Nephrology Flashcards
(233 cards)
1
Q
What is the average physiologic protein excretion in adults?
A
80mg/day (16-32mg albumin)
2
Q
What is a pathologic amount of protein excretion?
A
150mg or more
3
Q
Microalbuminuria
A
30-300mg/day
4
Q
Macroalbuminuria
A
> 300 mg/day
5
Q
Nephrotic range of protein
A
> 3-3.5g
6
Q
Causes of Proteinuria
A
Glomerular disease (most common-altered permeability)
Overflow (oveproduction of small proteins)
Tubular (diminished reabsorptive capacity)
7
Q
Glomerular Disease
A
Nephritic or nephrotic syndromes
Results in hypoalbuminemia due to loss of protein
Biopsy is gold standard of diagnosis
8
Q
Nephritic Syndrome
A
Inflammatory process with associated immunologic response leading to renal glomeruli damage
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)
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
11
Q
Primary Nephritic Syndromes
A
Post-infectious, IgA nephropathy, Henoch-Schonlein purpora, Pauci-immune glomerulonephritis, anti-glomerular basement membrane glomerulonephritis (Goodpastures)
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
13
Q
Post Infectious GN Presentation
A
Pt is oliguric, edematous, hypertensive, coca-cola urine w/ RBC casts, high ASO titers
14
Q
Post Infectious GN Treatment
A
Anti-hypertensives (ACE, ARB), salt restriction, diuretics (loops and thiazides)
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
16
Q
IgA Nephropathy Presentation
A
Coca-cola urine 1-3 days after URI or GI infection
Hematuria, proteinuria, increased IgA levels, normal complement
17
Q
IgA Nephropathy Treatment
A
Corticosteroids if proteinuria is1-3.5g/day
ACE, ARB if proteinuria, want BP <130/80
18
Q
Henoch-Schonlein Purpura
A
Systemic small vessel vasculitis associated w/ IgA deposition in vessel walls
Most common in kids, associated with infection
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
20
Q
DMARDs
A
Disease modifying antirheumatic drugs-azathioprine, cyclophosphamide, hydroxychloroquine, methotrexate
21
Q
Pauci-immune Glomerulonephritis (ANCA-associated)
A
Seen with small vessel vasculitis (granulomatosis with polyangitis, eosinophilic granulomatosis w/ polyangitis, microscopic polyangitis
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
23
Q
ANCA Associated GN Treatment
A
High dose corticosteroids, DMARDs
75% remission with treatment
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
25
Goodpastures Presentation
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
26
Goodpastures Treatment
Plasmapheresis to remove antibodies
| Corticosteroids and DMARDs to prevent new antibodies/inflammatory response
27
Nephrotic Syndrome Labs
Urine protein excretion >3.5g, hypoalbuminemia (<3g/dL), oval fat bodies in urinary sediment (from hyperlipidemia), deficient vitamin D, zinc and copper levels
28
Nephrotic Syndrome Presentation
Peripheral edema is hallmark (when serum albumin <2g), dyspnea, hyperlipidemia,
29
Nephrotic Syndrome
Significantly increased basement membrane permeability
30
Nephrotic Syndrome Treatment
Increased protein intake, salt restriction, thiazide and loop diuretics, high intensity statins, anticoags
31
Types of Nephrotic Syndromes
Minimal Change Disease, membranous nephropathy, focal segmentation glomeruulosclerosis (FSGS)
32
Minimal Change Disease
Increased glomerular permeability, foot process effacement
Mostly seen in kids (80% of all proteinuria)
men=women but boys>girls
33
Membranous Nephropathy
Most common primary nephrotic syndrome in adults
| Immune complex deposition in glomerular capillary walls result in increased permeability
34
Membranous Nephropathy Presentation
Asymptomatic; edema w/ frothy urine, high incidence of venous thromboembolism
Subnephrotic syndrome-classic nephrotic syndrome
35
Membranous Nephropathy Treatment
ACE/ARB if BP >125/75
| Corticosteroids in patients with no improvements after 6 months of conservative care
36
Focal Segmental Glomerulosclerosis (FSGS)
Increased permeability due to podocyte injury
37
FSGS Presentation
Proteinuria is initial presenttion
38
FSGS Treatment
Diuretics for edema, ACE/ARB to reduce proteinuria/HTN, Statins for hyperlipidemia, high dose corticosteroids for overt nephrotic syndrome for 16 weeks
39
Simple Renal Cyst Epidemiology
65-70% of renal masses, mostly >70
| Most common incidental finding with little clinical significance
40
Simple Renal Cyst
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
41
Simple Renal Cyst Presentation
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
42
Simple Renal Cyst Diagnositics
Ultrasound-sharply demarcated with smooth thin walls, anechoic, enhanced back wall
43
Complex Cyst Diagnostics
Ultrasound-thick walls/septations, calcifications, solid components, mixed echogenicity, vascularity
CT w/ and w/out contrast
44
Acquired Renal Cysts
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
45
Diagnostics of Acquired Renal Cysts
Ultrasound: Bilateral involvement, >4 cysts, diameter <0.5cm up to 2-3cm
46
Cyst Treatment
```
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
```
47
Autosomal Dominant Polycystic Kidney Disease (ADPKD)
```
Aggressive form (more common) is PKD1, slow growth is PKD2, 5% spontaneous
Irreversible decline in renal function by age 60 (50%)
```
48
ADPKD Pathology
Multiple cysts with bilateral involvement, gradual cyst growth, gradual loss of parenchyma, significant kidney enlargement, progressive decline in renal function (GFR)
49
ADPKD Clinical Presentation
Presents in 30s-40s with pain (abdominal, flank, back, chest), 50% have HTN*, large palpable kidneys*, frequent UTIs (treat with cipro), hematuria, mild proteinuria
50
ADPKD Diagnostics
Ultrasound for screen/monitoring
| CBC (anemia), CMP(decline kidney function), UA (blood, protein), genetic screening (PKD 1/2)
51
ADPKD Treatment
ACE/ARB, low sodium/caffeine, pain management, avoid nephrotoxic agents/contact sports, manage complications (infection, hemorrhage, etc)
Dialysis or transplant in end stage
52
Medullary Sponge Kidney
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
53
Complications of Medullary Sponge Kidney
Nephrolithiasis, UTI, hematuria, decreased urinary concentration, renal insufficiency (rare)
54
Medullary Sponge Kidney Diagnosis
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")
55
Medullary Sponge Kidney Treatment
No known therapy
Good hydration, thiazide diuretic for hypercalciuria, antibiotics for UTI
Maintain renal function to avoid decline
56
Medullary Cystic Disease (Nephronophthisis)
Autosomal recessive inheritance
Characterized by reduced urinary concentration (bland urinary sediment, polyuria, polydipsia) and chronic tubulointerstitial nephritis w/ renal cysts
57
Medullary Cystic Disease Diagnostic
Clinical characteristics, retinitis pigmentosa
Confirmed with genetic testing, ultrasound (normal-small kidney w/ increased echogenicity w/ loss of corticomedullary differentiation)
58
Medullary Cystic Disease Treatment
Supportive care, will end up on dialysis or kidney transplant
59
Renal Cell Carcinoma
Most common primary renal malignancy; 6-8th decade most common
SMOKING is huge risk factor, most are sporadic
60
RCC Pathology
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
61
RCC Presentation
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
62
RCC Diagnostics
```
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
```
63
RCC Treatment
Surgery is curative for stages 1-3
| Stage 4 becomes metastatic; can do surgery, radiation, systemic therapy-dependent on prognosis
64
Small Renal Mass
<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)
65
Small Renal Mass Management
Surgery (partial nephrectomy), thermal ablation if <3cm, surveillance if <2cm
66
Wilms Tumor
Most common (95%) primary renal malignancy in kids, usually sporadic
67
Wilms Tumor Pathology
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
68
Wilms Tumor Presentation
```
Abdominal mass (usually aymptomatic)
Can have: abdominal pain, hematuria, fever, hypertension
```
69
Wilms Tumor Diagnostics
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!
70
Wilms Tumor Treatment
Chemo and surgical excision
Refer to ped cancer center
Chest imaging for mets
71
Renovascular Disease
80-90% atherosclerotic
10-15% fibromuscular dysplasia
associated with accelerated target organ injury (LVH, renal fibrosis)
72
Renovascular Disease Presentation
Young onset/severe/resistant HTN, acute rise in normally stable BP
Serum creatinine raise >30% after ACE/ARB, abdominal bruit
73
Renovascular Disease Diagnostics
CTA most common, Renal arteriography is gold standard
Labs: elevated BUN and creatinine
Only test if intervention will be started
74
Atherosclerotic Renal Artery Stenosis
AKA Ischemic nephropathy; usually >45years
| reduced blood flow to kidney, involving aortic orifice or proximal main renal artery
75
Atherosclerotic Renal Artery Stenosis Diagnosis
Luminal occlusion of at least 60-75%
76
Atherosclerotic Renal Artery Stenosis Treatment
Treat HTN, monitor CKD, CV prevention w/statins/aspirin; revascularization (angioplasty with or without stent/bypass)
77
Fibromuscular Dysplasia
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
78
Fibromuscular Dysplasia Presentation
HA, pulsatile tinnitus, neck pain, flank/abdominal pain, HTN, bruits, TIA/stroke
Classified as multifocal (string of beads) or focal (circumferential or tubular stenosis)
79
Fibromuscular Dysplasia Management
ACE/ARB-check serum creatinine Q6M and duplex doppler Q6-12M
| OR: surgical (angioplasty-preferred treatment)
80
ACEs and ARBs in Kidneys
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!
81
What renovascular disease patient should get surgical treatment?
Short duration of ^ BP, failure/intolerance of medication therapy, recurrent flash pulmonary edema/refractory heart failure
82
Renal Ultrasonography
Choice test for obstructive disease, most commonly used initial test
Less sensitive for masses, can use doppler for vascular flow assessment
83
CT Scan
Gold standard for renal stones
Complementary to ultrasound, do WITHOUT contrast
loaves obstruction, evaluate tumors, diagnose RVT, high sensitivity for PKD
84
Radionuclide Scan
Preferred test in children bc it has less radiation than CT
| Finds obstructions, determines function of each kidney
85
MRI
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
86
Nephrogenic System Fibrosis
Fibrosis of skin, muscle, fascia, lungs and heart>wheelchair bound within weeks, only happens in those with renal failure w/ gad use
87
Renal Arteriography and Venography
Preferred test for polyarteritis nodes, can also identify arterial and venous occlusions
Used less than CT/MRI bc its more invasive
88
Intravenous Pyelogram (IVP)
AKA IV urogram
Assess caliceal anatomy, size and shape of kidney
Highsensitivity and specificity for stones
LOTS OF RADIATION and contrast use>infrequently used
89
Renal Biopsy
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
90
Hydronephrosis
Unilateral or bilateral edema of collecting system-fluid around kidneys
Almost always asymptomatic, but possible pain if obstructed
91
Hydronephrosis Diagnosis and Treatment
Ultrasound finds obstruction, CT if US is not diagnostic (non obstructive-can lead to diabetes insipidus)
Relieved by stent
92
Acute Kidney Injury
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
93
KDIGO (kidney disease: improving global outcomes) Classification
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
94
What is the most common cause of acute kidney injury?
Acute tubular necrosis (85%)
95
AKI Diagnosis
Ultrasound (maybe CT) and EKG
| Labs: UA (urine Na, urine osmolality), CBC, serum electrolytes, serum creatinine (>4mg/dL is serious renal impairment)
96
Diagnostic Studies to Distinguish AKI
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
Fractional Excretion of Sodium (FENa)
Most sensitive way to differentiate prerenal vs acute tubular necrosis (intrinsic)
<1% is prerenal, >3% is intrinsic, 1-3% is either or both
98
Prerenal Azotemia
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
Prerenal azotemia etiologies
Vascular depletion (hypovolemia from Addison's, DKA, vomitting, etc), low cardiac output (CHF), changes in vascular resistance (sepsis, shock, meds)
100
Medications that cause vascular resistance
ACEs, NSAIDs (chronic use), epi/norepi, dopamine, anesthetics, cyclosporine
101
Prerenal Azotemia Presentation
low-normal urine output, dry mouth/thirst/tenting turgor, hypotension, tachycardia, weight loss, edema (in CHF)
102
Prerenal Azotemia Diagnostics
```
Urinalysis (RBCs-no casts)
Serum electrolytes
BUN/creat ratio (>20:1)
Urine Na (<20 mEq/dL)
FENa (<1%)
```
103
Prerenal Azotemia Treatment
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
Intrinsic Renal Disease
```
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
Acute Tubular Necrosis Causes
```
Ischemic- preceded by prerenal azotemia, usually from prolonged low perfusion state; inadequate GFR and parenchymal perfusion
Toxin exposure (exogenous or endogenous)
```
106
Exogenous nephrotoxins
Vancomycin, ahminoglycosides, amphotericin B, antineoplastics, contrast dye
107
Contrast nephropathy
2nd leading cause of renal failure in hospitalized patients
Occurs 24-48 hours after exposure
Prevent with hydration, acetylcysteine and sodium bicarb
108
Endogenous Nephrotoxins
Heme containing products, uric acid (chemo, tumor lysis syndrome prevented with allopurinol), paraproteins (bence jones), rhabdomyolysis
109
Interstitial Nephritis
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
Presentation of Interstitial Nephritis
Fever, rash, arthralgia, plasma eosinophilia, RBC/WBC and white cell casts in UA
111
Interstitial Nephritis Course
Self-limiting recovering in weeks-months
| May need short term dialysis and short term high dose steroids
112
Intrinsic Renal Disease Diagnostics
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
Postrenal Azotemia
Obstruction! Can be nephrolithiasis, bladder stones, BPH, tumor, meds (anticholinergics) or poorly emptied bladder
114
AKI Treatment
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
AKI Complications
```
Volume regulation (retention>edema/HTN, hyponatremia), metabolic acidosis, hyperkalemia, hyperphosphatemia, excretory failure, metabolic failure, hypocalcemia, hypermagnesemia
Can have cardio, pulmonary, and infections also
```
116
Causes of death in AKI
Infections (30-70%; sepsis!), cardiovascular events (5-30%; CHF), GI/pul/neuro complications (7-30%), hyperkalemia or dialysis related
117
Chronic Kidney Disease
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
Causes of Chronic Kidney Disease
60% diabetes and hypertension
glomerulonephritis
cystic kidney
urologic diseases (obstructions, infections)
119
Stages of CKD
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
Who is at risk for CKD?
Hypertension, diabetics, >60 years, family hx, minorities
121
CKD Labs
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
When to refer CKD patients
every patient with GFR <60 (stages 3 and 4) to identify reversible processes, treatment, preparation for dialysis and transplant eval
123
CKD Management
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
Reversible Causes of CKD
Prerenal: hypotension, hypovolemia, meds
Intrinsic: meds (vac, amino glycoside, NSAIDs), contrast dye, infection
Postrenal: obstruction
125
Medications that can give false positive creatinine rise
Cimetidine, trimethoprim, cefotixin, flucytosine
126
What processes typically cause CKD progression?
Intra-Glomerular HTN nd hypertrophy, metabolic acidosis, tubulointerstitial disease
127
Metabolic Acidosis in CKD
Can worsen the disease, bone disease and cachexia
| Treat with sodium bicarb (but has poor tolerance)
128
Hyperphosphatemia in CKD
Phosphate binders required once GFR <25, if not treated can cause secondary hyperparathyroidism and renal osteodystrophy
129
Bone Disease in CKD
Common problem due to vitamin D deficiency, can be in form of: osteitis fibrous, osteomalacia, dynamic bone disease
130
Anemia in CKD
Usually when GFR <60, treat with erythropoietin prior to dialysis
131
Uremia
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
Dialysis
Diffusion of small molecules down their concentration gradient across a semi-permeable membrane
"washing" the blood
133
Indications for emergent dialysis
```
Acidosis (severe metabolic)
Electrolyte disturbance
Intoxication
Overload (of fluids)
Uremia
```
134
Indications for non-emergent dialysis
Uremia, fluid overload, hypertension, metabolic disturbance (chronic acidosis, hyperkalemia), nausea/vomiting/malnutrition
135
Types of Dialysis
Hemodialysis (normal), peritoneal dialysis, continuous renal replacement therapy (CRRT)
136
Complications of standard dialysis
Hypotension, disequilibrium syndrome, dialyzer reactions, clotting/bleeding, arrhythmias
137
Peritoneal Dialysis
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
Peritoneal Dialysis Complications
Peritonitis, exit site infection, poor dialysate drainage
139
Renal Transplant
Best option for replacement therapy when there are no contra indications
Median wait time is 2.6 years
140
Total Body Water
60% body weight
intracellular 40%, extracellular 20%
(TIE 60, 40, 20)
141
Extracellular Ions
Sodium, chloride and bicarb, protein
142
Intracellular Ions
Potassium, magnesium, protein and PO4/organics
143
Osmolality
total solute concentration in a fluid compartment
| ECF is calculated with Sodium, glucose and urea
144
Osmolality Ranges
Normal ECF is 280-295 most/kg
| Symptoms occur if >320 or<265
145
Osmol Gap
Normal is <10, elevated with high amounts of mannitol, ethanol, methanol, ethylene glycol
146
Tonicity
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
Extracellular Fluid Volume
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
Serum Sodium
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
Causes of hypovolemia
GI losses (bleeding, vomiting, diarrhea), renal losses (diuretics, diabetes insipidus), skin losses, sequestration (pancreatitis, obstruction), hemorrhage/bleed
150
Presentation of Hypovolemia
Increased thirst, decreased sweating/skin turgor, dry mucus membranes, oliguria w/ increased urine concentration, CNS depression, weakness/cramps, decreased BP/dizziness, increased pulse
151
Causes of Hypervolemia
Renal failure, nephrotic syndrome, hyperaldosteronism, Cushing's syndrome, pregnancy
Most common are liver disease and heart failure
152
Presentation of Hypervolemia
Edema, SOB, orthopnea, paroxysmal nocturnal dyspnea, JVD, hepatojugular reflex, crackles on pulm exam
153
Water Retention
Influenced by thirst and ADH
154
Salt Retention
Influenced by RAS
155
Hyponatremia
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
Hyponatremia Presentation
Na <125
| HA, dizziness, N/V, lethargy, weakness, confusion, hypoventilation, resp arrest, seizures, coma
157
Pseudohyponatremia
Falsly low serum Na with normal osmolality
Occurs with hyperlipidemia and hyperproteinemia
Laboratory artifact
158
Redistributive Hyponatremia
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
Hypoosmolar Hyponatremia
Hypovolemic, hypervolemic or euvolemic
160
Hypovolemic Hyponatremia
Renal losses (diuretics, osmotic diuresis, Addison's, hyperaldosteronism)
Non-renal losses
Treat by replacing fluid loss with isotonic fluid
161
Hypervolemic Hyponatremia
Hepatic cirrhosis, CHF, renal failure
| Treat with diuretics, dialysis, fluid restriction
162
Euvolemic Hyponatremia
SIADH, psychogenic polydipsia (maximally dilute urine), hypothyroidism, adrenal insufficiency
Treat with fluid restriction
163
SIADH-syndrome of inappropriate antidiuretic hormone secretion
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
Labs to evaluate hyponatremia
Urine Na and osmolality, serum Na and osmolality, CMP
| THEN TSH and serum cortisol
165
Treatment of Hyponatremia
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
What does rapid increase in serum sodium cause?
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
When do you use 3% NaCl?
Only in severe symptomatic cases (normal is 0.9%)
168
Rate of Hyponatremia Correction
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
Hypernatremia
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
Presentation of Hypernatremia
Often asymptomatic
| Thirst, signs of volume depletion, weakness, AMS, neuromuscular irritability, focal neurolgoci deficits, seizures/coma
171
Diabetes Insipidus
Urine dilute when it should be concentrated; non osmotic urinary water loss with elevated serum Na
172
Central Diabetes Insipidus
Due to impaired secretion of ADH, treated with desmopressin
173
Nephrogenic Diabetes Insipidus
Lack of kidney response to ADH>continued water loss with adequate ADH and low water levels
Treated with thiazides, amiloride, chlorpropamide and NSAIDs
174
Treatment of Hypernatremia
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
Aldosterone and Potassium
Aldosterone increases renal K excretion and Na reabsorption
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Hypokalemia
98% of the body potassium is intracellular
| 80%of patients on diuretics become hypokalemic
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Hypokalemia Presentation
Weakness, fatigue, cramps, hyporeflexia, flaccid ascending paralysis, hypercapnia, *cardia arrhythmia* (can be fatal)
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Hypokalemia EKG findings
Flattened T waves, prominent U waves, premature ventricular contractions, depressedST segments
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Causes of Hypokalemia
Transcellular shifts (brings K from cell to blood), renal losses (diuretics, MCC), extra renal losses (vomiting, diarrhea, burns, magnesium)
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Treatment of Hypokalemia
Replace potassium (oral is preferred but can do IV for NPO) NEVER push potassium, it will burn!
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Hyperkalemia
K >5, >6.5 is severe
| Presents with muscle weakness
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EKG Changes in Hyperkalemia
Potentially life threatening arrhythmia
| *peaked T waves*>wide QRS>junctional rhythm>vfib
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Hyperkalemia Causes
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
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Emergent Treatment of Hyperkalemia
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IV calcium (cardio protective), sodium bicarb IV push, insulin+D50W
Can also do albuterol, IV lassie and dialysis
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Non-emergent treatment of Hyperkalemia
Kayexalate (exchanged Na for K in gut), Lasix, correct underlying cause
Patiramer is new FDA approved drug
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Hypercalcemia
Calcium >10.1
Triggers release of calcitonin from thyroid inhibiting bone resorption
Common, usually midland self-limiting
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Hypercalcemia Presentation
"Stones bones abdominal moans and psychiatric groans" (kidney stones, bone pain, abdominal pain/N/V/anorexia/constipation, lethargy/fatigue/memory loss/psychosis/depression
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Causes of Hypercalcemia
Malignancy and hyperparathyroidism cause 90%
| Meds (thiazides, lithium antacids, vitamin A analogs)
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Labs for Hypercalcemia
Serum calcium (>13 malignancy), PTH and rPTH levels (low in cancer), TSH, cortisol, protein electrophoresis
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Hypercalcemia Treatment
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Volume expansion (saline) is #1
Can use calcitonin, pamidronate, zoledronic acid, dialysis (last case)
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Principles of Fluid management
Recognize fluid compartments, know normal daily losses of water and electrolytes and replace fluid losses wit appropriate solutions
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What is the normal water input/output?
2.6L/day
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What is the most common reason to give IV fluid?
Hypovolemia
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Third Spacing
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
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Types of IV Fluid
Cystalloids, colloids, blood/blood products
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Crystalloid
Fluid with crystal-forming elements (electrolytes) that easily pass through endothelial membrane
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Colloids
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
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Blood and blood products
Similar to colloids, stay in vascular space
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Types of crystalloids
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)
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Isotonic Crystalloids
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
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Hypertonic Crystalloid
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
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Hypotonic Crystalloid
0.5 or 0.25% saline
| used for maintenance fluid, distribute throughout total body water, inadequate for replacing volume deficits
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Dextrose
Used to treat hypoglycemia, starvation ketosis and used in Hypernatremia with free water deficit
Caution in diabetics!
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Albumin Preparations
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
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Types of Blood Products
Packed RBC
Platelets
Fresh Frozen Plasma
Cryoprecipitate
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Packed RBC
Prepared from whole blood, remain within vascular space
Used for blood transfusions, improves oxygen delivery to tissues
1 unit increases Hgb by 1g
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Platelets
Used in patients with thrombocytopenia or impaired platelet function to prevent or treat bleeding
Stored at room temp, used within 5 days
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Fresh Frozen Plasma
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
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Cryoprecipitate
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
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Bolus IVF
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
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Maintenance IVF
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
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Maintenance IVF Amounts
Typical doses are 75, 100 or 125ml/hr
| kg method determines by weight but not really used
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Maintenance IVF and Potassium
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
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Replacement IVF
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
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Replacement in Surgical Patients
Use urine output and vital signs as guides to the amount of fluid needed; normal post op UOP is 0.5ml/kg/hr
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Replacement in Burn Patients
"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
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Parkland formula
Total fluid required during first 24 hours=% of burns x body weight x 4ml
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Rule of Nines
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Each arm 9%
head 9%
ant/porterior trunks each 18%
Each leg 18%
perineum 1%
```
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What does an ABG measure?
pH, pO2 (oxygen concentration), O2 saturation, pCO2, HCO3
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Where do you draw an ABG?
Radial artery, can use brachial or femoral
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Acidemia/Alkalemia
pH<7.35/>7.45
| JUST the pH, not a specific disorder
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How many acid-base disorders can you have at once?
Up to 3 (2 metabolic and 1 respiratory)
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Respiratory Alkalosis Levels
^pH, low CO2 and HCO3
| CO2 is primary disturbance
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Respiratory Acidosis Levels
Low pH, high CO2 and HCO3
| CO2 is primary disturbance
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Metabolic Alkalosis
^pH, CO2, HCO3
| HCO3 is primary disturbance
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Metabolic Acidosis
Low pH, CO2 and HCO3
| HCO3 is primary disturbance
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Metabolic Acidosis Causes
High anion gap- MUDPILES: methanol, uremia, DKA, propylene glycol, iron/ioniazid, lactate, ethanol, salicylates
Non-anion gap- GI loss (diarrhea), renal loss, hyperchloremia
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Metabolic Acidosis Treatment
Sodium bicarb (temporary fix), allow for normal compensation (will happen through tachypnea)
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Metabolic Alkalosis Causes/treatment
Check Urine Chloride
<25: GI losses (vomiting, NG suction), diuretics, cystic fibrosis; These need fluids!
>25: Cushings, hyperaldosteronism, etc; treat cause, may need potassium
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Respiratory Acidosis Causes
Acute airway obstruction, leg disease (COPD), CNS depression, neuromuscular disorder (guillan-barre, MG), wrong ventilation settings
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Respiratory Acidosis Treatment
Treat underlying cause, Respiratory support (BiPAP) for acute only (chronic won't need it)
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Respiratory Alkalosis Causes
Hyperventilation/anxiety (lightheaded, palpitations), pain, CNS, pregnancy, high altitude, hypoxemia, hepatic encephalopathy
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Respiratory Alkalosis Treatment
Treat underlying cause
