Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI/GU > Genitourinary Exam 1 Cards > Flashcards

Genitourinary Exam 1 Cards Flashcards

1
Q

9 major renal functions

A

Excretion
Water and Electrolyte balance
Fluid volume
Plasma osmolality
RBC production regulation
BP regulation
Acid base balance
Vitamin D activation
Gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the kidney regulate RBC production?

A

It releases erythropoietin in response to hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does the kidney modulate blood pressure

A

Releases renin in response to low flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Renal medulla and cortex on biopsy

A

Cortex = Spaghetti and meatballs
Medulla = Bundles of pencils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Scar tissue

A

Not metabolically active and therefore does not need as much oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

More common nephron type

A

Cortical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Podocytes

A

Surround capillary loops in the glomerulus to remove trapped material and contract capillaries if needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Most common complaint and complication associated with a horseshoe kidney

A

UTI - Bacteria grow in pooling urine
Ureteropelvic junction obstruction
Kidney stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diagnosis and treatment of a horseshoe kidney

A

CT, Urinalysis, and Renal function
Manage disorders and complications as they arise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Urine filtrate

A

Plasma without proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Glomerular Filtration rate

A

Amount of filtrate formed over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Resorption of PCT

A

60% of HCl and H20 90% of bicarb
Secretes most wastes (urea, ammonia, creatinine, etc.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Loop of henle

A

Water goes out the descending
Sodium goes out the ascending
Most magnesium resorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where do loop diuretics work

A

Thick ascending loop of henle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Distal Convoluted tubule

A

May resorb urea
CALCIUM regulation Secretes K+
Regulates pH
Site of action for thiazide diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cortical collecting duct

A

Resorbs NaCl and H2O
Secretes K+
Aldosterone and K sparing diuretics work here

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Medullary collecting duct

A

Final modification of urine with some secretion and resorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do nephrons handle loss

A

They do not regenerate but hypertrophy in order to compensate for lost tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Maladaptive deterioration

A

Point at which nephrons can no longer compensate for losses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Amount of renal mass removal resulting in ESRD

A

80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Progression of nephron loss

A

Damage to glomeruli (via HTN) results in protein leakage which leads to inflammation and fibroblast activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

GFR of CKD

A

Under 60mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

2 Limitations of GFR

A

Can’t detect problems that are non-glomerular
May go up at the onset of renal disease
May appear stable in worsening disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

3 substances that can be used for GFR estimation

A

BUN, Creatinine, Cystatin C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Factors effecting GFR estimation

A

Body surface area - smaller body=less muscle mass
Age - declines with age
Gender - Males have more muscle and more creatinine
Race - AAs have more muscle and more creatinine - new recomendations don’t use race

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

3 factors that increase serum creatinine that are NOT renal failure

A

Meat intake
Creatine supplements
High muscle mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Medications that inhibit renal secretion of creatinine

A

Abx - cephalosporins, aminoglycosides, trimethoprim
Cimetidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Effect of liver disease on estimated GFR

A

Decreases creatine production leading to decreased creatinine, leading to higher eGFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Creatinine clearance in CKD

A

Enhanced in early stages, taken over by liver in late stages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Creatinine Clearance

A

Requires 24 hour collection of urine for creatinine testing and estimates the upper limit of the true GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

When does one need to finish collecting urine for a CrCl test

A

within 10 minutes of the 24 hour mark of beginning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Limitation of CrCl urine test

A

Cumbersome and has a tendency to overestimate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Cause of BUN:Cr above 20:1

A

Dehydration due to increased renal resorption - tubules must be working
Cell breakdown can also cause incresed BUN as well as decreased renal perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

4 things causing decreased BUN

A

Liver disease
Malnutrition
Sickle cell anemia
SIADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

BUN and GFR estimation

A

Less useful for estimation - much of it is resorbed is inversely proportional to GFR, and can change independantly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Cyastatin C and GFR

A

Not as impacted by race, gender, age as creatinine but still increased by things like male sex, fat mass, diabetes, etc.

Inverse relationship and EXPENSIVE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

3 indications for cyastatin C measurement

A

Elderly patients
Body builders
Acute Illness
(All have abnormal muscle mass)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Cockroft Gault equation

A

Estimates CrCl in a patient with stable Cr
Need age and body weight, sex
Overestimate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

MDRD study equation

A

Estimates GFR with body surface area and Cr
Needs age, sex, race
More accurate than CG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

CKD-EPI Study

A

More accurate GFR measurement than CG works best for mild or normal GFR
Better risk prediction
Uses serum creatinine, age, and sex (no longer modified by race)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Preferred GFR equation in US

A

CKD-EPI (no race)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Acute kidney injury

A

Sudden decrease in kidney function over hours or days with inability to manage fluid electrolytes, and acid base or excretion of waste products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Duration of AKI before we see a drop in labs

A

Can be up to 12-24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Azotemia

A

Increase of waste products in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Uremia

A

Symptomatic azotemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Anuria

A

Under 50 mL in 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Oliguria

A

50-400 mL in 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Polyuria

A

2500-3000 mL/day or more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

6 uremic symptoms

A

Weakness, tremors, dryness, HTN, Nausea, acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Most common cause of AKI

A

Prerenal azotemia (followed by intrinsic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Prerenal azotemia

A

Azotemia due to inadequate renal perfusion, hypovolemia, decreased cardiac output, or changed vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

BUN/Cr ratio of prerenal azotemia

A

Greater than 20:1 because kidneys think we are dehydrated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Fractional excretion of sodium in prerenal azotemia

A

Under 1% - kidneys think we are dehydrated - retain sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Clinical presentation or prerenal azotemia

A

Dehydration, Sepsis, diffuse abdominal pain and ileus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

MCC of postrenal obstruction in men

A

BPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

2 tests for postrenal obstruction

A

Bladder catheterization and/or abdominopelvic US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

BUN/Cr ratio of postrenal obstruction

A

Over 20:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Urine osmolality of postrenal obstruction

A

400mosm/kg or less

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

3 major causes of Acute Tubular Necrosis

A

Ischemia
Nephrotoxins
Sepsis - hypoperfusion or direct injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

5 Nephrotoxic antimicrobials

A

Gentamycin, Streptomycin (less so), Vancomycin, Sulfonamides, Cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

2 nephrotoxic antivirals and one antifungal

A

acyclovir, foscarnet, amphotericin B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

3 non pharm exogenous nephrotoxins

A

Radiographic contrast media, Chemo/immunosuppressants, Heavy metals etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Myoglobinuria

A

Due to rhabdomyolysis - urine appears dark brown but no detection of RBCs. False positive for hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Treatment for myoglobinuria

A

Rehydrate - may have high electrolytes and low calcium which correct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

3 other endogenous nephrotoxins

A

Hemoglobinuria (hemolysis)
Hyperuricemia (chemo - uric acid over 15-20 mg/dL)
Bence Jones protein - Obstructs tubules, multiple myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Clinical presentation of acute tubular necrosis

A

Uremia and arrhythmias may be noted
Low GFR with BUN:Cr under 20:1
Muddy brown casts
Elevated urine sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What does low BUN:Cr or elevated urine sodium mean

A

We are NOT resorbing anything

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Treatment for Acute tubular necrosis

A

Avoid volume overload, loop diuretics, or dialysis
Promote dietary interventions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Better long term outcome ATN patient

A

Non-oligouric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Classic presentation of acute glomerulonephritis

A

HTN, Edema, urine containing protein, RBCs, WBCs, and RBC casts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Crescent lesions

A

Severe breaks in glomerular walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Types of Glomerulonephritis

A

Immune complex destruction
Anti-GBM autoantibody destruction
C3 deposition
Pauci-immune (vasculitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

2 places edema is seen first

A

Scrotal and periorbital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Treatment for acute glomerulonephritis

A

Corticosteroids - high dose
Plasma exchange for goodpasture or pauci immune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Immune complex glomerulonephritis

A

Antigen-antibody complex lodges in GBM leading to its destruction by the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Anti-GBM associated glomerulonephritis

A

Autoantibodies against the GBM are produces - called Goodpature syndrome if the lungs are also effected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

C3 glomerulopathy

A

Caused by C3 deposition in the glomerulus - may result in low C3 levels. Minimal role played by immune globulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Monoclonal Ig-mediated glomerulonephritis

A

Monoclonal antibodies lodge in the GBM - no antigens are seen
Can be detected with serum protein electrophoresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Pauci-Immune GN

A

Associated with ANCAs (anti-neutrophillic cytoplasmic antibodies)
No immune complexes or complement involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

MCC of acute interstitial glomerulonephritis

A

Medications

Can also be infectious or immune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Classic triad of interstitial glomerulonephritis

A

Fever, rash, arthralgia (may not see ALL three)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Urine sediment of AIN

A

WBCs, RBCs, No protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

BUN:Cr ratio of Acute interstitial GN

A

under 20:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

BUN:Cr ratio for Glomerulonephritis

A

Greater than 20:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Broad or waxy urine casts

A

Chronic renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Hyaline casts

A

Exercise, diuretics, concentrated urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Fatty casts

A

Nephrotic syndrome (oval fat bodies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Granular casts

A

Chronic renal failure or ATN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Renal tubular epithelial cast

A

ATN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

RBC casts

A

Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

WBC casts

A

Interstitial or pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

2 diagnostics to rule out urethral obstruction

A

Urethral cath and bladder scan US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

4 things that increase and one thing that decreases when total body water drops

A

Increase:
SNS
RAAS
ADH
Thirst

Decrease:
ANP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Clinical presentation of isotonic fluid volume defecit

A

Altered mental status, low BP high HR, Weak pulse, Dry mucous membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Why does professor Jensen love lactated ringers?

A

They don’t have sodium in them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Treatment for volume overload

A

IV diuretics (loop), dialysis if no response to therapy, Restrict fluids and sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Clinical presentation of hyperphosphatemia

A

SOB, N/V, Hypocalcemia (hyperreflexia, trousseu and chvostek signs, carpopedal spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Clinical presentation of hypokalemia

A

Weakness, constipation, flattened T waves and ST depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Clinical presentation of hyperkalemia

A

Cramps, diarrhea, vomiting, hypotension, palpitations
Peaked T waves, lost P waves, Wide QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Treatment for hyperkalemia

A

Treat if EKG changes or neuromuscular symptoms
Block cardiac effects
Reduce plasma K+
Remove potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Blocking of cardiac effects in the hyperkalemic patient

A

IV calcium gluconate with cardiac monitoring
Repeat if EKG changes do not occur
Can potentiate toxicity of digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Reducing plasma potassium in hyperkalemic patient

A

Administer insulin followed by dextrose
Albuterol can also help

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Removal of potassium in the hyperkalemic patient

A

GI cation exchangers (Kayexalate, zirconium cyclosilicate, patiromir)

Loop or thiazide diuretics

Dialysis - can even electrolytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Isotonic hyponatremia

A

Usually means that there are extra molecules in the blood (fat or protein), skewing the data
Correct underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Hypertonic hyponatremia

A

Another osmotically active molecule is present such as glucose or radiocontrast
Correct underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Hypovolemic hyponatremia

A

Due to inappropriate salt loss (ie. GI, burns, dehydration)
Renally due to ACEIs, Diuretics, aldosterone deficiency, renal salt wasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Hypovolemic hyponatremia

A

Sodium is retained but even more water is retained - nephrotic syndrome, intrinsic renal fluid retention, heart failure, liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Euvolemic hyponatremia

A

SIADH, hypothyroidism, psychogenic polydipsia, beer potomania

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Clinical presentation of hyponatremia

A

Primarily neurologic due to cerebral edema
Confusion, lethargy, seizure
Less symptoms when chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Treatment of hypovolemic hyponatremia

A

Rehydration with normal saline
Use hypertonic saline if the condition is severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Treatment difference in chronic and acute hypernatremia

A

Acute - correct in 24 hours
Chronic correct more gradually

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

pH at which bicarbonate treatment is generally needed

A

pH under 7.2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Treatment for chronic metabolic acidosis in CKD

A

Bicarb replacement
Decreasing animal products in diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Mechanism of metabolic acidosis in AKI

A

Kidney unable to excrete acid and regenerate Bicarb

115
Q

How does acidosis affect potassium balance

A

It leads to hyperkalemia

116
Q

Situations in which to administer bicarb in severe AKI acidosis

A

Due to diarrhea
Waiting for dialysis
AKI readily reversible
Rhabdomyolosis without other dialysis indications

117
Q

Situations in which to dialyse in AKI acidosis

A

Severe AKI with volume overload
If organic acidosis from lactic or keto acids
pH under 7.1
Risk of volume overload if giving sodium

118
Q

Indications for dialysis in AKI

A

Azotemia and Uremia
Life threatening electolyte disturbances
Volume overload unresponsive to diuretics
Acidosis below 7.1

119
Q

Official definition of CKD

A

Presence of markers of kidney damage or GFR under 60 for 3+ months

120
Q

Kidney nephron response to a decrease in the number of functional nephrons

A

Hyperfiltration and Hypertrophy

121
Q

Cardiorenal syndrome nameing

A

Acute or Chronic is for BOTH organs
Renocardiac is the kidneys fault, Cardiorenal the hearts fault

122
Q

GFR CKD stages

A

1-5 w/ 3a and 3b
1 is normal (90+)
2 - 60-90
Down by 15 after than

123
Q

Albuminuria stages

A

A1 - Under 30 mg/g
A2 - 30/300
A3 - 300+

124
Q

Isosthenuria

A

Urine is the same concentration as blood

125
Q

Uremic frost

A

Crystallized urea excreted in sweat

126
Q

Cause of broad waxy casts in CKD

A

Dilated (Hypertrophied) Nephrons

127
Q

Clinical presentation of CKD in stages 1-2

A

Edema and HTN most common or signs of underlying disease

128
Q

Clinical presentation of stages 3 and 4 of CKD

A

Anemia, fatigue, anorexia, Abnormal calcium, phosphorous, vitamin D, PTH, Sodium, potassium, and water

129
Q

Clinical presentation of stage 5 CKD and ESRD

A

Marked disruption of ADLs and well being

130
Q

Medication most used for CKD

A

ACE/ARB - BUT don’t use in AKI!!

131
Q

CVD in CKD patients

A

Usually death is from cardiac complications before kidney problems
CKD patients build plaques faster and at lower cholesterol levels

132
Q

Goal BP for CKD patients

A

Less than 130/80mmHg okay if a little over

133
Q

ACEI/ARBs in CKD - monitoring

A

Check creatinine and K+ 7-14 days after starting or increase and reduce or stop drug if it has gone up over 30%

134
Q

Diuretics in CKD

A

Thiazides early on
Loop more effective when GFR is under 30
Over diuresis can cause AKI

135
Q

Drugs for lipid management in CKD

A

Statins = First line and recc’d for most pts
PSK-9 inhibitors and ezetimibe as adjunct therapy
Fibrates as last resort (can cause rhabdomyolosis

136
Q

Electrolyte abnormality to monitor for in ACE/ARB use

A

Hyperkalemia

137
Q

Atrial fibrilation treatment risk in Stage 5 and ESRD patients

A

Greater bleeding risk with anticoagulation

138
Q

Pericarditis in CKD

A

Retrosternal chest pain with friction rub, low voltage QRS, ALWAYS an indication for dialysis

139
Q

Typical mineral metabolism abnormality in CKD patients

A

Hyperphosphatemia
Hypovitaminosis D
Hypocalcemia

140
Q

Osteitis fibrosis cystica

A

MC form of renal osteodystrophy
Hyperphosphatemia leads to hyperparathyroidism which leads to osteoclast stimulation
High rates of bone turnover

141
Q

Adynamic bone disease

A

Suppression of PTH or low endogenous PTH = LOW bone turnover

142
Q

X-ray finding of osteitis fibrosa cystica

A

Brown tumors (hollow looking spots) on bones

143
Q

Controlling hyperphosphatemia in CKD mineral metabolism abnormalities

A

Initially use dietary intervention, later use oral phosphate binders

144
Q

CKD phosphate binders

A

Calcium carbonate (Tums, watch for atherosclerosis or hypercalcemia)
Sevelamer or Lanthanum (Non-calcium first line)
Aluminum hydroxide

145
Q

Management of PTH levels in CKD mineral metabolism abnormalities

A

Vitamin D3 (calcitriol) use to balance vitamin D
Cinacelcet - Increase sensitivity of the parathyroid gland good if increased phosphorus or Ca exclude calcitriol

146
Q

Hepcidin

A

Blocks GI iron absorption

147
Q

Treatment for iron deficiency in CKD

A

Ferrous sulfate, gluconate, fumarate, or citrate are approved
No iron if ferritin is over 500-800 ng/mL

148
Q

Erythropoietin treatment in CKD

A

Hold EPO until Hgb drops below 10
Goal is 10-11 for Hb numbers

149
Q

Epo dosing regimens and side effect

A

Epoiein 1-2x per week
Darbepoietin every 2-4 weeks
HTN seen in 20% of patients

150
Q

Treatment for hematologic coagulopathy

A

Due to PLT dysfunction
Only treat if symptomatic
Desmopressin and dialysis can help
Cryoprecipitate is rarely used
Severe protein loss can lead to HYPERcoagulability

151
Q

Good diuretics for high potassium

A

Loop diuretics

152
Q

Cause and treatment for metabolic acidosis of AKI

A

Loss of ability to excrete acid, maintain serum bicarb at 21+mEq/L

153
Q

Uremic encephalopathy

A

Due to aggregation of uremic toxins
Difficulty concentrating to altered mental status

154
Q

Uremic neuropathy

A

Indication to start dialysis
Symmetrical mixed neuropathy
Loss of vibration to clonus/muscle atrophy
Paresthesias

155
Q

Hypoglycemia of CKD

A

Due to decreased renal clearance of insulin
d/c metformin when Cr is above 1.4 or GFR is under 30

156
Q

CKD pregnancy

A

50% infant mortality rate
surviving infants are often premature
CKD progresses faster

157
Q

Sodium restriction for CKD

A

2g/d

158
Q

CKD protein restriction

A

May slow progression - careful if cachectic

159
Q

Water restriction for CKD

A

2L/d

160
Q

Potassium restriction for CKD

A

Less than 2g/d (50-60mEq) if GFR under 10-20 mL/min or hyperkalemic

161
Q

Medications to avoid or manage in CKD

A

Renally excreted drugs
Mg or Ph containing drugs
Morphine
NSAIDs and IV contrast (nephrotoxic)

162
Q

Indications for dialysis in CKD

A

When GFR reaches 5-10 mL/min
Uremic symptoms
Refractory metabolic disturbances
Unresponsive fluid overload

163
Q

Risk of peritoneal dialysis

A

Removes large amounts of albumin
Patients with abdominal surgeries may not by good candidates

164
Q

Diagnostic conditions for peritonitis

A

Over 100 WBC/mcL in peritoneal fluid with over 50% PMN
MCC staph

165
Q

Nephritic spectrum

A

Has more to do with inflammation
Under 3g/d proteinuria
Hematuria with RBC casts

166
Q

Nephrotic spectrum

A

Has more to do with proteinuria
Over 3g/day proteinuria
Bland urine sediment with oval fat bodies potentially

167
Q

Bergers disease

A

IgA nephropathy
Coca cola colored urine
Form of nephritis

168
Q

Clinical presentation of nephrotic syndrome

A

Hypoalbuminemia causing edema
Hyperlipidemia

169
Q

Immune complex deposition glomerulonephritis

A

Antigen-antibody complexes lodge in the GBM. GBM is destroyed in immune crossfire
Often associated with Strep infections, Berger disease, Lupus

170
Q

Anti-GBM associated glomerulonephritis

A

Autoantibody formation against the GBM
Called Goodpasture’s syndrome when it involves that Lungs AND Kidneys

171
Q

C3 glomerulopathy

A

C3 complement proteins lodge in the GBM causing its destruction -caused by an abnormal alternative complement pathway

172
Q

Monoclonal Ig-mediated glomerulonephritis

A

Excessive antibodies lodge in the GBM due to multiple myeloma or MGUS (monoclonal gammopathy of Undetermined significance)

173
Q

Pauci immune glomerulonephritis

A

Small vessel vasculitis associated with antineutrophilic cytoplasmic antibodies (ANCAs) caused by cell mediated autoimmune processes

174
Q

Clinical presentation of nephritis

A

Cola colored urine
Edema (periorbital and scrotal first) and HTN
Uremia eventually

175
Q

Glomerulonephritis associated with ANCA levels

A

Pauchi immune GN

176
Q

Purpose of an ASO titer

A

Helps evaluate for a recent streptococcal infection

177
Q

2 types of glomerulonephritis for which plasma exchange is recommended

A

Goodpasture disease
Pauci-immune GN

178
Q

General treatment for glomerulonephritis

A

Manage HTN and volume
May use high dose corticosteroids for immunosuppression

179
Q

Post infection glomerulonephritis

A

Bacterial or viral
MCC is GABHS
1-3 weeks after infection

180
Q

Treatment for post infectious glomerulonephritis

A

Support - antihypertensives, salt restrict, diuretics
Steroids are NOT helpful

181
Q

Henoch Schonlein purpura

A

Systemic small vessell vasculitis associated with IgA deposition in vessel walls
Purpura in lower extremities -supportive care

182
Q

MCC and criteria for nephrotic disease

A

DM is MCC
Over 3g of proteinuria/day

183
Q

Subnephrotic proteinuria

A

Proteinuria with few s/s

184
Q

Nephrotic syndrome

A

Peripheral edema seen with proteinuria

185
Q

Places we first see edema in nephrotic syndrome

A

Around eyes and scrotum

186
Q

Gross hematuria

A

We don’t need a microscope to visualize the blood

187
Q

Urine sediment of nephrotic syndrome

A

Oval fat bodies
Grape clusters
Maltese crosses with polarization

188
Q

Hypoalbuminemia

A

Serum protein under 3g/dL

189
Q

Hypoproteinemia

A

Serum protein under 6g/dL

190
Q

Why is ESR elevated in nephrotic syndrome?

A

Loss of proteins C and S

191
Q

When might we do a renal biopsy

A

When there is not an obvious cause such as DM

192
Q

Treatment for proteinuria in nephrotic syndrome

A

Increase dietary protein if loosing 10+ g/d
ACE/ARB to lower urine protein excretion by reducing glomerular capillary pressure

193
Q

Treatment for edema in nephrotic syndrome

A

Dietary salt restriction
Need larger doses of thiazide/loop diuretics bc they are protein bound

194
Q

Minimal change disease

A

A primary nephrotic syndrome
Common in children
Treat with prednisone for 8 weeks (children) or 16 weeks (adults

195
Q

Membranous nephropathy

A

Common in adults - immune complex deposition OR secondary to NSAIDs, cancer, etc.
May be asymptomatic or frothy urine

196
Q

Treatment for membranous nephropathy

A

ACE/ARB, Immunosuppressive agents, Transplant
50% progress to ESRD, 30% spontaneous remission

197
Q

Kidney v. bladder bleeding

A

Kidney will be more brown
Bladder will be more red
(just like GI tract)

198
Q

One size fits all response of the kidneys

A

Increase the RAAS

199
Q

Most common presenting symptom in Berger disease

A

episode of gross hematuria

200
Q

One thing that must be done when an acute on chronic kidney injury occurs

A

Stop ACE/ARB

201
Q

Amyloidosis

A

Secondary nephrotic syndrome due to extracellular deposition of amyloid protein
Low GFR, Enlarged kidneys
Limited treatment

202
Q

Progress of diabetic nephropathy

A

Hyperfiltration
Microalbuminuria (30-300 mg/dL)
Albuminuria

203
Q

When to treat diabetic nephropathy

A

As soon as microalbuminuria is found
Glycemic control
HTN treat to goal
ACE/ARB

204
Q

MCC of acute interstitial nephritis

A

Medication

205
Q

3 causes of chronic Tubulointerstitial Disease

A

Obstructive uropathy
Vesicoureteral reflux
Anagesic nephropathy

206
Q

How much analgesic tends to lead to nephropathy

A

1g/d for 3+ years

207
Q

Causes of obstructive uropathy

A

Enlarged prostate
Stones
cancer
Retroperitoneal fibrosis

Leads to reflux and scarring

208
Q

Potential s/s of obstructive uropathy

A

Pain - with a stone
Bladder distension
HTN
Can all be normal!!

209
Q

Labs for obstructive uropathy

A

May present with polyuria due to damaged tubules
Benign UA may have pyuria/hematuria
Elevted serum creatinine

210
Q

Imaging for obstructive uropathy

A

Should be done on all AKI and CKD patients with unknown cause
US is preferred, CT for stones

211
Q

Vesicoureteral reflux

A

Retrograde flow of urine while voiding due to misplaced sphincter

212
Q

Clinical presentation of vesicoureteral reflux

A

Frequent UTIs esp. in young children
HTN
May have mild/moderate proteinuria

213
Q

Imaging findings for vesicoureteral reflux

A

Assymetric kidneys - one will usually compensate for the other
Can use a US, CT, or Voiding cystourethrogram

214
Q

Treatment for vesicoureteral reflux

A

Maintain sterile urine in childhood
Surgical reimplantation (only works in children
ACE/ARB for HTN

215
Q

Analgesic nephropathy

A

Tubulointerstitial and papillary necrosis
Analgesics can be VERY concentrated in papillae

216
Q

Urine and imaging findings of analgesic nephropathy

A

Sloughed papillae in the urine
Small scarred kidney with calcifications on CT
Ring sign or golfball on tea seet with CT contrast

217
Q

Treatment for analgesic nephropathy

A

Renal decline stabilizes or improves slightly with analgesic removal

218
Q

Clinical findings of autoimmune interstitial nephritis

A

Polyuria w/ dilute urine, Volume depletion, Acidosis
Kidney scarring
Treatm underlying issue

219
Q

Nephrocalcinosis

A

Deposition of calcium in the renal parenchyma and tubules
Cauliflower florets in the kidneys

220
Q

Cause and risk factors for nephrocalcinosis

A

Increased urinary excretion of calcium, phosphate, or oxalate
Hyperparathyroidism
Vitamin D
Loop diuretics

221
Q

Clinical presentation of nephrocalcinosis

A

Often asymptomatic
May have hypercalcemia or hyperphosphatemia
Minimal proteinuria

222
Q

Imaging for nephrocalcinosis

A

US is best can use CT

223
Q

Single renal cyst

A

Usually not concerning and found incidentally
No HTN or ESRD signs present

224
Q

Routine management of benign renal cyst

A

Routine follow up
More likely to be cancerous if they have developed after initiation of dialysis

225
Q

Childhood medullary kidney disease

A

Juvenile Nephronophthisis
Autosomal recessive
Renal cysts in the corticomedullary junction and in the medulla

226
Q

Adult medullary kidney disease

A

MCKD - 20-70yrs
Autosomal dominant
Renal cysts in the corticomedullary junction and in the medulla

227
Q

S/S of medullary kidney disease

A

Hyperuricemia
HTN
Growth restriction for juvenile

228
Q

Treatment for medullary cystic kidney disease

A

No therapy to stop progression
Allopurinol for hyperuricemia
Does not recur in renal transplants

229
Q

s/s of Autosomal dominant PKD

A

Abdominal or flank pain
UTI/Stones
Palpable kidneys
Hematuria
Ultrasound to confirm
Can get cerebral aneurysms in the COW

230
Q

Two other places to check for cysts in PKD

A

Spleen and liver

231
Q

Tx for pain and hematuria associated with PKD

A

Analgesics, decomprassion for pain from bleeding, infection, stones
Hydration for bleeding, recurrent may be carcinoma

232
Q

Cerebral aneurysms PKD screening

A

Usually not recommended

233
Q

Antibiotics with cystic penetration for PKD

A

Quinolones, Bactrim

234
Q

Medications for ADPKD

A

Vasopressin receptor antagonists:
Ocreotide - decreased cyst growth
Tolvaptan

235
Q

4 risk markers indicating use of Tolvaptan in ADPKD

A

Mayo class 1C-E
Under 55 w/ GFR under 65
Kidney length over 16.5 cm in 50y/o
PROPKD score 6+

Patients 18+ with GFR 25+ and one of the above should be on something

236
Q

3 things that may slow progression of ADPKD

A

Avoidance of caffeine
Protein restriction
HTN Tx

237
Q

BBW for tolvaptan

A

Should be initiated in a hospital where serum sodium can be closely monitored
CI in liver disease, may cause thirst/polyuria

238
Q

Location of cysts in ARPKD

A

Cysts on collecting tubules only
Metabolic acidosis and HTN
Oligohydramnios (low amniotic fluid in utero)

239
Q

Presentation and treatment of autosomal recessive PKD

A

Cysts only visible after birth - no disease in parents
Manage HTN
Dialysis and transplant

240
Q

2 causes of renal artery stenosis

A

Atherosclerotic disease (by far most common)
Fibromuscular dysplasia (suspect in women under 40 w/ unexplained HTN)

241
Q

s/s, PE and labs for renal artery stenosis

A

Refractory or new onset HTN
AKI after ACEI
Abdominal bruit
Elevated BUN/Cr with ischemia

242
Q

Imaging for renal artery stenosis

A

Doppler US can show small or asymmetric kidneys on regular US
CT angiography may be less accurate and more expensive
MRA excellent but expensive
Renal angiography = Gold standard

243
Q

Treatment for renal artery stenosis

A

Medical management of HTN
Stenting produces good results
Bypass not superior

244
Q

Nephrosclerosis

A

Hypertensive nephropathy with sclerosis and interstitial fibrosis
More common in African Americans
Give ACE/ARB or thiazide diuretic

245
Q

Cholesterol atheroembolic disease

A

Emboli to the kidneys from vascular plaques, angiography is a risk factor

246
Q

s/s of cholesterol atheroembolic disease

A

1-2 weeks after inciting event
Worsening of HTN and renal function
May see livedo reticularis or localized gangrene

247
Q

Livedo reticularis

A

Webbing patter on legs

248
Q

Labs for cholesterol atheroembolic disease

A

Increased eosinophils, Cr, ESR
Def dx - kidney biopsy
Statins are most recommended

249
Q

MC kidney cancer

A

Renal cell carcinoma

250
Q

Risk factors for renal cell carcinoma

A

May be familial or dialysis related
HTN, analgesics, Obesity
SMOKING - biggest

251
Q

Clear cell carcinoma

A

Most common type of kidney cancer
Papillary tumors are less common but happen

252
Q

Clinical presentation of renal call carcinoma

A

Hematuria = most common
May see flank pain or abdominal mass
Cough or bone pain in metastasis
Usually found incidentally

253
Q

Stauffer syndrome

A

Abnormal liver function enzymes w/o metastasis - may just be a result of the carcinoma

254
Q

Imaging for renal cancer

A

US - for initial
CT to look at mass
MRI, Bone, Brain for mets

255
Q

Initial labs for renal cancer

A

CBC, LFT, UA

256
Q

Difference of PKD and cancer

A

PKD is more definied and evenly spread out

257
Q

Treatment for RCC

A

Radical nephrectomy
Chemotherapy has limited efficacy

258
Q

Wilms Tumor

A

Seen in pediatric patients
Due to abnormal kidney development - single unilateral lesion

259
Q

Clinical presentation of Wilms tumor

A

Abdominal pain
HTN
Hematuria

260
Q

Imaging for wilms tumor

A

US for first
CT/MRI for follow up
CBC,CMP, UA, Coag (you’re gonna do surgery)

261
Q

Wilms tumor treatment

A

Surgical resection - prognosis is often good
Recurrent disease is possible

262
Q

Oncocytoma

A

Common benign tumor that looks like RCC - treat like RCC

263
Q

Angiomyolipoma

A

Fat muscle and vessel tumor MC in women
Benign but can bleed
Embolize

264
Q

Organs that metastasize to kidney

A

Lung, stomach, other kidney

265
Q

Risk factors for kidney stones

A

Dehydration
High protein/salt intake
Gout

266
Q

Most common type of kidney stones

A

Calcium oxalate or phospjate
Visible on X-ray

267
Q

Clinical presentation of kidney stones

A

Acute severe flank pain - may follow ureters and be episodic
Nausea and vomiting

268
Q

Urinary stone labs

A

Hematuria
May have an abnormal pH of urine (high for calcium, low for uric acid)

269
Q

Litholink

A

Panel specifically looking for stones

270
Q

Imaging for renal stones

A

X-ray
US for pregnancy
CT - shows ALL stones

271
Q

Staghorn calculus

A

Stone that grows up into calyces

272
Q

Treatment for kidney stones

A

Try NSAIDs if not tried
IV fluids don’t help
Opioids may be needed for pain
Tamsulosin (a blocker)
Steroids

273
Q

Obstruction with infection

A

Medical emergency

274
Q

CIs for tamsulosin

A

Sulfa allergy
Lowers BP - orthostatic hypotension

275
Q

Stone passing criteria

A

Under 5mm - stone will pass
Over 10mm - will not pass

276
Q

Treatment for stuck kidney stone

A

Shock wave lithotripsy
- Avoid if may be pregnant
-Focus shockwaves
Ureteroscopic extraction
Percutaneous nephrolithotomy
- 15+mm or bottom of kidney

277
Q

Prevention for urinary stone disease

A

Consistent fluid intake
DONT decrease dietary calcium

278
Q

Things treat calcium stones

A

Thiazide diuretics help
Cellulose phosphate
Treat hypercalciuria (resorptive or renal)

279
Q

Hyperoxaluric stones

A

Some calcium
Often linked to IBD
Avoid vitamin C

280
Q

Hyperuricosuric stones

A

Mostly uric acid
Cut back on meat and beer - purines
Alipurinol

281
Q

Hypercitraturic stones

A

Due to diarrhea - drink lemonade

282
Q

Uric acid calculi

A

Hyperuricemia or abrupt cell death
Low pH and harder to see on X-ray
Potassium citrate or alopurinol

283
Q

Struvite calculi

A

P-bacteria - related to UTI
Often staghorn
Proteus, Pseudomonas, Providencia

284
Q

Cysteine calculi

A

Often genetic
Give citrate or bicarbonate
Double urine goal for these pts

GI/GU (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions