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Renal Systems > Week 1 LO > Flashcards

Week 1 LO Flashcards

1
Q

What are the seven major clinical presentations of renal disease?

A
  1. Acute kidney injury
  2. Chronic kidney disease
  3. Acute glomerulonephritis
  4. Nephrotic syndrome
  5. Isolated proteinuria
  6. Hypertension
  7. Ureteral Colic

Asymptomatic - #8

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2
Q

What are the usual symptoms of early chronic kidney disease (CKD)?

A

Usually asymptomatic thus importance of early screening labs - serum creatinine, urine albumin

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3
Q

What are the major signs of early CKD?

A
  1. Proteinuria (usually, and sooner than azotemia),
  2. Azotemia (always - elevated BUN, SCr, and CyC), (Blood Urea Nitrogen, Serum Creatinine, Cystatin C.)
  3. Hypertension (sometimes)
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4
Q

What are the usual signs & symptoms of late CKD?

A
  1. Hyperkalemia, hyperaldosterone, HTN, high phos, high iPTH (Intact parathyroid hormone)
  2. Hypocalcemia, hyponatremia, dyslipidemia,
  3. Neuropathy, fatigue, acidosis, dementia, nausea, edema, Anemia
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5
Q

What are the usual symptoms & stages of late CKD?

A

a. Stage G4, G5, sometimes G3b.
b. Uremic frost - build-up on skin; terrible smell; fatigue, nausea, vomiting, pruritus; seizures, confusion, peripheral neuropathy

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6
Q

What is the major sign of late CKD?

A

a. hyperkalemia

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7
Q 
What is the pathogenesis of the signs and symptoms of CKD?
1. Edema: 
2. Proteinuria: 
         A. Azotemia: 
3. Hematuria: 
4. Hypertension:
A
  1. Edema: salt & water retention
  2. Proteinuria: GBM leak (glomerular basement membrane)
    A. Azotemia: impaired filtration of nitrogenous waste
  3. Hematuria: capillary wall damage
  4. Hypertension: salt & water retention; disturbed homeostatic mechanisms
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8
Q

How is clinical CKD differentiated from the pathological diagnosis in the same patient?

A
  1. Clinical diagnosis is proteinuria, hematuria, HTN, AKI, acute GN, CKD, nephrotic syndrome, ureteral colic
  2. Pathologic diagnosis is diabetic nephropathy, HTN nephropathy, lupus nephritis, PSGN, urolithiasis, etc.
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9
Q

What are the normal adult ranges for BUN, serum creatinine, CrCl, eGFR, and urine albumin/protein?

MEMORIZE THESE!

A

a. BUN: 7–30 mg/dl (SI: 2.5–10.7 mmol/L)
b. SCr: 0.7–1.4 mg/dl (SI: 62–124 μmol/L)
c. CrCl: >100 ml/min in men, >90 ml/min in women
d. eGFR: >60 ml/min/1.73 m2 (not accurate in healthy people)

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10
Q

What are the usual signs & symptoms of acute glomerulonephritis (AGN)?

A 
Hematuria (micro or macro), 
oliguria, 
edema, 
HTN, 
fever, 
constitutional (N/V, HA, anorexia, pallor)
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11
Q

Where does the edema of AGN usually start? How does it typically progress overall? How does it typically progress over the course of a day for a patient?

A

a. Start in eyelids & face usually- “puffiness”
b. Always pitting
c. Progress downward  arm & leg edema
d. Migratory (face in AM, clear in afternoon, legs PM)

Differentiate with CKD which is dependent edema - only in legs, ankles, feet

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12
Q

What does the urine look like in patients with gross hematuria?

A

Ranges from orange–>red–>brown–>black; not shades of yellow.

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13
Q

Be able to describe the pathophysiology of type III hypersensitivity and the clinical implications of this for patients with AGN.

A

A. In type III HSR there is a soluble antigen floating in the blood. Body produces antibodies which attach to antigen forming immune complexes (IC’s).
B. Large and most medium IC’s cleared by macrophages
C. Small and some medium IC’s deposit in glomeruli, blood vessels (vasculitis/GN strong co-morbids), joints → complement activated → AGN, arthritis, and/or vasculitis

Another Answer:
Soluble antigen→ antibodies interact→  immune complexes→  deposited in glomeruli, blood vessels & joints→  activate complemen→t  vasculitis, arthritis, AGN

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14
Q

What are the most common etiologies of AGN?

A
  1. Postinfectious GN (history of rash? sore throat?)
  2. IgA nephropathy; Henoch-Schönlein purpura nephritis
  3. Lupus nephritis
  4. Membranoproliferative glomerulonephritis, type I
  5. Bacterial endocarditis
  6. Cryoglobulinemia
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15
Q

What clinical questions need to be asked of patients who present with AGN to help narrow down possible causes?

A

Ask: history of rash? Sore throat?

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16
Q

What are the usual signs and symptoms of anti-glomerular basement membrane (GBM) disease, a highly lethal subset of AGN?

(GoodPasture’s s/d)

A

A. Bloody sputum, chest pain, cough, dyspnea (come first)
B. Next will have hematuria
C. More common in men than women, ages 20–30 and 60–70.
D. This is Goodpasture’s Syndrome - extremely rare but lethal so you must consider

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17
Q

What is the correct management of a patient suspected of having anti-GBM disease?

A

Immediate hospitalization, will need immunosuppressives & plasmapharesis

Immediately hospitalize to rule out anti-GBM disease (Goodpasture syndrome); extremely high lethality w/o immunosuppressives (high dose steroids) and plasmapheresis

18
Q

What are the usual symptoms of the nephrotic syndrome?

A

A. Severe edema (3+/4+ pitting edema) - anasarca, ascites

B. polyuria

19
Q

What are the usual signs (labs) of the nephrotic syndrome?

A
  1. severe proteinuria (>3 g/d is considered “nephrotic syndrome level”)
  2. hypoalbuminemia,
  3. Dyslipidemia - hyperlipidemia, lipiduria (oily urine)
  4. No azotemia, no hypertension (unless present for some other reason)
20
Q

What is the pathogenesis of the signs and symptoms of nephrotic syndrome?

A

A. Kidney insult leads to lipiduria and massive proteinuria
B. Massive proteinuria causes:

  1. Increased hepatic LDL synthesis; decreased VLDL catabolism → increased LDL → dyslipidemia
  2. Loss of ApoC2, LPL → dyslipidemia
  3. Reduced clotting factors → thromboembolism
  4. Hypoalbuminemia → anascarca

Kidney insult → lipiduria & massive proteinuria→  reduced clotting factors leading to thromboembolism/ hypoalbuminemia leading to anasarca/ loss of ApoC2 & LPL leading to dyslipdemia

21
Q

What are the major causes of nephrotic syndrome in children?

A

Children: Minimal change disease

idiopathic, lithium, NSAIDs, leukemia, lymphoma, HIV, HCV, syphilis

22
Q

What are the major causes of nephrotic syndrome in Adults?

A

Adults: MGN=>Membranous glomerulonephritis (idiopathic, autoimmune, HBV, HCV, massive obesity)

A. Main is diabetic nephropathy

23
Q

What are the major causes of nephrotic syndrome in both children & Adults?

A

Both: FSGS=>Focal segmental glomerulosclerosis

(idiopathic, autoimmune, anabolic steroids, NSAIDs, radiation, HBV, HIV, sickle cell, congenital kidney problems, lymphoma)

24
Q

What is nephrotic syndrome level proteinuria (daily level)?

A

24 hour protein urine >3g

25
Q

How should a patient with asymptomatic proteinuria be worked up?

A

a. Check SCr or SCyC, BUN, electrolytes, blood pressure
b. Rule out diabetes
c. If >3g/day may have nephrotic syndrome
d. Repeat urine protein, SCr, BUN, electrolytes, BP in 1 month
e. Can refer to nephrologist after 2 elevated readings

26
Q

What organ(s) are primarily responsible for long-term regulation of blood pressure?

A

Kidneys

27
Q

What is Conn’s syndrome? How is it diagnosed?

Sx’s: HTN, Inc. Urination, CVD (Stroke etc.), Dec. vision, Mm weakness/tingling/spasms

A

a. Primary Hyperaldosteronism
b. Dx: plasma aldosterone: plasma renin activity ratio greater than 30
c. HypoKalemia = dec. Renin

28
Q

What are the usual signs and symptoms of ureteral colic?

A
  1. Intermittent, severe pain in low back or flank or abdomen
  2. May have nausea
  3. Move around a lot
  4. Gross or microscopic hematuria, proteinuria
29
Q

How is ureteral colic definitively diagnosed?

A

Imaging (renal US or CT scan)

30
Q

What are the usual signs & symptoms of the acute kidney injury (AKI)?

A

Edema, oliguria or anuria, HA, fatigue, anorexia, N/V, arrhythmias

31
Q

What is the pathogenesis of the symptoms of AKI?

A

a. Renal ischemia/angina → renal damage (kidney attack) → failure of filtration→ oliguria or anuria
1. Accumulation of urea & other products → HA, fatigue, N/V, anorexia
2. Hyperkalemia → arrhythmias

Acute kidney injury has three main causes: A sudden, serious drop in blood flow to the kidneys. Heavy blood loss, an injury, or a bad infection called sepsis can reduce blood flow to the kidneys. Not enough fluid in the body (dehydration) also can harm the kidneys.

32
Q

What are the usual symptoms of the acute kidney injury (AKI)?

A

Onset hours to days - HA, fatigue, anorexia, N/V, sudden onset edema, decreased urine production

Acute kidney injury has three main causes: A sudden, serious drop in blood flow to the kidneys. Heavy blood loss, an injury, or a bad infection called sepsis can reduce blood flow to the kidneys. Not enough fluid in the body (dehydration) also can harm the kidneys.

33
Q

What are the usual signs of AKI?

A
  1. Hyperkalemia → arrhythmias
  2. Elevated BUN due to filtration failure
  3. Hematuria + edema + HTN + acute onset → think AGN (subset of AKI)
  4. HTN not usually feature of other types of AKI put pt may have pre-existing HTN
34
Q

What are the major causes of prerenal, renal, and postrenal AKI?

A
  1. Pre-renal: CHF, hypotension, hypovolemia, liver cirrhosis, renal artery stenosis, renal vein thrombosis, Iatrogenic (NSAIDs, ACEi, ARB, diuretic overdose)
  2. Renal: acute glomerulonephritis, acute tubular necrosis, acute interstitial nephritis, tumor lysis syndrome, toxins, Iatrogenic (penicillins, cephalosporins, radiocontrast agents, aminoglycosides)
  3. Post-renal: Kidney stone, mass impinging ureter, BPH, obstructed catheter, neurogenic bladder.

A. Prerenal (vascular): 70%.

 1. Common etiologies: CHF, hypotension/hypovolemia, severe liver cirrhosis, renal vein thrombosis, severa RAS. 
 2. Also iatrogenic - NSAIDs, ACEi, ARB, diuretic    overdose. 
 3. Common picture of AKI: Elderly patient, mild or worse    dementia, restricted fluid access (or with vomiting, diarrhea, severe CHF)

B. Renal (intrinsic): tubular, glomerular, interstitial, vascular. AGN, Acute tubular necrosis, acute interstitial nephritis, many toxins, AKI. Iatrogenic - penicillins, cephalosporins, radiocontrast agents, aminoglycosides.

C. Postrenal (obstructive): kidney stone, mass impinging ureter, BPH, obstructed catheter

35
Q

What is the usual management of patients suspected of having AKI?

A

ER!!! Emergency dialysis (you don’t have this in office). Do not tell them to drink a lot of water. Do not give them an IV.

A. Send to hospital immediately
1. May need surgery or dialysis
B. Once cause is determined, potentially treat later
C. Diuretics do not improve outcomes in absence of volume overload.

36
Q

A. 55-yr-old man, long history of cigarette smoking with a chronic smoker’s cough, otherwise healthy
B. Noted pitting edema in his legs this morning
C. No other symptoms
D. SCr 1.6 mg/dl, BUN 31 mg/dl, eGFR (by CKD-EPI equation) 48 ml/min/1.73 m2, no proteinuria

What is his clinical syndrome?

A

Patient 1: early CKD (stage G3aA1a by the way)

37
Q

A. 14-year-old girl, previously healthy
B. Awoke with painful purpura on her legs
C. First morning urine dark
D. Mother noted her face was puffy and she felt feverish

What is her clinical syndrome?

A

Patient 2: AGN (r/o Henoch-Schönlein purpura nephritis)

Henoch-Schönlein purpura affects the small blood vessels of the skin, joints, intestines, and kidneys. It’s most common before age seven but can affect anyone.
Symptoms include reddish-purple spots on the lower extremities, swollen and sore joints, abdominal pain, or bloody urine.
The condition is often treated with steroids.

38
Q

A. 64-year-old man, history of coronary artery disease and hip osteoarthritis, on chronic NSAIDs
B. Over 1 wk, developed a persistent cough and started noticing intermittent bright red blood in his urine with back pain
C. In office, BP is 175/120 mmHg, urine dipstick is positive for blood and protein (both 3+), and he has bilateral 2+ pitting edema of his ankles

What is his clinical diagnosis? What is your response?

A

Patient 3: AGN w/ likely anti-GBM disease; send to hospital

39
Q

A. 42-year-old woman, history of irregular menstrual periods and dysmenorrhea, fatigue, currently taking levothyroxine
B. Found out her mother had aggressive breast cancer and started having to help take care of her (became very busy, not eating well)
C. She herself tested positive for BRCA1; extremely stressed
D. Started getting severe nausea, abdominal pain, restlessness not relieved by any position, but helped by taking ibuprofen

What is her clinical syndrome?

A

Patient 4: ureteral colic

40
Q

A. 71-year-old man, type I diabetes mellitus since age 17 yr, using insulin (basal and short-acting), refuses statins (highly skeptical of conventional medicine)
B. Diagnosed one year ago with retinopathy in left eye
C. Over the past month has become extremely fatigued, dyspneic, confused, anorexic, and has gained weight (~15 lb in 1 mon)
D. In office, BP is 160/105 mmHg, he has 3+ bilateral pitting edema of legs, has a positive fluid wave in abdomen, urine dipstick positive for glucose (4+), protein (1+), and blood (1+)

*What is his clinical syndrome?

A

Patient 5: late CKD (stage cannot be determined)

41
Q

A. 37-year-old man, history of scoliosis and back pain
B. Recent onset of fatigue and swollen face and ankles
C. Also noted oily sheen in toilet after urinating
D. In office BP 120/74 mmHg, urine dipstick 3+ protein, 3+ pitting edema of both lower legs almost to the knees and dorsa of his hands
E. BUN 24 mg/dl, SCr 1.0 mg/dl, eGFR >60 ml/min/1.73 m2

What is his clinical syndrome? What tests would confirm this?

A

Patient 6: nephrotic syndrome; serum lipids, 24 h urine protein, serum albumin

Renal Systems (11 decks)

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