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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
Q

alpha-1 blockers

A

tamulosin (Flomax)

relax prostate smooth muscle, blocking alpha stimulation

facilitates urine flow acts rapidly

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26
Q

BPH surgical treatment

A

transurethral prostatectomy (TURP)

removes prostatic tissue

risks sexual dysfunction

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27
Q

renal calculi pre disposing factors

A
  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
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28
Q

passing renal calculi

A

passes through ureters to bladder, causes renal colic and hematuria (microscopic or visible)

some become impacted in ureter and need to be removed

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29
Q

staghorn calculus

A

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

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30
Q

manifestations fo renal calculi

A

colic associated with passage of a stone

obstruction of urinary tract causes hydronephrosis-hydroureter proximal to obstruction

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31
Q

treatment of renal calculi

A

cystoscopy
shock wave lithotripsy
ureteral stents

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32
Q

cystoscopy

A

snares and removes stones that are lodged in distal ureter

grab and physically remove kidney stone

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33
Q

shock wave lithotripsy

A

stones lodge in proximal ureter are broken into fragments that are readily excreted

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34
Q

ureteral stents

A

increase the size of the ureter below to pass

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35
Q

urinary obstruction/retention

A

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
Q

manifestations of urinary obstruction/retention

A

hydrometer
hydronephrosis

dilation is reality seen on imaging

37
Q

causes of urinary retention/obstruction

A

bilateral (obstruction of bladder neck by prostate or stricture)

unilateral (stricture, calculus, tumor)

38
Q

diagnosing and treating urinary obstruction/retention

A

ultrasound, CT

remove obstruction or stenting

39
Q

glomerulonephritis

A

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
Q

anti GBM glomerulonephritis

A

autoAbs against particular collagen in GBM attack GBM

41
Q

circulating Ag-Ab and glomerulonephritis

A

plugs up the capillaries and causes localized infection and inflammation

leukocytes release lysosomal enzymes that cause injury to glomeruli

42
Q

symptoms of glomerulonephritis

A

hypertension
cola colored urine (due to RBCs)
nephritic range (<3 g/day) proteinuria

RBC casts in urine

AKI due to build up

43
Q

glomerulonephritis Treatment

A

control BP, limit renal damage, and monitor for recovery

44
Q

nephrotic syndrom

A

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
Q

Nephrotic system will cause the following conditions

A
  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
Q

nephrotic syndrome results from

A
  1. renal disease (glomerulonephritis or idiopathic dx of kidney)
  2. systemic disease (DIABETES**, SLE, amyloidosis) – uncontrolled damage
47
Q

diabetic nephropathy

A

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
Q

diabetic nephropathy clinical manifestions

A

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
Q

3 types/causes of acute kidney injury

A
  1. pre renal
  2. intrinsic
  3. post renal

sudden change (24hrs)

50
Q

pre renal causes of AKI

A

something going on BEFORE blood gets there

ex. blood loss/hemorrhage, osmotic diuresis, shock

51
Q

intrinsic causes of AKI

A

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
Q

post renal causes of AKI

A

problem with urinary system, beyond kidney, backs up to effect function

renal calculi
BPH

53
Q

clinical manifestations of AKI

A

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
Q

manifestations of renal failure

A

oliguria, low urine output (pre renal, intrinsic)

anuria no output (post renal)

oliguric renal failure is worse

55
Q

AKI recovery/treatment

A

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
Q

CKD/ESRD

A

retention of excessive byproducts of protein metabolism in blood

holds onto too much H+

57
Q

major causes of CKD

A

diabetes and HTN

also: polycystic kidney disease and glomerulonephritis

58
Q

clinical manifestations of CKD

A
  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
Q

treatment of CKD

A
  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
Q

dialysis

A

substitutes function of kidney by removing waste products (diffusion across membrane) and blood from pt.

two types: hemodialysis, peritoneal dialysis

life long

61
Q

hemodialysis

A

more common
its circulation is connected to machine removing and cleaning the blood

access on arterial and venous side

62
Q

peritoneal dialysis

A

uses patients own peritoneal membrane as the dialyzing machine

63
Q

body water distribution

A

2/3 of water is intracellular

1/3 of water is extra cellular (75% is interstitial, 25% is intravascular)

64
Q

diffusion in ECF

A

fluids and electrolytes diffuse freely between vascular and interstitial fluid compartments

interstitial space contains little protein bc of permeability (protein remains in blood)

65
Q

ICF diffusion

A

semipermeable membrane b/t ICF and ECF

freely permeable to water and impermeable to Na+ and K+

66
Q

important ions in fluid

A
  1. sodium
  2. potassium
  3. magnesium
  4. calcium
  5. phosphorus
  6. bicarbonate
  7. chloride
67
Q

sodium

A

most prevalent in ECF

imp. for transmission of nerve impulses

“water follows sodium”

68
Q

potassium

A

ICF

electrical impulses

69
Q

phosphorous

A

important in energy storage

electrical nutrality

works with magnesium

acts as a buffer in intracellular space

70
Q

bicarbonate

A

negative anion

principal buffer of body

neutralizes H+ and other organic ions

71
Q

chloride

A

negative

balances positive charge of cations

major role in renal function and fluid balance

72
Q

disturbances of water balance

A
  1. dehydration
  2. overhydration
  3. depletion of electrolytes
73
Q

dehydration

A

most common disturbance of water balance

either due to inadequate intake (diarrhea or vomiting) or excess H2O (comatose or debilitated patients)

74
Q

over hydration

A

caused by:

  1. excessive fluid intake when renal function is impaired
  2. excessive intake of fluids
  3. excessive administration of IV fluid
75
Q

depletion of electrolytes is caused by

A
  1. vomiting/diarrhea
  2. excessive diuretic usage
  3. excessvie diuresis in hyperglycemia
  4. renal tubular disease
76
Q

normal pH range of body

A

7.35-7.45

this is a must, we retain a pH despite large amounts of acid

77
Q

acid base balance

A

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
Q

acid base balance determination tests have ___ results

A

direct measurement of

  1. blood pH
  2. PCO2
  3. bicarbonate
79
Q

hendersen hassalbach eq.

A

makes H+ to CO2 to H2O

pH depends on ratio of bicarbonate to H2CO3

80
Q

respiratory control of carbonic acid

A

carbonic aid is dissolved as CO2 in plasma

hyperventilation lowers CO2 and H2CO3 in plasma

hypoventillation raises CO2 and H2CO3 in plasma

81
Q

renal control of bicarbonate

A

kidney selective reabsorb filtered bicarbonate

can manufacture bicarbonate to replace amounts lost in buffering acid from metabolic process

82
Q

pCO2, RR, and compensation

respiratory acidosis

A

increased pCO2

decrease in RR

kidney reabsorbs bicarbonate and makes more

this is caused by sleep apnea, rib fracture, narcotics, pneumonia)

83
Q

pCO2, RR, and compensation

respiratory alkalosis

A

increased RR

decreased pCO2

kidney increases bicarbonate excretion

caused by asthma, COPD, anxiety

84
Q

pCO2, RR, and compensation

metabolic acidosis

A

increased [Hydrogen] due to DKA, AKI, CKD, lactic acidosis

decreased pCO2

increases RR, makes more bicarbonate (if longstanding)

85
Q

pCO2, RR, and compensation

metabolic alkalosis

A

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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