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KCSU17 Patho/Pharm Submodule 2 > Urologic and Renal Disorders > Flashcards

Urologic and Renal Disorders Flashcards

1
Q

congenital urologic disorders

A

renal agenesis

duplications

malposition

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2
Q

renal agenesis

A

failure of one or both (rare) kidneys to develop

may be bilateral or unilateral

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3
Q

bilateral renal agenesis

A

both kidneys fail to develop

rare, associated with other congenital anomalies

incompatible with life, typically miscarried

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4
Q

unilateral renal agenesis

A

only have one kidney bc other failed to develop

common, asymptomatic

other kidney typically enlarges to compensate

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5
Q

duplications of urinary tract

A

can be complete (formation of extra ureter and renal pelvis) or incomplete (only upper part of excretory system)

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6
Q

malposition

A

kidney doesn’t migrate out in peritoneum, kidney fusion “horseshoe kidney”

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7
Q

urinary tract infections are typically caused by which organisms

A

caused by gram- negative bacteria

most common pathogen is E. coli (from lower digestive tract)

these organisms contaminate perianal and genital area and ascend urethra (also from blood, lamp, direct extension)

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8
Q

natural conditions protective against UTI

A

free urine flow (normal anatomy)
large urine volume (typically flushes it out)
complete bladder emptying (washes it out)
acid urine (so bacteria struggle to grow)

this area is normally sterile

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9
Q

predisposing factors to UTIs

A

impairing drainage of urine (kink, lrg prostate, stone)

stagnation of urine

injury to mucosa by kidney stones (allowing bacteria to go deeper)

introduction of catheter or instruments to bladder

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10
Q

cystitis and gender

A

only effects the bladder

women more likely than men to get it (shorter urethra)

sexual intercourse promotes transfer of bacteria

males are more likely to happen to older men nc large prostate interferes with complete bladder emptying

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11
Q

clinical manifestations of UTI/cystitis

A

during pain on urination
urinate frequently with low volume

no fever or leukocytosis on CBC

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12
Q

UA

A

urinalysis

compare number of epithelial cells to leukocytes

50-100 ??, 500+ UTI

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13
Q

pyelonephritis

A

infection of the upper urinary tract caused by

  1. ascending infection from bladder (ascending pyelo)
  2. cried to kidney from blood stream (hematogenous)

typically preceded by untreated UTI

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14
Q

main clinical indication of pyelonephritis

A

UA will show WBC casts

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15
Q

clinical manifestations of pyelonephritis

A

localized pain and tenderness over infected kidney (flank pain)

responds well to abx
can be chronic and lead to failure

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16
Q

prostatitis

A

inflammation of the prostate

two types:

  1. acute bacterial prostatitis
  2. chronic bacterial prostatitis

likelihood for infection increases with age bc more kinks in urethra

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17
Q

acute bacterial prostatitis

A

subset of UTI

caused by urethral organisms to invade prostatic duct

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18
Q

acute prostatitis symptoms

A

similar to UTI

fever, chills

systemic symptoms

perineal or rectal dull achy pain

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19
Q

treatment for acute prostatitis

A

4+ weeks of Abx (long course)

could result in prostatic abscess

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20
Q

chronic bacterial prostatitis

A

recurrent prostatitis (low grade, residual colonization)

no abscess here, systemic illness

abx therapy is challenging and long bc meds don’t get in here well

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21
Q

Benign Prostatic Hypertrophy

A

common, age related, non malignant nodular enlargement of central area of prostate

due to decreased cell death

prostate enlarges and pushes on bladder, applying pressure and causing difficulty voiding

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22
Q

classic symptoms of BPH

A 
wak stream 
hesitancy
frequency 
noctruia 
post-void dribbling
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23
Q

treatment of BPH

A
  1. alpha-2 blockers
  2. 5-alpha reductase inhibitors
  3. surgical
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24
Q

5 alpha reductase inhibitors

A

finasteride (Proscar)

gradual reduction in size of prostate

blocks affects of androgens on growth

causes atrophy of the prostate gland epithelial cells, reduces the volume by 20-30%

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25
alpha-1 blockers
tamulosin (Flomax) relax prostate smooth muscle, blocking alpha stimulation facilitates urine flow acts rapidly
26
BPH surgical treatment
transurethral prostatectomy (TURP) removes prostatic tissue risks sexual dysfunction
27
renal calculi pre disposing factors
1. high [salts] in urine -- salts saturates urine causing salts to precipitate and form calculi 2. urinary tract infections -- reduce solubility of salts in urine 3. urinary tract obstruction -- causes urine stagnation, promotes stasis and infection
28
passing renal calculi
passes through ureters to bladder, causes renal colic and hematuria (microscopic or visible) some become impacted in ureter and need to be removed
29
staghorn calculus
urinary stones that increase in size to form large branching structures that adopt to contour of pelvis and calyces massive, grows and fills space, must be surgically removed
30
manifestations fo renal calculi
colic associated with passage of a stone obstruction of urinary tract causes hydronephrosis-hydroureter proximal to obstruction
31
treatment of renal calculi
cystoscopy shock wave lithotripsy ureteral stents
32
cystoscopy
snares and removes stones that are lodged in distal ureter grab and physically remove kidney stone
33
shock wave lithotripsy
stones lodge in proximal ureter are broken into fragments that are readily excreted
34
ureteral stents
increase the size of the ureter below to pass
35
urinary obstruction/retention
blockage of urine outflow leads to progressive dilation of urinary tract proximal to obstruction eventually causes compression atrophy of kidneys can cause UTI, kidney stones
36
manifestations of urinary obstruction/retention
hydrometer hydronephrosis dilation is reality seen on imaging
37
causes of urinary retention/obstruction
bilateral (obstruction of bladder neck by prostate or stricture) unilateral (stricture, calculus, tumor)
38
diagnosing and treating urinary obstruction/retention
ultrasound, CT remove obstruction or stenting
39
glomerulonephritis
inflammation of glomeruli caused by Ag-Ab rxn within glomeruli mechanisms: 1. anti-GBM 2. circulating Ag-AB complexes filter and trapsed in glomeruli and incite inflammation 3. connective tissue disorders
40
anti GBM glomerulonephritis
autoAbs against particular collagen in GBM attack GBM
41
circulating Ag-Ab and glomerulonephritis
plugs up the capillaries and causes localized infection and inflammation leukocytes release lysosomal enzymes that cause injury to glomeruli
42
symptoms of glomerulonephritis
hypertension cola colored urine (due to RBCs) nephritic range (<3 g/day) proteinuria RBC casts in urine AKI due to build up
43
glomerulonephritis Treatment
control BP, limit renal damage, and monitor for recovery
44
nephrotic syndrom
marked loos of protein in urine >3 g/day urine protein excretion > preodcuiton of protein albumin levels fall causing edema due to 3rd spacing
45
Nephrotic system will cause the following conditions
1. AKI/CKD 2. Anascarca (3rd spacing to abdomen) and Ascites (edema everywhere) 3. Lipid abnormalities (increases cholesterol to maintain onchoitc levels) children have good prognosis but adults will often get CKD/ESRF
46
nephrotic syndrome results from
1. renal disease (glomerulonephritis or idiopathic dx of kidney) 2. systemic disease (DIABETES**, SLE, amyloidosis) -- uncontrolled damage
47
diabetic nephropathy
common disorder in US progressive kidney damage caused by uncontrolled diabetes more common in Type 1 bc of small vessel dx its develop glomerulosclerosis (hard, inflexible GBM) can't get rid of their wastes (accumulates in blood)
48
diabetic nephropathy clinical manifestions
progressive impairment of renal function (less able to excrete wastes and acids) protein loss no treatment, but control of glucose and HTN can help ultimately leads to renal failure
49
3 types/causes of acute kidney injury
1. pre renal 2. intrinsic 3. post renal sudden change (24hrs)
50
pre renal causes of AKI
something going on BEFORE blood gets there ex. blood loss/hemorrhage, osmotic diuresis, shock
51
intrinsic causes of AKI
problem with kidney itself;f, plenty of blood her but kidney doesn't do its job 85% of it caused by acute tubular necrosis toxins (medications, Hgb, myoglobin, uric aci, bench jones proteins)
52
post renal causes of AKI
problem with urinary system, beyond kidney, backs up to effect function renal calculi BPH
53
clinical manifestations of AKI
acute renal failure fluid overload (more fluid that it can deal with, backs up into lungs) hyperkalemia**** metabolic acidosis (no way to deal with H+, pH drop and enzyme dysfunction
54
manifestations of renal failure
oliguria, low urine output (pre renal, intrinsic) anuria no output (post renal) oliguric renal failure is worse
55
AKI recovery/treatment
with good care, will recover easy to find but hard to figure out what caused it treatment is to dix underlying cause (shock, blockage?) may be treated with dialysis until function returns
56
CKD/ESRD
retention of excessive byproducts of protein metabolism in blood holds onto too much H+
57
major causes of CKD
diabetes and HTN also: polycystic kidney disease and glomerulonephritis
58
clinical manifestations of CKD
1. weakness, loss of appetite, n/v 2. anemia (due to chronic dx, chronic k disease, and IDA) 3. toxic manifestations from retained waste products (encephalopathy, seizures, and puritis) 4. edema 5. hypertension 6. metabolic acidosis
59
treatment of CKD
1. aggressive treatment of HTN to limit progression 2. control diabetes 3. correct electrolyte disturbances (esp. K+ and PO4) 4. correct endocrine dysfunction (2 hyperparathyroidism) 5. prepare for renal replacement therapy
60
dialysis
substitutes function of kidney by removing waste products (diffusion across membrane) and blood from pt. two types: hemodialysis, peritoneal dialysis life long
61
hemodialysis
more common its circulation is connected to machine removing and cleaning the blood access on arterial and venous side
62
peritoneal dialysis
uses patients own peritoneal membrane as the dialyzing machine
63
body water distribution
2/3 of water is intracellular 1/3 of water is extra cellular (75% is interstitial, 25% is intravascular)
64
diffusion in ECF
fluids and electrolytes diffuse freely between vascular and interstitial fluid compartments interstitial space contains little protein bc of permeability (protein remains in blood)
65
ICF diffusion
semipermeable membrane b/t ICF and ECF freely permeable to water and impermeable to Na+ and K+
66
important ions in fluid
1. sodium 2. potassium 3. magnesium 4. calcium 5. phosphorus 6. bicarbonate 7. chloride
67
sodium
most prevalent in ECF imp. for transmission of nerve impulses "water follows sodium"
68
potassium
ICF electrical impulses
69
phosphorous
important in energy storage electrical nutrality works with magnesium acts as a buffer in intracellular space
70
bicarbonate
negative anion principal buffer of body neutralizes H+ and other organic ions
71
chloride
negative balances positive charge of cations major role in renal function and fluid balance
72
disturbances of water balance
1. dehydration 2. overhydration 3. depletion of electrolytes
73
dehydration
most common disturbance of water balance either due to inadequate intake (diarrhea or vomiting) or excess H2O (comatose or debilitated patients)
74
over hydration
caused by: 1. excessive fluid intake when renal function is impaired 2. excessive intake of fluids 3. excessive administration of IV fluid
75
depletion of electrolytes is caused by
1. vomiting/diarrhea 2. excessive diuretic usage 3. excessvie diuresis in hyperglycemia 4. renal tubular disease
76
normal pH range of body
7.35-7.45 this is a must, we retain a pH despite large amounts of acid
77
acid base balance
regulator mechanisms to neutralize and eliminate acids as soon as they are produced (lung and kidney) 1. blood buffer (resist pH change) 2. lungs (control carbonic acid [ ]) 3. kidney (controls [bicarbonate]
78
acid base balance determination tests have ___ results
direct measurement of 1. blood pH 2. PCO2 3. bicarbonate
79
hendersen hassalbach eq.
makes H+ to CO2 to H2O pH depends on ratio of bicarbonate to H2CO3
80
respiratory control of carbonic acid
carbonic aid is dissolved as CO2 in plasma hyperventilation lowers CO2 and H2CO3 in plasma hypoventillation raises CO2 and H2CO3 in plasma
81
renal control of bicarbonate
kidney selective reabsorb filtered bicarbonate can manufacture bicarbonate to replace amounts lost in buffering acid from metabolic process
82
pCO2, RR, and compensation respiratory acidosis
increased pCO2 decrease in RR kidney reabsorbs bicarbonate and makes more this is caused by sleep apnea, rib fracture, narcotics, pneumonia)
83
pCO2, RR, and compensation respiratory alkalosis
increased RR decreased pCO2 kidney increases bicarbonate excretion caused by asthma, COPD, anxiety
84
pCO2, RR, and compensation metabolic acidosis
increased [Hydrogen] due to DKA, AKI, CKD, lactic acidosis decreased pCO2 increases RR, makes more bicarbonate (if longstanding)
85
pCO2, RR, and compensation metabolic alkalosis
results from increased plasma bicarbonate or net loss of acid (loss of gastric juices, chloride depletion, excess mineralocorticoid, excess antacids occurs with K deficiency compensation is to decrease RR but this is not sufficient bc we still need to breath

KCSU17 Patho/Pharm Submodule 2 (14 decks)

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