urgency, dysuria

38
Q

bladder cancer treatment

A

chemo based on stages
- stage 1: intravesical chemo
- advanced stage: systemic chemo

39
Q

glomerulonephritis

A

a variety of conditions that cause inflammation of glomeruli
-can be focal or diffuse
-3rd leading cause of kidney failure
-primarily an immune process

40
Q

where does damage occur with glomerulonephritis

A

-glomerulus: a delicate network of arterioles within the bowman’s capsule (all blood goes through)
-Tubules

41
Q

glomerular blood flow

A

there are 2 renal arteries -> an afferent artery that takes blood in and an efferent artery that return blood
pressure difference that helps push chemicals, toxins, ect out of the vessels to filter the blood and sends them to the urine

42
Q

what organ takes up a large amount of the bodies cardiac output

A

the kidney
needs high enough BP to profuse the kidney and allow glomeruli to work

43
Q

what cells help with the production of urine

A

podocytes

44
Q

3 layers of the capillary membrane in the glomerulus

A

1) endothelium
2) basement membrane (most issues happen here)
3) podocytes

45
Q

production of urine

A

starts by podocytes -> fluid travels the nephron -> particles are excreted and reabsorbed -> final concentration of urine

46
Q

type 2 sensitivity rx

A

reactions occur on the cell surface and result in direct cell death or malfunction

47
Q

type 3 sensitivity rx

A

immune complexes are deposited into tissues and the resulting inflammation destroys the tissue

48
Q

etiology of glomerulonephritis

A

1) antibodies attach to antigens of the glomerular basement membrane (anti GBM antib’s) type 2 rx ~5%
2) antibodies react w/ circulating antigens and are deposited as immune complexes in the GBM type 3 rx ~90%

49
Q

characteristics of acute glomerulonephritis

A

-abrupt onset
HARP
-hematuria
-azotemia (build up of waste products)
-retention (edema, oliguria, HTN)
-proteinuria

50
Q

acute glomerulonephritis triggers

A

-post infections (strep)
-primary disease (berger disease)
-multisystem disease aka secondary (goodpasture syndrome, systemic lupus, vasculitis)

51
Q

bergers disease

A

antibody IGA builds up in the kidney which causes inflammation within the glomerulus

52
Q

goodpasture syndrome

A

a disorder where a person has anti GBM antibodies (the 5% cause) -> the glomerular basement membrane looks very similar to the basement membrane of the lungs so these pts present to the hospital w/ a hemoptysis bc the anti GBM are not only attacking the glomerular but also the lungs basement membrane causing the pts to cough up blood
resp & renal problems -> look for anti GBM antibodies

53
Q

acute glomerulonephritis pathogenesis

A

trigger -> immune complexes form -> complement activated -> release of mediators -> tissue injury -> hematuria, proteinuria & decreased GFR

54
Q

chronic glomerulonephritis

A
  • long term inflammation of the glomerulus (scare tissue which cannot filter or produce urine effectively)
    -presents like acute
    -prognosis: slow then ESRD
55
Q

nephrotic syndrome

A

the glomerulus is too permeable to plasma proteins which is measured by elimination of >3g of protein per day
do 24hr urine

56
Q

nephrotic syndrome etiology

A

glomerulonephritis
DM

57
Q

nephrotic syndrome pathogenesis

A

increased glomerular permeability -> proteinuria -> hypo albuminemia
specifically lose a lot of albumin

58
Q

result of losing large amount of albumin w/ nephrotic syndrome

A

third spacing because fluid begins to shift

59
Q

nephrotic syndrome clinical manifestations

A

-edema
-htn (kidneys want more volume so activate raas)
-liver problems (hyperlid, hypercoag, loss of antithrombin 3 & plasminogen)

60
Q

why do we see liver problems w/ nephrotic syndrome

A

we are spilling protein and losing fluid so the liver will have increased lipid levels & some proteins lost include antithrombin 3 and plasminogen (precursor to plasmin which helps breakdown clots -> risks for PEs & DVTs

61
Q

glomerulopathy

A

DM & HTN complications

62
Q

glomerulopathy: DM comps

A

-major complication
-gross thickening of the GBM (so doesn’t filter particles & fluid as effectively) -> less urine & more toxin build up
-leads to ESRD

63
Q

glomerulopathy: HTN comps

A

decreased renal perfusion -> sclerotic glomerular changes d/t increased pressure on the blood vessels

64
Q

glomerulopathy manifestations

A

hematuria, oliguria (<400ml/d), fluid retention, increased BUN/Cr, proteinuria and low albumin

ABSN (150 decks)

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