Nephrology

Front 1

What are the causes of ECF volume increases?

Back 1

CHF, cirrhosis, kidney disease, hypoalbuminemia

Front 2

How would a patient with ECF volume overload present?

Back 2

edema, weight gain, JVP elevation, pulmonary edema, pleural effusion

Front 3

How do you manage a patient with ECF volume overload?

Back 3

treat underlying cause, Na+ restriction, diuretics

Front 4

What are the side effects of diuretics?

Back 4

hypotension, hypokalemia, hyponatremia.

Front 5

What are the causes of ECF volume depletion?

Back 5

diarrhea, sweating, burns, diuretics

Front 6

How does a patient with ECF volume depletion present?

Back 6

low JVP, dry mucous membranes, weight loss, tachycardia, hypotension, depressed fontanels, oliguria

Front 7

How do you manage a patient with ECF volume depletion?

Back 7

oral rehydration, isotonic saline IV

Front 8

What are some of the causes of hyponatremia?

Back 8

Low Na+ due to TOO MUCH water! causes: too much ADH due to low bp, stress, pregnancy, cortisol, low tyroid, cancers, drugs

Front 9

What are the S/S of hyponatremia?

Back 9

usually none if gradual, but if acute: headache, confusion, seizures, coma due to brain swelling.

Front 10

How do you treat hyponatremia?

Back 10

treat underlying cause, fluid restriction, give hypertonic saline to move fluid into ICS, treat slowly to avoid brain injury

Front 11

What are the causes of hypernatremia?

Back 11

Condition due to LOW WATER!! seen in patients who are unable to obtain fluids (elderly, infants, etc), patients in coma, glycouria (ie. DM) diabetes insipidus.

Front 12

What are the S/S of hypernatremia?

Back 12

thirst, if acute: coma, seizures,

Front 13

What causes hypokalemia?

Back 13

insulin therapy, diarrhea, DM, Conn's syndrome, MI, high aldosterone, diuretics, metabolic alkalosis

Front 14

What are the S/S of hypokalemia?

Back 14

muscle weakness, ventricular arrhythmias, hyperglycemia

Front 15

Why are patient with hypokalemia alkaline?

Back 15

When K+ is lost from cells, it gets replaced by H+ and Na+ which makes cells acidic. The kidneys then think the body is acidic and they secrete extra ammonium (acid) making the blood alkaline.

Front 16

How do you treat hypokalemia?

Back 16

use a K+ sparing diuretic, oral KCl, IV KCl (for very low K+), high K+ foods

Front 17

What causes hyperkalemia?

Back 17

due to K+ leaking out of cells, secondary to insulin deficiency, rhabdomyolysis, hemolysis, impaired kidney excretion, metabolic acidosis

Front 18

what are the S/S of hyperkalemia?

Back 18

muscle weakness, stiffness, cardia arrhythmias (peaked T waves, no P waves, wide QRS)

Front 19

How do you treat hyperkalemia?

Back 19

give calcium and insulin (stablizes ECG and shifts K+ into cells), diuretics or dialysis

Front 20

When would you refer a diabetic patient to a nephrologist?

Back 20

1. renal insufficiency: GFR <15

2. hematuria

3. SCr elevated >30% when on ACE or ARB

4. >300mg protein in 24hr urine specimen

5. diabetic nephropathy unlikely at this time

Front 21

What is GFR based on? (3)

Back 21

1. age

2. weight

3. creatinine clearance

Front 22

What two areas detect changes is ECF volume?

Back 22

1. carotid baroreceptors

2. juxtaglomerular apparatus

Front 23

What substances regulate ECF volume in the body?

Back 23

1. renin

2. aldosterone

3. angiotensin

4. catecholamine

Front 24

What is diabetes inspidus?

Back 24

When there is not enough ADH and too much fluid is being lost.

Front 25

What lab findings would be present in DI?

Back 25

1. high serum Na

2. high serum osmolarity (=highly concentrated)

3. low urine osmolarity (=diluted)

4. polyuria and thirst

5. ADH low (if lack of excretion from pituitary) or normal if no response from the kidneys

Front 26

What are the S/S of DI?

Back 26

1. polyuria,

2. thirst

Front 27

How do you treat DI?

Back 27

hormonal replacement of ADH, thiazide diuretics, oral fluid replacement.

Front 28

What is SIADH?

Back 28

Syndrome of inappropriate ADH - too much ADH = fluid overload!!

Front 29

What lab findings would be present in SIADH?

Back 29

1. low serum Na

2. low serum osmolarity

3. high urine osmolarity

4. high ADH levels

5. low serum Ca2+

Front 30

What are the S/S of SIADH?

Back 30

1. edema/fluid retention

2. olgiuria

Front 31

What causes SIADH?

Back 31

some cancers (eg. lung), drugs

Front 32

How do you treat SIADH?

Back 32

hypertonic solution, lithium, fluid restriction

Front 33

What are the causes of Metabolic alkalosis?

Back 33

1. vomiting

2. loss of HCl

3. hypokalemia

Front 34

What lab values are indicative of metabolic alkalosis?

Back 34

high pH, high bicarb, possibly low K+, low H+

Front 35

What are the causes of metabolic acidosis with an anion gap? (KARMEL)

with out an anion gap?

Back 35

K-ketoacidosis

A-aspirin

R- Renal failure

M- methanol

E-ethalene glycol

L- lactic acidosis (hypovolemic/cardiogenic shock, sepsis, cirrhosis)

without - diarrhea,

Front 36

How do you treat metabolic acidosis?

Back 36

treat underlying condition, administer NaBicarb

Front 37

What lab values are indicative of metabolic acidosis?

Back 37

low pH, low bicarb, increased anion gap

Front 38

What are the main characteristic of AKI?

Back 38

decreased GFR, elevation of BUN and Cr, olgiuria

Front 39

What are major S/S of AKI?

Back 39

fatigue, altered mental status, nausea, vomiting, pruritis, seizures, anorexia, hyperkalemia, acidosis

Front 40

What clinical findings are present in AKI?

Back 40

myoclonus, pericardial rub, edema, pulmonary rales

Front 41

What lab investigations would you do for suspected AKI?

Back 41

BUN, SCr, lytes, CBC w/diff, urine dipstick, microscopy, urine Na, urine Cr.

Front 42

Differentiate between nephrotic syndrome and actue nephritic syndrome

Back 42

nephrotic: >3.5g urine protein in 24 hrs, low serum albumin, high cholesterol, edema - condition of protein loss in the urine causing low oncotic pressure and subsequent edema

nephritic: RBCs in urine, RBC casts, edema, HTN - condition of AKI and Na and H2O retention leading to edema.

Front 43

Differentiate between pre, intra, and post renal AKI?

Back 43

pre-diminised blood flow to kidneys

intra - damage to renal parenchyma

post - UT obstruction

Front 44

How would you investigate pre-renal AKI?

Back 44

urine dipstick, serum osmolality (>500mmol/L). BUN:Cr (>20:1), no blood or protein in the urine

Front 45

What are the causes of pre-renal AKI?

Back 45

shock (cardiogenic, hemorrhagic), CHF

Front 46

How do you treat pre-renal AKI?

Back 46

volume replenishment (IV NS)

Front 47

What lab findings would be indicative of intra-renal AKI?

Back 47

normal serum osmolarity, BUN:Cr <20:1, Na excretion >3%, urine would show: RBC, RBC casts, WBC, WBC casts, proteins

Front 48

What are the main clues in a urine analysis that AKI is glomerular in origin?

Back 48

RBCs, RBC casts, >2-3g protein in 24hr sample.

Front 49

What is post streptococcal glomerulonephritis? What are the S/S? What is the treatment?

Back 49

immune complex build up in the glomeruli leading to AKI. usually occurs 2-3 weeks post-infection. S/S: hematuria, oliguria, HTN, proteinuria. Tx: supportive

Front 50

What is IgA nephropathy (aka Berger's disease)?

Back 50

IgA complex build up in glomeruli usually at the time of a URTI. S/S: painless, gross hematuria Tx: steroids

Front 51

What is Henoch Schonlein purpura? How is it different from IgA nephropathy?

Back 51

Due to deposition of IgA complex in glomeruli and may lead to CKD. Similar to IgA but has systemic presentation of: purpura, arthalgia, abd pain (triad of symptoms: abd pain, arthritis, purpura) Tx: pain killers, supportive bc spontaneously resolves

Front 52

Name the types of focal nephritic syndromes

Back 52

1. mild postinfectious glomerulonephritis

2. mild IgA nephropathy

3. thin basement membrane disease

4. proliferative glomerulonephritis

5. early lupus

Front 53

Name the types of diffuse nephritis syndromes

Back 53

1/ postinfectious glomerulonephritis

2. poliferative glomerulonephritis

3. advanced lupus

4. glomerulonephritis

Front 54

If a patient had protein in the urine and hypoalbuminemia, dyslipidemia and edema but NO hematuria, what kind of kidney disease would they have? (Nephritic, nephrotic, or pre-renal?)

Back 54

nephrotic

Front 55

How do you differentiate between glomerular vs. tubulo-interstitial AKI?

Back 55

glomerular- RBC, RBC casts, proteinuria

tubulo-interstitial: WBC, WBC casts,

Front 56

What are the two main types of tubulo-interstitial disease? How do you distinguish between the two?

Back 56

1. acute tubular necrosis

2. interstitial nephritis

IN is an allergic rxn to drugs and presents with additional S/S: rash, fever, high Cr.

Front 57

What is polycystic KD? What are the S/S?

Back 57

cyst formation on kidneys bilaterally

S/S: HTN, pain, kidney stones, hematuria, UTI

Front 58

How would you investigate polycystic KD?

Back 58

ultrasound, urine analysis

Front 59

Who does proximal renal tube acidosis usualy occur in? What is it? What are the S/S?

Back 59

Young kids,

failure of proximal tubules to reabsorb bicarb from the urine creating metabolic acidosis

S/S: confusion, failure to thrive, low resp rate, dehydration, fatigue, polydispia

Front 60

What are the S/S of renal cell carcinoma?

Back 60

hematuria, flank pain, palpable abdominal mass, weight loss, anorexia, etc.

Front 61

What causes renal vein thrombosis? How do you investigate it? How do you treat it?

Back 61

renal veins become clogged by thrombi for various reasons, or by tumor

Ix: renal vein angiography or doppler, US, CT

Tx: anticoagulation w/ heparin

Front 62

A patient presents with HTN, flank bruits, and hypokalemia. What is the main DDx? How would you investigate this? How would you manage this?

Back 62

renal artery sclerosis (bruit is main clue)

Ix: angiography, doppler, CT, MRIangio, labs

Tx: manage risk factors, angioplasty, meds: antiHTN

Front 63

What is hemolytic uremia syndrome?

Back 63

When the RBC are prematurely destroyed and clog the filtering system in the kidneys leading to AKI. Usually occurs following E.coli poisoning.

Front 64

What defines CKD?

Back 64

GFR <60ml/min for >3months

proteinuria or hematuria, or anatomical abnormalities

Front 65

What is the recommended medical therapy to improve proteinuria?

Back 65

ACE or ABR (bc acts on distal tubules)

Front 66

List ways to prevent the progression of CKD?

Back 66

DM control, HTN control, reduce proteinuria, dyslipidemia control, smoking cessation

Front 67

How would you investigate generalized edema?

Back 67

H&PE, urinalysis, blood tests: albumin, BUN, SCr, lytes, LFT. Further testing: abd US, CT.

Want to determine if CHF, cirrhosis, kidney disease, hypoalbunemia

Front 68

What causes the edema in nephrotic syndrome?

Back 68

high secretion of protein in the urine =low protein in the blood = low oncotic pressure = fluid is lost to the ECF

Front 69

How do you treat nephrotic syndrome?

Back 69

corticosteroids, rare occasions: immunosuppresants. if HTN then ACEi

Front 70

What are the S/S of acute proliferative glomerulonephritis (aka postinfectious GN)?

Back 70

hematuria, oliguria, HTN, proteinuria, edema

Front 71

Differentiate between postinfectious GN (aka acute proliferative GN), IgA GN, and Henoch-Schnolen Purpura.

Back 71

Similar: IgA complexes clog glomeruli causing hematuria, oliguria, HTN and protienuria.

Diff: PIGN: 2-3 weeks post streptococcal infection. IgA GN: at same time as URTI. HSP: has systemic symptoms of purpura, arthritis, abd pain.

Front 72

What is Goodpasture's syndrome? What are the S/S? How is it diagnosed? How do you treat it?

Back 72

1. autoimmune disease where the basement membrane of the LUNGs and KIDNEYs are attacked by anti-glomerular basement membrane antibodies (anti-GBM)

2. fatigue, wt loss, night sweats, lung symptoms: hemoptysis, cough, SOB, crackles, resp failure, PE, chest pain. Renal symptoms: hematuria, edema, HTN, uremia. Other: hepatosplenomegaly, anemia, cyanosis

3. DDx confirmed by anti-GBM antiboides, Labs: Iron deficiency anemia, Chest x-ray, renal biopsy (cresent formation on microscopy)

4. plasma exchange, immunosuppressives, corticosteroids

Front 73

What are the 3 main classification of AKI? Give examples of what causes each type

Back 73

1. Pre-renal: shock, vomiting, diarrhea, diuretics, CHF, Hypotension, trauma

2. intra-renal: inflammation, toxins, drugs, infection, tubular necrosis, idiopathic

3. post-renal - obstruction: enlarged prostate, kidney stones, tumors, strictures, injury

Front 74

How do you investigate AKI?

Back 74

H&PE, CBC with diff, serum Na, K, Cl, HCO, urinalysis, US of kidneys (to determine if pre, intra or post renal AKI)

Front 75

How do you treat AKI? (generally)

Back 75

Treat is tailored to diagnosis of pre, intra or post renal AKI.

1. correct volume: if depleted-rehydrated, if overloaded: diurese. correct K+: if hyper: insulin, Calcium gluconate, saline, lasix, dialysis. metabolic acidosis: dialysis, sodium bicarb. catheter: used for obstruction

Front 76

What are the two main causes of renal artery stenosis? Who is most likely to acquire each?

Back 76

1. atherosclerosis - older males, smokers

2. fibromuscular dysplasia - young females <30yo

Front 77

How does angiotensin raise BP?

Back 77

1. causes generalized arteriole constriction

2. increases Na & H2O retention

Front 78

What are the S/S of renal artery stenosis?

Back 78

severe HTN, asymmetric renal size, bruits, hypokalemia, increased SCr, pulmonary edema

Front 79

What is the gold standard for investigating renal artery stenosis?

Back 79

renal arteriography

Front 80

What are the causes of SIADH? (list 2 from each of the 5 categories)

Back 80

1. pulmonary disorders: acute respiratory failure, infections

2. tumors - pulmonary, mediastinal

3. CNS disorders - stroke, mass lesions

4. Drugs - SSRIs, MAOIs, carbamazapine, tricyclics

5. Misc. - HIV, idiopathic

Front 81

List at least 5 risk factors for renal cell carcinoma

Back 81

1. obesity

2. CKD

3. PKD

4. HTN

5. smoking

6. sickle cell

7. toxicity

Front 82

What is the classic triad of symptoms in renal cell carcinoma?

Back 82

flank pain, hematuria, abdominal mass

Front 83

How would you investigate a suspected renal cell carcinoma? How is it treated?

Back 83

1. US, CT, MRI, labs, urinalysis, biopsy

2. surgery (partial or full nephrectomy), immunotherapy - often resistant to chemo

Front 84

What is renal vein thrombosis? Who is most likely to acquire it?

Back 84

occlusion of the renal vein due to thrombi. Most common in children but still very rare

Front 85

What are the symptoms of renal vein thrombosis? How does it differ from renal artery stenosis?

Back 85

S/S: flank pain, gross hematuria, nausea, anorexia, edema, scrotal swelling, proteinuria, elevated SCr, tender abdominal mass in infants, signs of dehydration

Artery stenosis - more likely to affect older males with risks of athrosclerosis. causes HTN, and pre-renal AKI (possibly)

Front 86

What is the gold standard to investigate renal vein thrombosis?

Back 86

renal venography,

Front 87

How do you treat renal vein thrombosis?

Back 87

anticoagulation - warfarin/heparin

clot buster - tPA pr PCI

monitor fluids and lytes

treat underlying disease (ie. nephrotic syndrome)

Front 88

What is hemolytic uremia syndrome?

Back 88

severe life threatening complication of E.coli poisoning. E. coli toxins cause cell injury and cell death in the kidneys which induces the coagulation cascade. causes obstruction of small renal vessels but destroying RBC

Front 89

What are the classic symptoms of hemolytic uremia syndrome?

Back 89

anemia, thrombocytosis (high platelets), renal failure

other S/S: bloody diarrhea, lethargy, bruising, swelling, dehydration, oliguria, nausea, vomiting

Front 90

How do you manage hemolytic uremia syndrome?

Back 90

supportive (fluids, lytes, analgesics, TPN, antihypertensives)

blood transfusions

dialysis

Front 91

What is proximal renal tubular acidosis?

Back 91

failure of the proximal tubules to reabsorb bicarb from the urine/filtrate

Front 92

How does a patient with proximal renal tubular acidosis present?

Back 92

metabolic acidosis - headache, confusion, LOC, lethargy, coma, hyperkalemia, warm flushed skin, nausea, vomiting, Kussmaul breathing

Front 93

What investigations would lead you to believe a patient has proximal renal tubule acidosis?

Back 93

metabolic acidosis that is unexplained by other normal anion gap causes (ie. diarrhea, fistula, drugs)

urine pH <5.3

hyperkalemia

ECG suggestive of hyperkalemia

Front 94

How do you treat proximal renal tubule acidosis?

Back 94

sodium bicarb to restore normla pH. restore lytes

Front 95

What causes hyperkalemia?

Back 95

metabolic acidosis, DKA, renal failure, ACE inhibitors, IV intake