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Foundations 2 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What is the average physiologic protein excretion in adults?

A

80mg/day (16-32mg albumin)

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2
Q

What is a pathologic amount of protein excretion?

A

150mg or more

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3
Q

Microalbuminuria

A

30-300mg/day

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4
Q

Macroalbuminuria

A

> 300 mg/day

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5
Q

Nephrotic range of protein

A

> 3-3.5g

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6
Q

Causes of Proteinuria

A

Glomerular disease (most common-altered permeability)
Overflow (oveproduction of small proteins)
Tubular (diminished reabsorptive capacity)

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7
Q

Glomerular Disease

A

Nephritic or nephrotic syndromes
Results in hypoalbuminemia due to loss of protein
Biopsy is gold standard of diagnosis

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8
Q

Nephritic Syndrome

A

Inflammatory process with associated immunologic response leading to renal glomeruli damage

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9
Q

Nephritic Syndrome Clinical Presentation

A

Periorbital edema, swollen lips, puffy pale face, “Coca Cola” urine (RBC casts), hypertension, occasional WBCs, proteinuria (but <3.5g/day)

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10
Q

Rapidly Progressing Glomerulonephritis (RPGN)

A

Severe injury to glomerular capillary wall, GBM and bowman’s capsule; progresses to renal failure in weeks-months
Most severe and clinically urgent end of nephritic spectrum

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11
Q

Primary Nephritic Syndromes

A

Post-infectious, IgA nephropathy, Henoch-Schonlein purpora, Pauci-immune glomerulonephritis, anti-glomerular basement membrane glomerulonephritis (Goodpastures)

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12
Q

Post Infectious Glomerulonephritis

A

1-3 weeks after Group A strepinfection (pharyngitis or impetigo)
Good prognosis in kids, but adults prone to CKD

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13
Q

Post Infectious GN Presentation

A

Pt is oliguric, edematous, hypertensive, coca-cola urine w/ RBC casts, high ASO titers

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14
Q

Post Infectious GN Treatment

A

Anti-hypertensives (ACE, ARB), salt restriction, diuretics (loops and thiazides)

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15
Q

IgA Nephropathy

A

AKA Bergers Disease, most common primary GN worldwide
IgA deposition in glomerular mesangium leading to an inflammatory response
Most common in kids/young adults

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16
Q

IgA Nephropathy Presentation

A

Coca-cola urine 1-3 days after URI or GI infection

Hematuria, proteinuria, increased IgA levels, normal complement

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17
Q

IgA Nephropathy Treatment

A

Corticosteroids if proteinuria is1-3.5g/day

ACE, ARB if proteinuria, want BP <130/80

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18
Q

Henoch-Schonlein Purpura

A

Systemic small vessel vasculitis associated w/ IgA deposition in vessel walls
Most common in kids, associated with infection

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19
Q

Henoch-Schonlein Presentation

A

Palpable purpura in legs and butt w/ arthralgia and abdominal symptoms
Decreased GFR
No definitive treatment but can try plasmapheresis and DMARDs

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20
Q

DMARDs

A

Disease modifying antirheumatic drugs-azathioprine, cyclophosphamide, hydroxychloroquine, methotrexate

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21
Q

Pauci-immune Glomerulonephritis (ANCA-associated)

A

Seen with small vessel vasculitis (granulomatosis with polyangitis, eosinophilic granulomatosis w/ polyangitis, microscopic polyangitis

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22
Q

ANCA Asscoiated GN Presentation

A

Fever, malaise, weight loss, purport
90% have respiratory symptoms with nodular lesions that can bleed
Labs are ANCA positive, slight hematuria and proteinuria

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23
Q

ANCA Associated GN Treatment

A

High dose corticosteroids, DMARDs

75% remission with treatment

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24
Q

Anti-glomerular Basement Membrane Glomerulonephritis (Goodpastures)

A

GN + pulmonary hemorrhage
Basement membrane injury from anti-GBM antibodies
Accounts for 10-20% of patients with RPGN
Peak in 2-3rd decades and 6-7th decades

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25
Q

Goodpastures Presentation

A

Typically have lung injury
20-60% preceded by URO; hemoptysis, dyspnea, RPGN
Labs have anti-GBM antibodies, proteinuria, sputum shows hemosiderin-laden macrophages
Pulmonary infiltrates on CXR

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26
Q

Goodpastures Treatment

A

Plasmapheresis to remove antibodies

Corticosteroids and DMARDs to prevent new antibodies/inflammatory response

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27
Q

Nephrotic Syndrome Labs

A

Urine protein excretion >3.5g, hypoalbuminemia (<3g/dL), oval fat bodies in urinary sediment (from hyperlipidemia), deficient vitamin D, zinc and copper levels

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28
Q

Nephrotic Syndrome Presentation

A

Peripheral edema is hallmark (when serum albumin <2g), dyspnea, hyperlipidemia,

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29
Q

Nephrotic Syndrome

A

Significantly increased basement membrane permeability

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30
Q

Nephrotic Syndrome Treatment

A

Increased protein intake, salt restriction, thiazide and loop diuretics, high intensity statins, anticoags

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31
Q

Types of Nephrotic Syndromes

A

Minimal Change Disease, membranous nephropathy, focal segmentation glomeruulosclerosis (FSGS)

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32
Q

Minimal Change Disease

A

Increased glomerular permeability, foot process effacement
Mostly seen in kids (80% of all proteinuria)
men=women but boys>girls

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33
Q

Membranous Nephropathy

A

Most common primary nephrotic syndrome in adults

Immune complex deposition in glomerular capillary walls result in increased permeability

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34
Q

Membranous Nephropathy Presentation

A

Asymptomatic; edema w/ frothy urine, high incidence of venous thromboembolism
Subnephrotic syndrome-classic nephrotic syndrome

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35
Q

Membranous Nephropathy Treatment

A

ACE/ARB if BP >125/75

Corticosteroids in patients with no improvements after 6 months of conservative care

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36
Q

Focal Segmental Glomerulosclerosis (FSGS)

A

Increased permeability due to podocyte injury

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37
Q

FSGS Presentation

A

Proteinuria is initial presenttion

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38
Q

FSGS Treatment

A

Diuretics for edema, ACE/ARB to reduce proteinuria/HTN, Statins for hyperlipidemia, high dose corticosteroids for overt nephrotic syndrome for 16 weeks

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39
Q

Simple Renal Cyst Epidemiology

A

65-70% of renal masses, mostly >70

Most common incidental finding with little clinical significance

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40
Q

Simple Renal Cyst

A

Develop in cortex and medulla with solitary or multiple, unilateral/bilateral, <1 cm or >10cm, clear to straw-colored fluid filled, round or oval, with a single epithelial layer lining

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41
Q

Simple Renal Cyst Presentation

A

No clinical manifestations
Rupture rares>flank pain, hematuria
Infection rare>insidious fever, vague limbo-abdominal pain, +/-hematuria or pyuria
HTN rare due to. compression of renal parenchyma

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42
Q

Simple Renal Cyst Diagnositics

A

Ultrasound-sharply demarcated with smooth thin walls, anechoic, enhanced back wall

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43
Q

Complex Cyst Diagnostics

A

Ultrasound-thick walls/septations, calcifications, solid components, mixed echogenicity, vascularity
CT w/ and w/out contrast

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44
Q

Acquired Renal Cysts

A

Most common reason is chronic renal failure
dialysis increases risk of development (yearly screening every 3-5 years after dialysis)
Rarely symptomatic, small-normal kidneys, may increase risk of RCC

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45
Q

Diagnostics of Acquired Renal Cysts

A

Ultrasound: Bilateral involvement, >4 cysts, diameter <0.5cm up to 2-3cm

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46
Q

Cyst Treatment

A 
Excision based on Bosniak classification 
Pain: acetaminophen or NSAIDs if normal kidney function
Persistent pain (cysts >5cm): percutaneous aspiration w/ injection of sclerosing agent, laparoscopic unroofing
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47
Q

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

A 
Aggressive form (more common) is PKD1, slow growth is PKD2, 5% spontaneous
Irreversible decline in renal function by age 60 (50%)
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48
Q

ADPKD Pathology

A

Multiple cysts with bilateral involvement, gradual cyst growth, gradual loss of parenchyma, significant kidney enlargement, progressive decline in renal function (GFR)

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49
Q

ADPKD Clinical Presentation

A

Presents in 30s-40s with pain (abdominal, flank, back, chest), 50% have HTN, large palpable kidneys, frequent UTIs (treat with cipro), hematuria, mild proteinuria

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50
Q

ADPKD Diagnostics

A

Ultrasound for screen/monitoring

CBC (anemia), CMP(decline kidney function), UA (blood, protein), genetic screening (PKD 1/2)

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51
Q

ADPKD Treatment

A

ACE/ARB, low sodium/caffeine, pain management, avoid nephrotoxic agents/contact sports, manage complications (infection, hemorrhage, etc)
Dialysis or transplant in end stage

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52
Q

Medullary Sponge Kidney

A

Congenital disorder, mostly sporadic and asymptomatic
Characterized by dilation of collecting tubules (1+ renal papillae in 1 or both kidneys) and medullary cysts of variable sizes

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53
Q

Complications of Medullary Sponge Kidney

A

Nephrolithiasis, UTI, hematuria, decreased urinary concentration, renal insufficiency (rare)

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54
Q

Medullary Sponge Kidney Diagnosis

A

not until 4-5th decade
Intravenous pyelography (IVP) with “brush” or linear striations radiating outward from calyces
Multidetector-row CT (IVP like image with “brush”)

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55
Q

Medullary Sponge Kidney Treatment

A

No known therapy
Good hydration, thiazide diuretic for hypercalciuria, antibiotics for UTI
Maintain renal function to avoid decline

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56
Q

Medullary Cystic Disease (Nephronophthisis)

A

Autosomal recessive inheritance
Characterized by reduced urinary concentration (bland urinary sediment, polyuria, polydipsia) and chronic tubulointerstitial nephritis w/ renal cysts

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57
Q

Medullary Cystic Disease Diagnostic

A

Clinical characteristics, retinitis pigmentosa
Confirmed with genetic testing, ultrasound (normal-small kidney w/ increased echogenicity w/ loss of corticomedullary differentiation)

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58
Q

Medullary Cystic Disease Treatment

A

Supportive care, will end up on dialysis or kidney transplant

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59
Q

Renal Cell Carcinoma

A

Most common primary renal malignancy; 6-8th decade most common
SMOKING is huge risk factor, most are sporadic

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60
Q

RCC Pathology

A

75-85% clear cell-deletion of chromosome 3p, usually a solid mass in the proximal tubule
10-15% papillary-proximal tubule; stage 1 has good prognosis and stage 2 is aggressive

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61
Q

RCC Presentation

A

Triad (but not usually together): Hematuria, abdominal mass, flank pain
left-sided scrotal varicocele, weight loss, metastasis to lungs, brain, bone, liver and lymph nodes; paraneoplastic syndromes

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62
Q

RCC Diagnostics

A 
Abdominal CT with and without contrast, MRI is second line (if CT/US non-diagnostic)
tissue biopsy (through full or partial nephrectomy) for solid renal mass
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63
Q

RCC Treatment

A

Surgery is curative for stages 1-3

Stage 4 becomes metastatic; can do surgery, radiation, systemic therapy-dependent on prognosis

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64
Q

Small Renal Mass

A

<4cm with enhancement on contrast imaging, solid or complex cystic
Male is more likely to be malignant
<2cm has 20-40% chance of benign
>4cm 20-30% chance of RCC (malignant)

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65
Q

Small Renal Mass Management

A

Surgery (partial nephrectomy), thermal ablation if <3cm, surveillance if <2cm

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66
Q

Wilms Tumor

A

Most common (95%) primary renal malignancy in kids, usually sporadic

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67
Q

Wilms Tumor Pathology

A

Usually a solitary lesion composed of blastemal, stroll and epithelial cells surrounded by a pseudo capsule
Due to abnormal renal development leading to proliferation of cells

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68
Q

Wilms Tumor Presentation

A 
Abdominal mass (usually aymptomatic)
Can have: abdominal pain, hematuria, fever, hypertension
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69
Q

Wilms Tumor Diagnostics

A

Histologic confirmation through excision or biopsy
Initial study is ultrasound (CT or MRI if not enough info); Labs: coag studies, CBC, Ca, liver function, UA, renal function
ALWAYS evaluate other kidney for comparison!

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70
Q

Wilms Tumor Treatment

A

Chemo and surgical excision
Refer to ped cancer center
Chest imaging for mets

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71
Q

Renovascular Disease

A

80-90% atherosclerotic
10-15% fibromuscular dysplasia
associated with accelerated target organ injury (LVH, renal fibrosis)

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72
Q

Renovascular Disease Presentation

A

Young onset/severe/resistant HTN, acute rise in normally stable BP
Serum creatinine raise >30% after ACE/ARB, abdominal bruit

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73
Q

Renovascular Disease Diagnostics

A

CTA most common, Renal arteriography is gold standard
Labs: elevated BUN and creatinine
Only test if intervention will be started

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74
Q

Atherosclerotic Renal Artery Stenosis

A

AKA Ischemic nephropathy; usually >45years

reduced blood flow to kidney, involving aortic orifice or proximal main renal artery

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75
Q

Atherosclerotic Renal Artery Stenosis Diagnosis

A

Luminal occlusion of at least 60-75%

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76
Q

Atherosclerotic Renal Artery Stenosis Treatment

A

Treat HTN, monitor CKD, CV prevention w/statins/aspirin; revascularization (angioplasty with or without stent/bypass)

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77
Q

Fibromuscular Dysplasia

A

Usually women <50 years
Noninflammatory, nonatherosclerotic disorder leading to arterial stenosis, occlusion, aneurysm, dissection and tortuosity leading to reduced blood flow to kidney; commonly in carotids and renal artery

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78
Q

Fibromuscular Dysplasia Presentation

A

HA, pulsatile tinnitus, neck pain, flank/abdominal pain, HTN, bruits, TIA/stroke
Classified as multifocal (string of beads) or focal (circumferential or tubular stenosis)

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79
Q

Fibromuscular Dysplasia Management

A

ACE/ARB-check serum creatinine Q6M and duplex doppler Q6-12M

OR: surgical (angioplasty-preferred treatment)

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80
Q

ACEs and ARBs in Kidneys

A

These blunt effect of auto regulation leading to reduced GFR which can possibly cause AKI
Acute kidney injury will happen within 3-4 days-check creatinine levels in 5-7 days and 1 week after to monitor!

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81
Q

What renovascular disease patient should get surgical treatment?

A

Short duration of ^ BP, failure/intolerance of medication therapy, recurrent flash pulmonary edema/refractory heart failure

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82
Q

Renal Ultrasonography

A

Choice test for obstructive disease, most commonly used initial test
Less sensitive for masses, can use doppler for vascular flow assessment

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83
Q

CT Scan

A

Gold standard for renal stones
Complementary to ultrasound, do WITHOUT contrast
loaves obstruction, evaluate tumors, diagnose RVT, high sensitivity for PKD

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84
Q

Radionuclide Scan

A

Preferred test in children bc it has less radiation than CT

Finds obstructions, determines function of each kidney

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85
Q

MRI

A

Gold standard for renal vein thrombosis (with renal venography and CT)
Further valor masses
Caution with gadolinium with GFR <30-can lead to nephrogenic system fibrosis

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86
Q

Nephrogenic System Fibrosis

A

Fibrosis of skin, muscle, fascia, lungs and heart>wheelchair bound within weeks, only happens in those with renal failure w/ gad use

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87
Q

Renal Arteriography and Venography

A

Preferred test for polyarteritis nodes, can also identify arterial and venous occlusions
Used less than CT/MRI bc its more invasive

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88
Q

Intravenous Pyelogram (IVP)

A

AKA IV urogram
Assess caliceal anatomy, size and shape of kidney
Highsensitivity and specificity for stones
LOTS OF RADIATION and contrast use>infrequently used

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89
Q

Renal Biopsy

A

Indicated for nephritic and nephrotic syndromes and unexplained AKI
Can do open renal, trans jugular renal or percutaneous (uses US and local anesthesia) renal biopsy

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90
Q

Hydronephrosis

A

Unilateral or bilateral edema of collecting system-fluid around kidneys
Almost always asymptomatic, but possible pain if obstructed

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91
Q

Hydronephrosis Diagnosis and Treatment

A

Ultrasound finds obstruction, CT if US is not diagnostic (non obstructive-can lead to diabetes insipidus)
Relieved by stent

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92
Q

Acute Kidney Injury

A

Precipitous and significant decrease in GFR (>50%) over a period of hours-days (but <3 months) with accompanying accumulation of nitrogenous waste in the body and inability to maintain fluid and electrolyte balance

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93
Q

KDIGO (kidney disease: improving global outcomes) Classification

A

Increase in serum creation by >0.3mg/dL within 48 hoursOR ^ in serum creatinine to >1.5x baseline within last 7 days OR urine volume <0.5mL/kg/hour for 6 hours

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94
Q

What is the most common cause of acute kidney injury?

A

Acute tubular necrosis (85%)

95
Q

AKI Diagnosis

A

Ultrasound (maybe CT) and EKG

Labs: UA (urine Na, urine osmolality), CBC, serum electrolytes, serum creatinine (>4mg/dL is serious renal impairment)

96
Q

Diagnostic Studies to Distinguish AKI

A

Prerenal: BUN/creat ratio >20:1, Na excretion <1%
Intrinsic: BUN/creat ratio <20:1, Na excretion >3%
Postrenal: BUN/Creat ratio <20:1

97
Q

Fractional Excretion of Sodium (FENa)

A

Most sensitive way to differentiate prerenal vs acute tubular necrosis (intrinsic)
<1% is prerenal, >3% is intrinsic, 1-3% is either or both

98
Q

Prerenal Azotemia

A

Characterized by inadequate blood perfusion to the kidneys-leaves kidneys unable to properly filter blood, patients are often critically ill
poor perfusion is usually in multiple organs>multiple organ failure

99
Q

Prerenal azotemia etiologies

A

Vascular depletion (hypovolemia from Addison’s, DKA, vomitting, etc), low cardiac output (CHF), changes in vascular resistance (sepsis, shock, meds)

100
Q

Medications that cause vascular resistance

A

ACEs, NSAIDs (chronic use), epi/norepi, dopamine, anesthetics, cyclosporine

101
Q

Prerenal Azotemia Presentation

A

low-normal urine output, dry mouth/thirst/tenting turgor, hypotension, tachycardia, weight loss, edema (in CHF)

102
Q

Prerenal Azotemia Diagnostics

A 
Urinalysis (RBCs-no casts)
Serum electrolytes
BUN/creat ratio (>20:1)
Urine Na (<20 mEq/dL)
FENa (<1%)
103
Q

Prerenal Azotemia Treatment

A

Depends on etiology, but will all get fluids empirically;
Volume depletion-fluid resuscitation
Volume overload-diuresis, inotropes, fluid restriction
Vascular resistance-treat cause, inotropes

104
Q

Intrinsic Renal Disease

A 
Tubular disease (85%), glomerular diseases, vascular disease, interstitial disease
Characterized by damage or injury within renal parenchyma making it unable to keep its gradients (necrosis, apoptosis, inflammatory response)
105
Q

Acute Tubular Necrosis Causes

A 
Ischemic- preceded by prerenal azotemia, usually from prolonged low perfusion state; inadequate GFR and parenchymal perfusion
Toxin exposure (exogenous or endogenous)
106
Q

Exogenous nephrotoxins

A

Vancomycin, ahminoglycosides, amphotericin B, antineoplastics, contrast dye

107
Q

Contrast nephropathy

A

2nd leading cause of renal failure in hospitalized patients
Occurs 24-48 hours after exposure
Prevent with hydration, acetylcysteine and sodium bicarb

108
Q

Endogenous Nephrotoxins

A

Heme containing products, uric acid (chemo, tumor lysis syndrome prevented with allopurinol), paraproteins (bence jones), rhabdomyolysis

109
Q

Interstitial Nephritis

A

Characterized by edema and tubular damage from interstitial inflammation
Drugs are the most common cause, but can also be related to infection (CMV, strep)

110
Q

Presentation of Interstitial Nephritis

A

Fever, rash, arthralgia, plasma eosinophilia, RBC/WBC and white cell casts in UA

111
Q

Interstitial Nephritis Course

A

Self-limiting recovering in weeks-months

May need short term dialysis and short term high dose steroids

112
Q

Intrinsic Renal Disease Diagnostics

A

Hallmark: unable to concentrate urine
Tests: urine- dark granular casts, sodium >30
ABG-metabolic acidosis
Serum-FENa >2-3%, BUN/creat ratio <20:1

113
Q

Postrenal Azotemia

A

Obstruction! Can be nephrolithiasis, bladder stones, BPH, tumor, meds (anticholinergics) or poorly emptied bladder

114
Q

AKI Treatment

A

Correct any abnormalities (fluids, electrolytes, uremic), treat underlying conditions, prevent complications
Dose-adjust medications per GFR, possible short term dialysis and use of diuretics

115
Q

AKI Complications

A 
Volume regulation (retention>edema/HTN, hyponatremia), metabolic acidosis, hyperkalemia, hyperphosphatemia, excretory failure, metabolic failure, hypocalcemia, hypermagnesemia
Can have cardio, pulmonary, and infections also
116
Q

Causes of death in AKI

A

Infections (30-70%; sepsis!), cardiovascular events (5-30%; CHF), GI/pul/neuro complications (7-30%), hyperkalemia or dialysis related

117
Q

Chronic Kidney Disease

A

Kidney disease lasting >3 months evidenced by structural or functional abnormalities w/ or without decreased GFR
OR
presence of GFR <60 for 3 months with or without other signs of kidney damage

118
Q

Causes of Chronic Kidney Disease

A

60% diabetes and hypertension
glomerulonephritis
cystic kidney
urologic diseases (obstructions, infections)

119
Q

Stages of CKD

A

1: normal GFR >89 with albuminuria
2: GFR 60-89 with albuminuria
3: GFR 30-59
4: GFR 15-29
5: ESRD, GFR<15-symptoms start here, need to be on dialysis

120
Q

Who is at risk for CKD?

A

Hypertension, diabetics, >60 years, family hx, minorities

121
Q

CKD Labs

A

Urine dipstick- microalbumin
Creatinine
uPRO/uCR ratio- ratio <0.3 is 300mg protein excreted in 24 hours, <3 is 3g excreted in 3 hours, between is kidney disease but not nephrotic syndrome
UA- sediment analysts, RBC/casts (nephritic), WBC/casts (infection), crystals for stones

122
Q

When to refer CKD patients

A

every patient with GFR <60 (stages 3 and 4) to identify reversible processes, treatment, preparation for dialysis and transplant eval

123
Q

CKD Management

A

Prevention is key! control hyperglycemia and hypertension, review meds (need ACE/ARB for proteinuria), quit smoking, treat cholesterol, low protein diet, renal vitamins (K, Ca, Phos, Mg)

124
Q

Reversible Causes of CKD

A

Prerenal: hypotension, hypovolemia, meds
Intrinsic: meds (vac, amino glycoside, NSAIDs), contrast dye, infection
Postrenal: obstruction

125
Q

Medications that can give false positive creatinine rise

A

Cimetidine, trimethoprim, cefotixin, flucytosine

126
Q

What processes typically cause CKD progression?

A

Intra-Glomerular HTN nd hypertrophy, metabolic acidosis, tubulointerstitial disease

127
Q

Metabolic Acidosis in CKD

A

Can worsen the disease, bone disease and cachexia

Treat with sodium bicarb (but has poor tolerance)

128
Q

Hyperphosphatemia in CKD

A

Phosphate binders required once GFR <25, if not treated can cause secondary hyperparathyroidism and renal osteodystrophy

129
Q

Bone Disease in CKD

A

Common problem due to vitamin D deficiency, can be in form of: osteitis fibrous, osteomalacia, dynamic bone disease

130
Q

Anemia in CKD

A

Usually when GFR <60, treat with erythropoietin prior to dialysis

131
Q

Uremia

A

Retention of nitrogen waste from kidney dysfunction, Develops when GFR <15
N/V, anorexia, fatigue, confusion, pericarditis, platelet dysfunction, neuropathy, sexual dysfunction, seizures, encephalopathy, asterisks, coagulopathy

132
Q

Dialysis

A

Diffusion of small molecules down their concentration gradient across a semi-permeable membrane
“washing” the blood

133
Q

Indications for emergent dialysis

A 
Acidosis (severe metabolic)
Electrolyte disturbance
Intoxication
Overload (of fluids)
Uremia
134
Q

Indications for non-emergent dialysis

A

Uremia, fluid overload, hypertension, metabolic disturbance (chronic acidosis, hyperkalemia), nausea/vomiting/malnutrition

135
Q

Types of Dialysis

A

Hemodialysis (normal), peritoneal dialysis, continuous renal replacement therapy (CRRT)

136
Q

Complications of standard dialysis

A

Hypotension, disequilibrium syndrome, dialyzer reactions, clotting/bleeding, arrhythmias

137
Q

Peritoneal Dialysis

A

Done at home with catheter in abdominal wall; dialysate solution introduced into peritoneal cavity, toxins diffuse across peritoneal capillarie across the peritoneal membrane andante the peritoneum, then the “dirty” fluid is drained from the cavity

138
Q

Peritoneal Dialysis Complications

A

Peritonitis, exit site infection, poor dialysate drainage

139
Q

Renal Transplant

A

Best option for replacement therapy when there are no contra indications
Median wait time is 2.6 years

140
Q

Total Body Water

A

60% body weight
intracellular 40%, extracellular 20%
(TIE 60, 40, 20)

141
Q

Extracellular Ions

A

Sodium, chloride and bicarb, protein

142
Q

Intracellular Ions

A

Potassium, magnesium, protein and PO4/organics

143
Q

Osmolality

A

total solute concentration in a fluid compartment

ECF is calculated with Sodium, glucose and urea

144
Q

Osmolality Ranges

A

Normal ECF is 280-295 most/kg

Symptoms occur if >320 or<265

145
Q

Osmol Gap

A

Normal is <10, elevated with high amounts of mannitol, ethanol, methanol, ethylene glycol

146
Q

Tonicity

A

Ability of the combined effect of all the solutes to generate osmotic drive-in force that causes water movement from one compartment to another
affecting the sizes of cells (to increase ECF tonicity solute must be confined to ECF compartment)-sodium, glucose and mannitol effect this

147
Q

Extracellular Fluid Volume

A

Determined by the total amount of sodium in ECF (where 90-95% of body sodium is located)
Increased Na increases ECFV>hypervolemia
Decreased Na decreases ECFV>hypovolemia

148
Q

Serum Sodium

A

Refers to the amount of water relative to sodium in the ECF-abnormal levels are a sign of water regulation disorder
High Na value=too little water relative to sodium

149
Q

Causes of hypovolemia

A

GI losses (bleeding, vomiting, diarrhea), renal losses (diuretics, diabetes insipidus), skin losses, sequestration (pancreatitis, obstruction), hemorrhage/bleed

150
Q

Presentation of Hypovolemia

A

Increased thirst, decreased sweating/skin turgor, dry mucus membranes, oliguria w/ increased urine concentration, CNS depression, weakness/cramps, decreased BP/dizziness, increased pulse

151
Q

Causes of Hypervolemia

A

Renal failure, nephrotic syndrome, hyperaldosteronism, Cushing’s syndrome, pregnancy
Most common are liver disease and heart failure

152
Q

Presentation of Hypervolemia

A

Edema, SOB, orthopnea, paroxysmal nocturnal dyspnea, JVD, hepatojugular reflex, crackles on pulm exam

153
Q

Water Retention

A

Influenced by thirst and ADH

154
Q

Salt Retention

A

Influenced by RAS

155
Q

Hyponatremia

A

Most common electrolyte abnormality in hospitalized patients
Symptoms are more severe with faster decrease
Mild: 125-135, Mod: 120-125, Severe <120 (life threatening w/ seizures)
Most common with extremes of age

156
Q

Hyponatremia Presentation

A

Na <125

HA, dizziness, N/V, lethargy, weakness, confusion, hypoventilation, resp arrest, seizures, coma

157
Q

Pseudohyponatremia

A

Falsly low serum Na with normal osmolality
Occurs with hyperlipidemia and hyperproteinemia
Laboratory artifact

158
Q

Redistributive Hyponatremia

A

Osmotically active solutes in extracellular space that draw water from cell diluting the serum Na concentration
Hyperglycemia is a common cause
Add 1.5mEq/L to sodium value for every 100mg serum glucose>100

159
Q

Hypoosmolar Hyponatremia

A

Hypovolemic, hypervolemic or euvolemic

160
Q

Hypovolemic Hyponatremia

A

Renal losses (diuretics, osmotic diuresis, Addison’s, hyperaldosteronism)
Non-renal losses
Treat by replacing fluid loss with isotonic fluid

161
Q

Hypervolemic Hyponatremia

A

Hepatic cirrhosis, CHF, renal failure

Treat with diuretics, dialysis, fluid restriction

162
Q

Euvolemic Hyponatremia

A

SIADH, psychogenic polydipsia (maximally dilute urine), hypothyroidism, adrenal insufficiency
Treat with fluid restriction

163
Q

SIADH-syndrome of inappropriate antidiuretic hormone secretion

A

Impaired free water excretion but sodium is still excreted
Concentrated urine (>100) with low serum osmolality and euvolemia
Caused by Small cell lung cancer
Treat with fluid restriction

164
Q

Labs to evaluate hyponatremia

A

Urine Na and osmolality, serum Na and osmolality, CMP

THEN TSH and serum cortisol

165
Q

Treatment of Hyponatremia

A

If Na is <125 or symptomatic hospitalize!
Treat based on underlying cause with slow correction
Traditional treatment for chronic is demeclocycline, vaptans are new treatment

166
Q

What does rapid increase in serum sodium cause?

A

Cerebral pontine myelinolysis (CPM)-irreversible demyelination in pons and extra-pontine areas causing dysarthria, dysphagia, seizures, hypotension, quadriparxsis 1-3 days after over correction

167
Q

When do you use 3% NaCl?

A

Only in severe symptomatic cases (normal is 0.9%)

168
Q

Rate of Hyponatremia Correction

A

6-12 mEq/L in the 1st 24 hours, <18 in 48 hours
If chronic stay <8 in first 24 hours
Check serum Na levels every 2-4 hours

169
Q

Hypernatremia

A

Hypertonic disorder due to serum sodium >145 (too little water to sodium)
Caused by too little water, too much salt or excessive water loss (GI, skin, renal)
Presentation due to brain shrinkage from increased ECF osmolality

170
Q

Presentation of Hypernatremia

A

Often asymptomatic

Thirst, signs of volume depletion, weakness, AMS, neuromuscular irritability, focal neurolgoci deficits, seizures/coma

171
Q

Diabetes Insipidus

A

Urine dilute when it should be concentrated; non osmotic urinary water loss with elevated serum Na

172
Q

Central Diabetes Insipidus

A

Due to impaired secretion of ADH, treated with desmopressin

173
Q

Nephrogenic Diabetes Insipidus

A

Lack of kidney response to ADH>continued water loss with adequate ADH and low water levels
Treated with thiazides, amiloride, chlorpropamide and NSAIDs

174
Q

Treatment of Hypernatremia

A

Hospitalize if severe, stop water loss and replace water deficit
Usually just use free water but can use IV or NG tube
Too rapid of replacement with shift water into brain cells causing seizures, brain damage and CPM

175
Q

Aldosterone and Potassium

A

Aldosterone increases renal K excretion and Na reabsorption

176
Q

Hypokalemia

A

98% of the body potassium is intracellular

80%of patients on diuretics become hypokalemic

177
Q

Hypokalemia Presentation

A

Weakness, fatigue, cramps, hyporeflexia, flaccid ascending paralysis, hypercapnia, cardia arrhythmia (can be fatal)

178
Q

Hypokalemia EKG findings

A

Flattened T waves, prominent U waves, premature ventricular contractions, depressedST segments

179
Q

Causes of Hypokalemia

A

Transcellular shifts (brings K from cell to blood), renal losses (diuretics, MCC), extra renal losses (vomiting, diarrhea, burns, magnesium)

180
Q

Treatment of Hypokalemia

A

Replace potassium (oral is preferred but can do IV for NPO) NEVER push potassium, it will burn!

181
Q

Hyperkalemia

A

K >5, >6.5 is severe

Presents with muscle weakness

182
Q

EKG Changes in Hyperkalemia

A

Potentially life threatening arrhythmia

peaked T waves>wide QRS>junctional rhythm>vfib

183
Q

Hyperkalemia Causes

A

Factitious (hemolytic anemia, fist clenching), impaired excretion (renal failure, Addison’s, hypoaldosteronism), drugs (ACE/ARB, NSAIDs, K sparing diuretics), increased intake (only in renal impaired), rhabdo, acidosis, low insulin

184
Q

Emergent Treatment of Hyperkalemia

A 
IV calcium (cardio protective), sodium bicarb IV push, insulin+D50W
Can also do albuterol, IV lassie and dialysis
185
Q

Non-emergent treatment of Hyperkalemia

A

Kayexalate (exchanged Na for K in gut), Lasix, correct underlying cause
Patiramer is new FDA approved drug

186
Q

Hypercalcemia

A

Calcium >10.1
Triggers release of calcitonin from thyroid inhibiting bone resorption
Common, usually midland self-limiting

187
Q

Hypercalcemia Presentation

A

“Stones bones abdominal moans and psychiatric groans” (kidney stones, bone pain, abdominal pain/N/V/anorexia/constipation, lethargy/fatigue/memory loss/psychosis/depression

188
Q

Causes of Hypercalcemia

A

Malignancy and hyperparathyroidism cause 90%

Meds (thiazides, lithium antacids, vitamin A analogs)

189
Q

Labs for Hypercalcemia

A

Serum calcium (>13 malignancy), PTH and rPTH levels (low in cancer), TSH, cortisol, protein electrophoresis

190
Q

Hypercalcemia Treatment

A 
Volume expansion (saline) is #1
Can use calcitonin, pamidronate, zoledronic acid, dialysis (last case)
191
Q

Principles of Fluid management

A

Recognize fluid compartments, know normal daily losses of water and electrolytes and replace fluid losses wit appropriate solutions

192
Q

What is the normal water input/output?

A

2.6L/day

193
Q

What is the most common reason to give IV fluid?

A

Hypovolemia

194
Q

Third Spacing

A

Fluid accumulation in interstitial of tissues (edema)
In areas that normally don’t have fluid (ascites, edema with burns, pleural effusions)
Can cause hypovolemia eve though they look fluid overloaded

195
Q

Types of IV Fluid

A

Cystalloids, colloids, blood/blood products

196
Q

Crystalloid

A

Fluid with crystal-forming elements (electrolytes) that easily pass through endothelial membrane

197
Q

Colloids

A

Never first line!
Fluids that have large organic macromolecules and electrolytes and are retained in the intravascular space (expand vascular compartment)
Used when crystalloids fail to sustain plasma volume due to low osmotic pressure
We don’t use dextran or hydroxyethyl starch

198
Q

Blood and blood products

A

Similar to colloids, stay in vascular space

199
Q

Types of crystalloids

A

Isotonic (same salt concentration as body and blood-GO TO!)
Hypertonic (higher salt concentration)
Hypotonic (lower salt concentration)
Dextrose (usually for NPO patients, never bolus)

200
Q

Isotonic Crystalloids

A

Normal Saline (0.9%)
Lactated Ringer Solution (lactate, K, Ca and NaCl)
Plasma-Lyte (less Cl, most physiologic solution)
These distribute uniformly throughout ECF, use for treatment of dehydration/hypovolemia

201
Q

Hypertonic Crystalloid

A

3% Saline, use with caution!
best fro life-threatening hyponatremia with significant water excess
Good for neurosurgical patients to decrease cerebral edema
Can cause CPM if done too quickly

202
Q

Hypotonic Crystalloid

A

0.5 or 0.25% saline

used for maintenance fluid, distribute throughout total body water, inadequate for replacing volume deficits

203
Q

Dextrose

A

Used to treat hypoglycemia, starvation ketosis and used in Hypernatremia with free water deficit
Caution in diabetics!

204
Q

Albumin Preparations

A

Colloid
5% or 25% albumin
Used in edematous patient sot mobile interstitial fluid into the vascular space
Helpful in liver disease, peritonitis, burns or third spacing

205
Q

Types of Blood Products

A

Packed RBC
Platelets
Fresh Frozen Plasma
Cryoprecipitate

206
Q

Packed RBC

A

Prepared from whole blood, remain within vascular space
Used for blood transfusions, improves oxygen delivery to tissues
1 unit increases Hgb by 1g

207
Q

Platelets

A

Used in patients with thrombocytopenia or impaired platelet function to prevent or treat bleeding
Stored at room temp, used within 5 days

208
Q

Fresh Frozen Plasma

A

Contains ALL factors of the soluble coagulation system, used to correct major bleeding complications in patients on warfarin/with vitamin K deficiency, anyone bleeding with high INR

209
Q

Cryoprecipitate

A

Prepared by thawing fresh frozen plasma and collecting the precipitate
Has high concentration of factor 8 and fibrinogen
Used in patients with low fibrinogen with massive hemorrhage or consumptive coagulopathy

210
Q

Bolus IVF

A

Saline, Lactate ringer and plasma-lyme can be given as bolus in hypovolemia (dehydration, acute blood loss, sepsis)
Can give 250ml-1L at a time
Caution in heart failure

211
Q

Maintenance IVF

A

Maintains/accounts for ongoing water/electrolyte loss-goal is water and electrolyte balance
Used when patients aren’t eating or drinking normally
Crystalloids are typically used with low dose slow drip

212
Q

Maintenance IVF Amounts

A

Typical doses are 75, 100 or 125ml/hr

kg method determines by weight but not really used

213
Q

Maintenance IVF and Potassium

A

Potassium can be added to treat hypokalemia or for maintenance fluids if the patient is NPO
NEVER BOLUS the K is added!
Use caution in kidney disease

214
Q

Replacement IVF

A

Corrects existing water and electrolyte deficits from GI, urinary, skin, blood loss or third spacing
Monitor vital signs, urine output and clinical picture to determine effectiveness
Use caution with Na imbalances

215
Q

Replacement in Surgical Patients

A

Use urine output and vital signs as guides to the amount of fluid needed; normal post op UOP is 0.5ml/kg/hr

216
Q

Replacement in Burn Patients

A

“parkland formula” or rule of nines to estimate fluid needed; replace with lactated ringer or plasma-lyte: 1/2 the amount in first 8 hours, 1/4 during next 2 sets of 8 hours

217
Q

Parkland formula

A

Total fluid required during first 24 hours=% of burns x body weight x 4ml

218
Q

Rule of Nines

A 
Each arm 9%
head 9%
ant/porterior trunks each 18%
Each leg 18%
perineum 1%
219
Q

What does an ABG measure?

A

pH, pO2 (oxygen concentration), O2 saturation, pCO2, HCO3

220
Q

Where do you draw an ABG?

A

Radial artery, can use brachial or femoral

221
Q

Acidemia/Alkalemia

A

pH<7.35/>7.45

JUST the pH, not a specific disorder

222
Q

How many acid-base disorders can you have at once?

A

Up to 3 (2 metabolic and 1 respiratory)

223
Q

Respiratory Alkalosis Levels

A

^pH, low CO2 and HCO3

CO2 is primary disturbance

224
Q

Respiratory Acidosis Levels

A

Low pH, high CO2 and HCO3

CO2 is primary disturbance

225
Q

Metabolic Alkalosis

A

^pH, CO2, HCO3

HCO3 is primary disturbance

226
Q

Metabolic Acidosis

A

Low pH, CO2 and HCO3

HCO3 is primary disturbance

227
Q

Metabolic Acidosis Causes

A

High anion gap- MUDPILES: methanol, uremia, DKA, propylene glycol, iron/ioniazid, lactate, ethanol, salicylates
Non-anion gap- GI loss (diarrhea), renal loss, hyperchloremia

228
Q

Metabolic Acidosis Treatment

A

Sodium bicarb (temporary fix), allow for normal compensation (will happen through tachypnea)

229
Q

Metabolic Alkalosis Causes/treatment

A

Check Urine Chloride
<25: GI losses (vomiting, NG suction), diuretics, cystic fibrosis; These need fluids!
>25: Cushings, hyperaldosteronism, etc; treat cause, may need potassium

230
Q

Respiratory Acidosis Causes

A

Acute airway obstruction, leg disease (COPD), CNS depression, neuromuscular disorder (guillan-barre, MG), wrong ventilation settings

231
Q

Respiratory Acidosis Treatment

A

Treat underlying cause, Respiratory support (BiPAP) for acute only (chronic won’t need it)

232
Q

Respiratory Alkalosis Causes

A

Hyperventilation/anxiety (lightheaded, palpitations), pain, CNS, pregnancy, high altitude, hypoxemia, hepatic encephalopathy

233
Q

Respiratory Alkalosis Treatment

A

Treat underlying cause

Foundations 2 (4 decks)

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