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Quarter 3 > Clin Med Exam 3 > Flashcards

Clin Med Exam 3 Flashcards

1
Q

Most common intrinsic cause

A

Acute Tubular Necrosis

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2
Q

Causes of Prerenal (decreased perfusion)

A 
True volume depletion
Hypotension
Edematous state
Selective renal ischemia
Drugs (NSAIDs, ACE-I)
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3
Q

Intrinsic causes

A

Renal ischemia
Sepsis
Nephrotoxins

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4
Q

Acute Tubular Necrosis d/t IV Contrast

A

Contrast causes tubular epith cell toxicity and Renal medulary ischemia frm vasoconstriction

Risk factors:
Pre-existing renal dz
Volume depletion
Repeated dose of contrast

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5
Q

Reduction in GFR will only occur if:

A

there is a Bilateral obstruction or an issue LOW

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6
Q

Obstruction most commonly d/t

A

Prostatic dz (hyperplasia or CA)
or Mets
or Neurogenic bladder

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7
Q

Normal urine output

A

1-2 L /day

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8
Q

Oliguric (little urine)

A

<400 mL in 1 day

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9
Q

Anuric

A

<50- 100 mL in 2 day

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10
Q

Muddy brown casts

A

Acute Tubular Necrosis

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11
Q

FENa

A

How is kidney handling sodium? (Na)

% of filtered Na that is actually excreted in urine

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12
Q

FENa <1%

A

Pre-Renal

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13
Q

FENa >2%

A

Intra-renal (Acute tubule necrosis)

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14
Q

FENa is NOT useful for:

A

Pts on diuretics

pts in AKI (bc serum Cr is not stable)

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15
Q

When to perform Renal biopsy

A

No other explanation
Cr markedly elevated or significantly worsening quickly

Purpose: to prevent ESRD

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16
Q

Contra to Renal biopsy

A 
Bleeding issues
Severe HTN
Pyelonephritis
Renal tumor
Solitary native kidney
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17
Q

Life threatening complications of Acute Kidney Injury

A 
Volume imbalance
Metabolic Acidosis
Hyperkalemia, Hyperphosph
Uremia
HypOOOcalcemia
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18
Q

Severe AKI can cause

A

Altered mental status

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19
Q

First step to managing AKI

A

Correct volume status (this can improve or reverse AKI)

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20
Q

Fluid challenge

A

identify Pre-renal failure

Crystalloid isotonic IVF

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21
Q

Pt doesn’t respond to Fluid challenge

A

Likely Acute Tubular Necrosis or other forms of Intrinsic or Post renal

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22
Q

If pt is still producing urine,

A

give diuretic

BUT should not be used for prolonged tx

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23
Q

Metabolic acidosis happens in AKY why?

A 
Not excreting the acid
Not making bicarb
Low GFR
Many causes of AKI produce inc acids
Diarrhea net loss of bicarb
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24
Q

Tx of Metabolic Acidosis

A

Dialysis or

Bicarb administration

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25
Q

Dialyze pts with Metabolic Acidosis IF

A

Not producing urine (or V little)
Volume overloaded
pH <7.1

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26
Q

Bicarb can make what worse?

A

Volume overload

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27
Q

When to give bicarb for Metabolic Acidosis?

A 
Pt is not volume overloaded
no other indication for acute dialysis
ESP IF:
diarrhea is cause
ph <7.1 and awaiting dialysis
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28
Q

Low Calcium

A

Chvostek sign (face)
Trousseaus sign (arm)
Paresthesias
Tetany

NEED IV Calcium (but don’t replace too quickly)

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29
Q

If pt has no sx and Calcium is low,

A

correct the High phosphate with: Phosphate binders

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30
Q

Uremia

A

urine in the blood

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31
Q

Uremia can lead to

A

Pericarditis
Neuropathy
Decline in mental status

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32
Q

Uremia is more common in

A

CHRONIC kidney dz

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33
Q

Leading cause of kidney failure

A

DM and HTN

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34
Q

Those with CKD and DM are at much higher risk of also developing

A

Cardiovascular dz

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35
Q

CHRONIC Kidney Dz

A

3 OR MORE MONTHS OF:
Decreased kidney fx (GFR <60)
OR
Kidney Damage (Albuminuria ACR 30 or more, abnormal imaging, abnormal urinary sediment, hx transplant)

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36
Q

RBC casts

A

GLOMERULOnephritis

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37
Q

Pts “at risk” for developing CKD should be screened by:

A

Urine ACR

Serum Cr to estimate GFR (eGFR)

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38
Q

Uremic syndrome

A

accumulation of metabolic Waste products or Uremic toxins

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39
Q

Uremic syndrome

A

seen w profound decrease in GFR

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40
Q

Uremic syndrome

A

Fatigue, anorexia, n/v, pruritus, bruising, METALLIC tase in mouth, SOB, DOE, Pericarditis, restless leg syndrome, seizure, encephalopathy

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41
Q

Secondary hyperparathyroidism

A

Hyper-phosphatemia, hypocalcemia, decrease in vitamin D

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42
Q

Secondary hyperparathyroidism

PTH

A

High phosphorus
Low Ca2+

In an effort to raise Ca levels, we stimulate PTH

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43
Q

Meds that lower GFR

A

ACE-I

NSAIDs

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44
Q

ACE-I and ARBs

A

dilate Efferent arteriole, decreasing glomerular pressure

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45
Q

When ACE-I and ARBs can be harmful:

A

Bilateral Renal Artery Stenosis

caution in Acute Kidney Injury (may see acute reduction in GFR and hyperkalemia)

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46
Q

When to refer to nephrologist

A

GFR <30

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47
Q

Chronic intertubulo dz of kidney

A

Obstructive uropathy
Reflux uropathy
Analgesic uropathy

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48
Q

Chronic tubulointerstitial

A

spares the glomeruli

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49
Q

Chronic tubulointerstitial dz General findings

A

Polyuria
Hyperkalemia
UA nonspecific- proteinuria (<2), broad waxy casts

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50
Q

Obstructive sx

A

PAIN, change in UOP, HTN, hematuria, inc serum Cr

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51
Q

Obstructive pathology UA

A

Hematuria, pyuria, bacteriuria but often bland

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52
Q

Obstructive pathology US

A

Detect mass, hydroureter, hydronephrosis

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53
Q

Reflux Nephropathy

A

the result of Vesicoureteral Reflux (VUR)

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54
Q

VUR

A

urine can extravasate into the interstitium–> inflammatory response–> scarring/fibrosis of kidney

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55
Q

Reflux Nephropathy

A

typically in young children w hx of recurrent UTI

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56
Q

Analgesic Nephropathy

A

long term consumption of Analgesics (often seen in those w chronic back pain)

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57
Q

Analgesic Nephropathy labs

A

Often no sx
Labs show elevated serum Cr
UA: hematuria, sterile pyruia, mild proteinuria
Anemia

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58
Q

Analgesic Nephropathy

CT Scan:

A

Renal papillary necrosis/calcification

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59
Q

Nephrotic syndrome

A

Non-inflamm
Proteinuria: >3.5
“foamy” oval fat bodies
More edema than in the other

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60
Q

Proteinuria >3.5g/day

A

Nephrotic syndrome

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61
Q

Nephrotic synd: primary dz (3 subtypes)

A

Minimal change dz
Membranous nephropathy
Focal segmental glomerulosclerosis

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62
Q

Nephrotic synd: secondary dz

A

Diabetic nephropathy

Amyloidosis

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63
Q

Oval fat bodies

Lipiduria

A

Nephrotic synd

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64
Q

Minimal change dz (MCD)

A

Most common nephrotic synd in KIDS

Most idiopathic, but can be secondary following URI or Allergic rxn

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65
Q

1st line tx for Minimal change dz (primary nephrotic synd)

A

Prednisone

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66
Q

MCD Minimal change dz primarily affects

A

Podocyte

podocyte foot process fusion

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67
Q

Membranous nephropathy

A

adults
peak in 40s, 50s

Primarily idiopathic, thought to be immune mediated

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68
Q

Membranous nephropathy sx

A

Typical of Nephrotic synd

RISK OF CLOT

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69
Q

Tx for Membranous nephropathy

A

Supportive, immunosupp, transplant

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70
Q

Adverse risk factors for Membranous nephropath

A

Male sex, older age >50YO

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71
Q

FSGS

A

specific pattern under microscope given this name

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72
Q

FSGS

A

> 70% present with typical Nephrotic synd sx

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73
Q

FSGS greater risk

A

African American

3-4x more common men

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74
Q

FSGS

A

Damage to podocyte,

Sclerosis

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75
Q

FSGS tx

A

Supportive, Immunosupp, Dz specific tx for if secondary dz

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76
Q

Poor outcome for FSGS IF

A

Nephrotic range proteinuria
African american
Renal insuff

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77
Q

What to order if you suspect Minimal change nephropathy

A

UA

Serology

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78
Q

Diabetic Nephropathy (secondary dz)

A

Most common cause of ESRD in US

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79
Q

Diabetic nephropathy

A

usually in pts who have had DM for 10-20 yrs BUT may be present at time of dz in those with DM Type II

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80
Q

Diabetic nephropathy

A

Morphologic changes in kidney
inc proteins in urine
Albuminuria >300

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81
Q

Tx of Diabetic nephropathy

A 
Strict glycemic control
BP control
ACE-I, ARBs
Statin therapy
Dialysis/ transplant
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82
Q

Renal Amyloidosis

A

abn shaped protein that CLUMP together, can deposit in gomerulus

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83
Q

Renal Amyloidosis screening

A

SPEP and UPEP

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84
Q

Renal Amyloidosis tx

A

Refer to nephro

Tx underlying cause

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85
Q

SPEP and UPEP

A

Multiple Myeloma

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86
Q

C-ANCA and P-ANCA

A

GPA

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87
Q

Microalbuminurie

A

Early sign:
Diabetic nephropathy
Kidney damage

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88
Q

Test of choice to RULE OUT obstruction

A

Renal US

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89
Q

Test of choice to DIAGNOSE Kidney stone/Nephrolithiasis

A

CT non contrast

90
Q

Gold standard test to DIAGNOSE Renal Vein Thrombosis (clot)

A

MRI

91
Q

Renal biopsy can aid in the dx of:

A 
Unexplained AKI
Nephrotic synd
Acute Nephritic synd
Mass
Assess for rejection after transplant
92
Q

Cystourethrogram

A

Contrast injected, X Rays taken while pt is voiding “real time”

Test for VUR,
Bladder distortion
Fistula
Perforation

93
Q

Cystoscopy (camera into bladder) used to diagnose

A

Interstitial Cystitis “painful bladder synd”

Bladder tumor, tone, or scarring

94
Q

Nephritic syndrome

left side

A

Hematuria
Glomerulonephritis
Rapidly prog GN (RPGN)

95
Q

Nephrotic syndrome

right side

A 
Asymptomatic proteinuria 
Nephrotic synd (edema)
96
Q

Glomerulonephritis

A

is INFLAMMATORY

usually deposits of immune complexes

97
Q

Glomerulonephritis

A 
Coca colored, smoky
RBC casts
protein <3
Elevated Cr, dec GFR
Oliguria (little UOP)
HTN
98
Q

RPGN

A

more severe GN

CRESCENT formation

99
Q

CRESCENT

A

RPGN

100
Q

IgA Nephropathy

“Berger”

A

Most common cause of primary GN in the world

Think everybody loves Bergers

101
Q

IgA Nephropathy

A

Young Asains and Whites
20s-30s
1-2 DAYS AFTER URI

102
Q

IgA Nephropathy is assoc with

A

Celiac
Liver cirrhosis
HIV
EBV

103
Q

Tx for IgA if pt has persistent proteinuria >1
elevated Cr
reduced GFR or
HTN

A

ACE-I/ ARB

104
Q

Post Strep GN

A

1-3 WEEKS after infection

Labs: Low C3 complement, ASO titer, + strep culture

105
Q

Tx for Post Strep GN

A

Supportive

should feel better in 2 weeks

106
Q

IgA Vasculitis/HSP

A 
Tetrad:
Artralgias
Palpable purpura
Abdominal pain
Renal dz*
107
Q

IgA Vasculitis/HSP

A

This is an immune mediated SYSTEMIC vasculitis

unique bc it has all the other system sx

108
Q

IgA Vasculitis/HSP

A

Adults are at increased risk of PROGRESSIVE Renal dz

Tx: supportive

109
Q

Anti GBM/Goodpasture

A

“Syndrome”: GN and pulm

“Disease”: GN, pulm dz, AND anti-GBM antibodies

110
Q

Anti GBM/Goodpasture

A

Peak for males: 30s

Peak for females: 50-70s

111
Q

Anti GBM/Goodpasture sx

A

classic RPGN (rapidly progressive GN, with CRESCENT)

may need dialysis

112
Q

Anti GBM/Goodpasture pulm sx

A

Alevoolar hemmorhage, Hemoptysis, SOB

Tx: Plasmapharesis and Immunosupp (PRednisone and Cycloph)

113
Q

Tx for Anti-GBM/Goodpasture

A

Dialysis
Plasmapharesis
Immunosupp (Prednisone and Cyclosporine)

114
Q

Tx for IgA Nephropathy

A

ACE-I/ARB w the criteria

115
Q

Tx for Post Strep and IgA Vasculitis/HSP

A

Supportive

116
Q

Tx for Anti-GBM/Goodpasture

A 
Plasmapharesis
Immunosupp (Prednisone and Cycloph)
117
Q

SLE Nephritis

A 
LUPUS
Anti-ds DNA antibodies
Non whites
Elevated Cr
Confirm w biopsy
118
Q

Pauci Immune (3 subcategories)

A

GPA: Granulomatosis w Polyangitis
MPA: Microscopic Polyangitis
EGPA: Eisinophillic Granulomatosis w Polyangitis

119
Q

Pauci Immune

A

all end in “PA” for Polyangitis

ANCA-associated

120
Q

C-ANCA

A

GPA: Granulomatosis w Polyangitis

Upper AND Lower
Necrotizing granulomos

“Saddle nose”, cough, SOB, nodules/infiltrate/cavitations on CXR

121
Q

All of ANCA associated are

A

Classically RPGN (rapidly progressing)

122
Q

Unique characteristic of MPA: Microscopic Polyangitis

A

SPARES upper resp tract

No granuloma

123
Q

P-ANCA associated

A

MPA: spares upper, no granulomas
EGPA: asthma and eisonophils

124
Q

Tx for all 3 types of ANCA associated (very necessary! Poor prognosis w/o Tx)
GPA
MPA
EGPA

A

Immunosupp

  • Corticosteroid
  • Cytoxic agents
125
Q

EGPA: Eisinophilic Granulomatosis w Polyangitis

“Churg Strauss”

A 
Asthma and Eisinophils
3 phases:
1. Atopic, Allergic rhinitis, Asthma
2. Eisinophilic infiltrate
3. Vasculitis
126
Q

Tx for Polycystic Kidney Dz

A

Strict BP control, low salt
TOLVAPTAN
Dialysis, Transplant, Analgesics

127
Q

Gene for A. Dominant PKD

A

PKD1 or PKD2

128
Q

Sx of PKD

A

HTN, pain, HEMATURIA, Hx of UTI and stones

129
Q

Other complications of PKD

A

INTRAcranial aneurysm
Hepatic cysts
Valvular heart dz

130
Q

Tx for PKD

A

TOLVAPTAN

131
Q

Autosomal Recessive form of PKD

A

PKHD1 gene
Kidneys AND Hepatobiliary system

K and H

132
Q

Autosomal Recessive form of PKD

A

Kids and infants

133
Q

Autosomal Recessive PKF

A

PKHD1 gene
Kidneys and Liver-biliary
Enlarged kidneys AND Liver fibrosis

134
Q

Severe cases of A. Recessive PKD

A 
Neonates have ERD
Respiratory distress
Big kidneys
HTN
Portal HTN (liver)
Feeding diff and FTT
135
Q

When can you see Autosomal PKF on Ultrasound?

A

after 24 weeks gestation

136
Q

Tx of PKD

A

Supportive with multi-disc

137
Q

Definitive Diagnosis of Autosomal Recessive PKF (infants and kids)

A

Genetic testing

Early screening: Ultrasound

138
Q

ACUTE Kidney Injury results in

A

Retention of urea and nitrogenous waste

Dysregulation of volume and electrolytes

139
Q

Criteria for ACUTE kidney injury based on

A

Serum Cr OR

Urine output

140
Q

Sometimes Cr isn’t a good measure of GFR because

A

Cr hasnt had time to build up

Cr was removed by dialysis

141
Q

What is most often used for diagnosing ACUTE kidney injury?

A

KDIGO

142
Q

Dx ACUTE kidney injury

A

Inc in Serum Cr 0.3 or more within 48 hours

Inc in Serum Cr 1.5x baseline

Urine volume <0.5 for 6 hours

143
Q

Huge risk for developing AKI

A

Hospitalized pts

60% of ICU pts develop AKI

144
Q

AKI in hospital is most often d/t

A

Pre-Renal or

Acute Tubular dz (Intrinsic)

145
Q

Most common etiology of ACUTE kidney injury

A

Acute Tubular Necrosis (Intrinsic)

146
Q

Rate of occurence

A
  1. ATN (Intrinsic)
  2. Pre-Renal (perfusion)
  3. Obstruction least common
147
Q

Causes of Pre-Renal (perfusion)

A 
Volume depletion (n/v/d/burn)
Hypotension
Edema
Renal ischemia (also in intrinsic)
Drugs (NSAIDs, ACE-I)
148
Q

Intrinsic causes

A

Renal ischemia (in pre-renal also)
Sepsis
Nephrotoxins

149
Q

Risk factors of developing Acute Tubular Necrosis (ATN- Intrinsic cause)

A

Pre-existing Renal dz
Volume depletion
Repeated dose

150
Q

Most common causes of Post-renal obstruction

A

Prostate dz
Cancer
Neuro dz

151
Q

How can UA be helpful in diagnosing Acute Kidney Injury?

A

Cr
GFR
FENa (how is kidney excreting sodium)

152
Q

Signs of ACUTE kidney injury

A

Muddy brown casts

*pathognomic for ATN

153
Q

Normal Creatine for M and F

A

M 0.6-1.2

F 0.5-1.1

154
Q

FENa is <1

A

Pre-Renal etiology

155
Q

FENa is helpful in distinguishing

A

Pre-Renal AKI from ATN (Intrinsic)

156
Q

Biggest reason to perform Renal imaging

A

Assess for Obstruction

157
Q

Danger with obstruction, Predispose for

A

UTI –> Urosepsis –> Kidney failure

158
Q

When to do Renal biopsy?

A

If Cr is MARKEDLY ELEVATED or

SIG WORSENS in couple days

159
Q

Importance of getting a Biopsy when indicated

A

More definitive tissue dx
Therapeutic intervention
Prevent ESRD*

160
Q

Contra to getting Renal Biopsy

A 
Bleeding diathesis
Severe HTN
Pyelonephritis
Renal tumor
One kidney
161
Q

1st Step when dealing with ACUTE Kidney injury?

A

Volume challenge to see if it can be corrected

162
Q

If pt meets these things, do a fluid challenge:

A

Clinical hx of volume depletion (vomiting/diarrhea)
Physical showing Hypovolemia (hypotension/tachy), and/or
Oliguria (little urine)

163
Q

How much fluid to give for a fluid challenge?

A

1-3 L to start

If they DONT RESPOND issue is probably ATN or other Intrinsic

164
Q

What 2 things are we looking for in Fluid Challenge?

A

Increase Urine output

Increased Kidney function (Cr or GFR)

165
Q

If a pt is volume overload but still peeing, can give DIURETICS but

A

not a long term solution

166
Q

What is the MOST EFFICIENT method of volume removal?

A

Dialysis

167
Q

Diuretics are

A

Temporizing measure

168
Q

Recap:

Tx of Volume overload

A

Diuretics (temporary)

Dialysis

169
Q

Tx of Metabolic Acidosis

A

Dialysis

Bicarb administration

170
Q

How to treat Metabolic Acidosis is pt is VOLUME OVERLOADED?

A

Dialysis

Bicarb can make volume overload WORSE

171
Q

When to use Dialysis to treat Metabolic Acidosis?

A

(it is pretty much preferred)
Not producing urine
Volume overloaded
pH <7.1

172
Q

When to give bicarb to treat Metabolic acidosis?

A

Volume status is normal (not overloaded)
Acidosis d/t DIARRHEA
ph <7.1 and waiting for dialysis

173
Q

Hyperkalemia as a result of AKI

A

Very few sx UNTIL YOU DIE

“it’s: A F A C T”

174
Q

Hyperkalemia as a result of AKI, Sx can include:

A

Impaired neuromuscular transmission
Cardiac abnormalities

Arrhythmia
Flaccid paralysis
Asc musc weakness
Conduction abnormality
T waves
175
Q

Tx for Hyperkalemia

A

Insulin to drive K into cells

Remove extra K with Dialysis

176
Q

Hypocalcemia sx

A

Paresthesia
Chvostek
QT prolongation

177
Q

Hypocalcemia tx if pt is symptomatic

A

IV calcium

178
Q

Hypocalcemia tx if pt is asymtpomatic

A

if High Phosphorus levels are present also, 1st step is to correct Phosphorus!

179
Q

Hypocalcemia, no symptoms, and Phosphate is >5.5

A

Tx with Dietary phosphate binders

180
Q

Low ca, no symptoms, HIGH phosphate, what do we treat with?

A

Serum ionized Ca low: Ca Acetate or Ca Carbonate

Serum ionized Ca high: Aluminum hydroxide, Lanthanum Carbonate

181
Q

Serum ionized Ca low

A

Calcium Acetate or

Calcium Carbonate

182
Q

Serum ioinized Ca is high

A

(Wierd names)
Aluminum hydroxide
Lanthanum carbonate

183
Q

Dialysis should be given to peeps with SEVERE UREMIA “urine in the blood”

A

Pericarditis
Neuropathy
Unexplained AMS

184
Q

Females usually get

A

Pyelonephritis (kidney) or

Cystitis (bladder)

185
Q

Only upper tract one

A

Pyelo

186
Q

UTI Risk factors (3)

A

Reduced urine flow
Promotion of colonization (sex, spermicide, recent abx)
Facilitate ascent (catheter, incontinence)

187
Q

Special populations regarding UTIs

A

Pregnant
Men
Comorbidities, Immunocomp, Underlying urology conditions

188
Q

Acute SIMPLE Cystitis

A

confined to bladder

No s/s suggestive of Upper urinary tract or systemic

189
Q

Systemic sx suggestive of Acute COMPLICATED UTI

A

Fever

Chills, fatigue, malaise, Flank pain, CVA tenderness, Pelvic/perineal pain in men

190
Q

Sx of Acute SIMPLE Cystitis

A

Dysuria, frequency, urgency

+/- hematuria and suprapubic discomfort

191
Q

Culture for Acute SIMPLE Cystitis?

A

Not recommended, unless:

  • Atypical presentation/dx uncertain
  • Suspect COMPLICATED
  • Unresolving sx
  • Suspect abx resistance
  • Special pops
192
Q

Culture results (if you ordered one) of Acute SIMPLE cystitis

A

> 10^3 CFU = DIAGNOSTIC

193
Q

Culture results (if you got one) of Acute SIMPLE cystitis

A

> 10^2 in combination with Typical sx= POSITIVE culture

194
Q

Tx of Acute SIMPLE Cystitis

A

Abx:
Nitrofurantoin (Macrobid)
Bactrim
Fosfomycin

195
Q

Tx of Acute SIMPLE Cystitis in PREGNANT

A

Fosfomycin or Augmentin

196
Q

Do NOT give to pregnant for Acute SIMPLE Cystitis

A

Fluoroquinolones

197
Q

Tx for Acute SIMPLE Cystitis

A

Nitro (5 days)
Bactrim (3 days)
Fosfo (single dose)

198
Q

Is f/u culture needed with Acute SIMPLE cystitis?

A

NOT IF SX RESOLVE, unless:

You are pregnant

199
Q

Acute Pyelonephritis

A

Systemic sx
Involving kidney parenchyma and Renal pelvis

Flank pain, fever, malaiaise

200
Q

MORE labs for Pyelo suspicion

A

Always UA with C and S

201
Q

Results indicating Pyelo

A

WBC casts

CFU > 10^5

202
Q

Do you order CBC and BMP for Acute Pyelo?

A

Not unless pt is hospitalized

203
Q

Imaging for Acute Pyelo? Not unless:

A

Severely ill
Sx persist even after 48-72 hrs of Abx
Suspect Obstruction
Recurrent sx w/in few wks of tx completion

204
Q

What imaging to order with Acute Pyelo?

A

CT A/P with AND without contrast

205
Q

Tx for Mild-Moderate Acute Pyelo

A

Fluoroquinolones

(Cipro or Levo) 5-7d

206
Q

Other considerations for Acute Pyelo tx

A

If pathogen is susceptible to Bactrim, can do that instead

If E.Coli resistance >10%, then give initial does of Rocephin before discharging pt

207
Q

F/u for Acute Pyelo

A

WITHIN 48-72 HOURS

208
Q

Need f/u culture for Acute Pyelo?

A

Not unless you are pregnant

209
Q

When is Acute Pyelo considered Severe? –> Hospitalization

A

Critically ill, Hemodynamically unstable, Pers high fever, Bad pain, Obstruction, Renal dysfx, Unable to eat/drink, Worried about compliance

210
Q

Tx of Acute Pyelo for Severe/Inpatient

A

IV Abx

  • Fluoroquinolones
  • ER Cephalosporin
  • ER PCN
  • Carbapenem
  • Aminoglycoside

+supportive

211
Q

Primary tx for Acute Pyelo

A

Nitro
Bactrim
Fosfo

212
Q

Acute pyelo things you HAVE TO ORDER

A

UA, C and S

213
Q

Acute Pyelo labs

A

WBC Casts

CFU >10^5

214
Q

Acute Pyelo tx for outpatient

A

Fluoroquinolones

215
Q

IC/Painful bladder synd

A

Abscence of infection

>6 weeks

216
Q

Associations with IC/Painful bladder synd

A

IBS
Fibromyalgia
>40 YO

217
Q

Crazy pathophys of IC/Painful bladder syndrome

A 
Glycosaminoglycan layer
Urothelial inj
Pro-inflammaotry
Mast cell
Fibrosis
Neural hypersens
Neuropathic pain
Voiding dysfx
218
Q

Presentation of IC/Painful bladder synd highly VARIABLE

In men, usually:

A

Pelvic pain with Sexual dysfx

219
Q

What you may see on Cytoscopy (camera) with IC/Painful bladder syndrome

A

Altered urothelium

  • Glomerulations
  • Hunner lesions
220
Q

1st line tx for IC/Painful bladder syndrome

A

Behavior/lifestyle

Pyridium OTC

221
Q

2nd line tx for IC/Painful bladder syndrome

A

Oral: TCA(Amitriptyline), Pentosan Polysulfate(Elmiron), Antihistamine(Hydroxyzine)

Other: Lidocaine, PT

222
Q

Tx for Overactive blader

A

1st line: Behavioral

2nd line: Antimuscarinics (Oxybutynin, Tolterodine, Solifenacin), Beta-agonist (Mirabegron)

Quarter 3 (17 decks)

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