nephro Flashcards

1
Q

horseshoe kidney

A

kidneys are linked and wrap around the aorta

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2
Q

how is fluid volume controlled

A

sodium

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3
Q

consequences of hyponatremia

hypernatremia

A

hypotension, cardvascular collapse, death

hypertension, pulmonary edema, death

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4
Q

proteinuria is usually = what

A

renal disease

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5
Q

how does the respiratory system regulate pH

A

by adding or taking away CO2

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6
Q

how does the renal system regulate pH

A

adding or taking away HCO3

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7
Q

respiratory compensation of acidosis

alkalosis

A

acidosis: ventilation increases, takes away CO2, shifts the equation to CO2 and H2O
alkalosis: decreases ventilation, retains CO2, shifts equation to H and HCO3

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8
Q

renal compensation of acidosis

alkalosis

A

acidosis: HCO3 is retained, H+ is excreted
alkalosis: HCO3 is secreted, H+ is retained

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9
Q

causes of metabolic acidosis

A

renal failure

ketoacidosis

ingestion of acid (aspirin overdose)

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10
Q

causes of respiratory acidosis

A

respiratory failure

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11
Q

causes of metabolic alkalosis

A

prolonged vomiting

ingestion of large amounts of bicarbonate

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12
Q

causes of respiratory alkalosis

A

hyper ventillation

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13
Q

what is the function of clinically useful diuretics

why do they work

A

causes an increased secretion of Na

water follows Na

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14
Q

regulators of sodium homeostasis

A

Hypothalamus/pituitary: ADH

Baroreceptors in the atria: Atrial natrietic peptide

sympathetic nervos system

RAAS

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15
Q

T/F use of diuretics can completely eliminate Na from the body

A

false, the body will eventually reach a new equilibrium

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16
Q

diruetic drug classes

A

carbonic anhydrase inhibitors

osmotic agents

thiaizide and thiazide-like agents

loop agents

potassium sparing

ADH antagonists

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17
Q

carbonic anhydrase

A

enzyme responsible for splitting H+ off H2CO3 or synthesizing H2O and CO2 f

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18
Q

inhibition of carbonic anhydrase causes what

A

alkaline urine

metabolic acidosis

minimal sodium loss

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19
Q

most important carbonic anhydrase inhibitor

what is this most used for

what does it do

A

acetazolamide (diamox)

acute mountain sickness

speeds acclimation process and treats symptoms

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20
Q

indications for the use of carbonic anhydrase inhibitors

A

open angle glaucoma

epilepsy

acute mountain sickness

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21
Q

functions of osmotic diuretics

A

increase tubule osmolality

increase renal ultrafiltrate

increase urine flow

preferential to water but electrolytes are also lost

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22
Q

osmotic diuretics

primary uses

complications iwth use

A

Mannitol glycerin, isosorbide

acute renal failure, increased ICP

may worse pulmonary edema, not useful for anuria

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23
Q

two instances where mannitol is particularly useful

how can you determine mannitol is a good therapy

A

acute renal failure due to hemoylsis or rhabdomyolysis

Mannitol IV increases urine flow, good response to test dose indicates it will work well

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24
Q

where is most Na reaborbed in euvolemia

expanded volume

dehydration

A

proximal tubule

less in the proximal tubule, increases Na excretion to urine

significant increase in Na reabsorption in PT

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25
Q

what are the functions of thiazide diuretics

A

inhibitors of Na/Cl symport in the tubule (increases Na/Cl excretion)

come inhibit carbonic anhydrase

some have a direct vascular effect

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26
Q

three thiazide drugs

A

hydrochlorothiazide

benzathiazide

bendroflumethazide

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27
Q

most important thiaizide like diuretic

A

chlorthalidone

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28
Q

side effects of thiazide drugs

A

HYPOKALEMIA

postural hypotension

change in glucose tolerance

hypercalcemia, uricemia

hyponatremia

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29
Q

complications of hypokalemia

A

muscle weakness

muscle soreness

heart arrhytmia

death

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30
Q

function of loop diuretics

A

blocks tubule reabsorption of Na

significantly increases Na+ and Cl-

venous dilation

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31
Q

T/F osmotic diuretics are useful in decreasing blood volume and Na

A

false

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32
Q

most important loop diuretic

A

furosemide (lasix)(

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33
Q

ADRs of loop diuretics

A

ototoxicity (deafness, vertigo, usually reversible)

excessive fluid and Na loss (hypotension, postural hypotension)

loss of electrolytes (K, Cl, Ca, Mg)

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34
Q

two types of potassium sparing diuretics

A

luminal membrane agents (triameterene)

mineralcorticoid antagonist (spirolactione)

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35
Q

T/F luminal membrane postassium sparing diuretics are very effective

A

false, they are not very effective and are usually combined with thiazides or loops

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36
Q

luminal diuretic toxicity

A

GI upset

increase urinary calcium

hyperkalemia, especially with Ace inhibitors or NSAIDs

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37
Q

what is the function of mineralocorticoid receptor antagonists

A

blocks the effect of aldosterone, preventing retention of NA and water, prevents excretetion of K and H+

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38
Q

T/F mineralocorticoid rececptor agonists can prevent cardiac remodeling

T/F they are typically not used as a sole medication

A

true, maybe

true

39
Q

toxicity related to aldosterone antagonsists

A

hyperkalemia

antiandrogenic effects (gynecomastia, ↓hirsuitism)

40
Q

issues with hyperkalemia

A

malaise

palpitation

muscle weakness

fatal arrhytmia

41
Q

non-selective ADH antagonists

A

lithium

demeclocycline

42
Q

T/F patients with pulmonary edema related to CHF will have almost immediate relief with lasix due to decreased heart workload

A

true, lasix will cause vasodilation

43
Q

wht are vaptans

A

selective vasopressin receptor blockers

44
Q

diuretic combinations

A

loop+thiazide (useful in pts who are refractory to loop diuretics)

loop/thiazide + potassium sparing

45
Q

T/F androgens are needed for BPH

A

true, specifically DHT

46
Q

what is 5-alpha reductase

A

the enzyme that converts T to DHT

47
Q

why are obese men at increased risk to BPH

A

because they have higher levels of estradiol because they have more aromatase to convery T into E

48
Q

obstructive BPH symptoms

A

—Decreased force & caliber of urine stream

—Difficulty initiating flow (“hesitancy”)

—Sensation of incomplete emptying

—Double voiding (2nd void within 2 hours)

—Straining to urinate

—Post-void dribbling

49
Q

irritative symptoms of BPH

A

—Urgency

—Frequency

—Nocturnal voiding

—All due to bladder pressure changes from partial outflow tract obstruction

50
Q

treatment strategies for BPH

A

—Observation

—Herbs, dietary

—Medical treatment

—Surgical treatment

51
Q

why might BPH symptoms spontaneously remit

A

lifesyle changes or ↓androgens

52
Q

dietary strategies to combat BPH

A

decreased fatty food intake

saw palmetto

53
Q

medical treatment of BPH

A

alphablockers

5-alpha reductase blockers

54
Q

how can the autonomic influences of the destrusor muscle be modified

A

cholinergic drugs can cause urgency and frequency

anitcholinergics will cause urinary retention

55
Q

what type of autonomic receptor is found in the bladder sphincter

A

alpha receptors

56
Q

blocking alpha 1 receptors leads to…

blocking alpha 2 leads to…

A

relaxation of the bladder sphincter

relaxation of the bladder and vascular smooth muscle, lowering BP

57
Q

what is the advantage of Alpha 1 blockers (tamsulosin, silodosin) over alpha 1 and 2 blockers (doxazosin, terazosin)

A

alpha 1 blockers will only work on the prostate and bladder

alpha 1 and 2 wil work on vascular smooth muscle as well

58
Q

Most important ADR for alpha1 blockers

how to prevent issue

A

orthostatic hypotension more common in volume/salt depleted patients

educate them on what is happening and give them their first dose in the office

59
Q

less common ADRs with alpha receptor blockers

A

CYP interaction

ejaculatory dysfunction

60
Q

T/F selective alpha blockers are 100% selective

A

false, they can still cross react

61
Q

advantages of 5-alpha reductase inhibitors

A

treats BPH and male pattern baldness

can also lower prostate cancer risk

62
Q

5-alpha reductase inhibiors

A

dutasteride

finasteride

63
Q

side effects of 5 alpha reductase inhibitors

A

diminished libido

erectile dysfunction

gynecomastia

64
Q

what is the time difference between symptomatic relief of BPH beteween alpha 1 blockers vs 5-alpha reductase inhibitors

A

7-10 days vs 6-12 months

65
Q

possible use of aromatase inhibiors in BPH treatment

A

might able to improve the estrogen/test ratio in overweight men

66
Q

why are elderly men at higher risk for UTI

A

atrophy of urinal muscosa

BPH

67
Q

Dx of UTI requires what

A

clinical suspcion + 100,000mL in voided samples or 1,000-10,000 in catheter samples

68
Q

T/F a culture needed to treat a UTI

A

false, culture is useful but you can start treatment without it

69
Q

typical UA results with UTI

A

cloudy or bloody

increased WBCs, bacturia, RBCs

casts = pyelonephtitis)

70
Q

cystitis symptoms

A

irritative voiding symptoms (frequency, urgency, pain)

hematura

fever (commonly in kids)

71
Q

pyelonephritis symptoms

A

fever, nausea, vomiting, diarrhea

flank pain

with or without voiding symptoms

72
Q

what would indicate high clinical suspcion of UTI in peds

A

unexplained fever in female <5

73
Q

typical pathogens for UTI

A

80-85% come from coliforms

15-20% from strep or enterococcus

hematogenous seeding is rare

74
Q

typical coliforms in UTI

A

enterobacter

escherichia

klebsiella

serratia

75
Q

when would an abnormal bacteria or fungus be suspected for a UTI

A

indwelling catheter

bed ridden

immunosuppresedd

76
Q

Treatment of UTI

A

fluids

vitamin C/cranberry juice

Abx

77
Q

T/F abx are always needed for cystitis and pyelonephritis

A

false, they are usually necessary for cystitis but always for pyelonephritis

78
Q

typical drugs for UTI

A

bactrim

nitrofurantonin

2nd gen cephalosporins

amoxicilin

fluoroquinolones

79
Q

complications of a UTI

A

untreated cystitis can lead to pyelonephritis

poorly treated pyelonephritis can produce kidney damage

80
Q

strategies to combat repeat UTI

A

◦Hydrate well

◦Empty bladder before/after intercourse (IC)

◦Antibiotic before IC

◦Apply antibiotic ointment to urethral meatus before IC

◦Long term low dose antibiotic therapy

81
Q

symptoms of acute prostatitis

A

—Fever is common

—Perineal, sacral, suprapubic pain/discomfort

—Irritative voiding symptoms

82
Q

PE and lab findings associated with acute prostatitis

A

enlarged and painful prostate

leukocytosis with left shift

UA with pyuria, bacturia, hematuria

positive cultures for G- bacteria

83
Q

inpt treatment of prostatitis

out patient

A

IV ampicillina and aminoglycoside (gent)

cipro or other fluoroquinolone

84
Q

significant differences between chronic and acute prostatitis

A

chronic prostatitis is more common in ment between 40-60

no fever with chronic

85
Q

causes of chronic prostatitis

A

very few are due to low grade infections

some are due to atypical infections

the majority are due to non-pecific inflammtion

86
Q

hallmark signs of bacterial chronic prostatitis

A

Urine and blood culture negative with leukocytes and bacteria in prostatic secretions

87
Q

best treatment for chronic bacterial prostatitis

A

bactrim for 6-12 weeks

88
Q

causes of ED

A

medical disorders (vascular compromise, DM, androgen insufficiency)

iatrogenic (ADRs from HTNdrugs, sequela from surgery)

pysch

89
Q

what is the function of PDE-5 inhibitors in treating ED

A

limits the action of phosphodiesterase, increasing duration of nitric oxide effect

nitric oxide increases blood flow to corpus cavernosum

90
Q

PDE-5 inhibitor examples

A

sildenafil (PRN)

tadalafil (daily)

91
Q

off label use of PDE-5 inhibitors

A

BPH (tadalafil)

pulmonary HTN (sildenafil, tadalafil)

92
Q

signficant ADRs with PDE-5 inhibitors

most common

other

A

priapism (contraindicates with organic nitrates)

headache, flushing, nasal congestion

color vison, hearing loss

93
Q

when would prostaglandin E analog be used to treat ED

example

fucntion

A

when pts can’t use PDE-5 inhibitors

alprostadil by urethral suppository or injection

probably relaxes corpus cavernosum smooth muscle