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Patho > Week 9: Renal > Flashcards

Week 9: Renal Flashcards

1
Q

What are the basic functions of the renal system? (4)

A

Water/ion homeostasis
Removes metabolic wastes: urea, uric acid, creatinine and toxins
Secretes hormones: EPO, renin, activates vitamin D3
Plays a role in gluconeogenesis

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2
Q

What is the basic structure of kidneys?

A

paired and located in the upper dorsal region of abdominal cavity

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3
Q

What are the different regions of the nephron?

A

renal corpuscle, proximal convoluted tubule, loop of henle, distal convoluted tubule, collecting tubules

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4
Q

How much cardiac output goes through the renal artery?

A

20%

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5
Q

Explain the renal tubular processes (4)

A

Filtration: removal of substances from blood into renal tubule at the glomerulus

Secretion: removal of substances from blood into renal tubule at peritubular capillaries

Reabsorption: return of substances from renal tubule into blood at peritubular capillaries

Excretion: removal of substances from renal tubule through urine

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6
Q

What is the function of the renin-angiotensin system? What are the two major hormones in play?

A

regulates blood pressure and maintain blood volumes

Angiotensin II - potent vasoconstricting factor
Aldosterone from adrenal cortex - facilitates sodium reabsorption

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7
Q

How is renin synthesized into angiotensin II?

A

Renin is synthesized by the liver into angiotensinogen, then converted to angiotensin I & II in the lungs by angiotensin converting enzyme

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8
Q

Where is antidiuretic hormone (ADH) released from and what is it’s role?

A

Released from the posterior pituitary
Acts on the renal tubules to allow for water reabsorption that depends upon the formation of a salt gradient by the loop of henle

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9
Q

Where is atrial natriuretic peptide (ANP) released from and what is it’s role? What hormone does it oppose?

A

Released from cells of the cardiac atria in response to increased stretch
Role: Counters fluid-conserving effects to reduce blood volume, relieves blood pressure
Works opposite aldosterone

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10
Q

What are the major tests of renal function (4)?

A
  • urinalysis
  • blood chemistry: blood urea nitrogen measures urea, serum creatinine reflects GFR and functional capacity of kidneys
  • creatinine clearance: clearance is the amt of some substance that is cleared from the blood by the kidneys per unit time, can be used to estimate GFR
  • GFR: provides an assessment of renal function
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11
Q

What is measured in a UA and what are the normal findings (6)?

A
  1. color (yellow to amber)
  2. consistency (clear to slightly hazy)
  3. specific gravity (1.003-1.030)
  4. pH (5-6.5)
  5. glucose, ketones, nitrites, hemes and protein (negative)
  6. microscopic exam for casts, crystals and cells (absence)
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12
Q

Define diuretic

A

agents that increase water excretion

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13
Q

Explain (generally) how osmotic, loop, thiazide, and potassium-sparing diuretics work

A

Osmotic diuretics: acts at proximal tubule to shift the osmotic balance
Loop diuretics: work by inhibiting symporters in the loop of Henle - destroys the salt gradient and prevents water reabsorption under the influence of ADH from the collecting tubules
Thiazide diuretics: block the Na+Cl- symporter in the distal convoluting tubule to block sodium reabsorption, thus water remains in the lumen of the renal tubule for excretion
Potassium-sparing diuretics: work in the collecting ducts and inhibits aldosterone, blocks Na+ reabsorption and increases K+ retention

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14
Q

Define glomerulonephritis

A

several pathological states usually involves inflammation of glomerulus

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15
Q

What are causes of glomerulonephritis (Primary 1 vs. Secondary 4)

A

Primary: intrinsic to kidney
Secondary: associated with infections (post-streptococcal GN, bacterial endocarditis), drugs, systemic disorders (lupus or vasculitis) or diabetes

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16
Q

S/S of glomerulonephritis (5)

A

depends on the form of GN but may include hematuria, proteinuria, hypertension, edema and fatigue

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17
Q

S/s of acute nephritis syndrome (5)

A

hematuria, proteinuria, azotemia (nitrogen in the blood), edema, hypertension

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18
Q

Define rapidly progressive glomerulonephritis

A

progression of renal failure over days to weeks often in the context of nephritic syndrome

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19
Q

What is the defining characteristic of rapidly progressive glomerulonephritis?

A

Formation of crescents initiated by passage of fibrin into the Bowman’s capsule which stimulates proliferation of the endothelial cells

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20
Q

What is Goodpasture syndrome?

A

autoimmune disease caused by formation of antibodies to the basement membrane

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21
Q

Define nephrotic syndrome

A

constellation of findings resulting from glomerular permeability and protein loss to the urine

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22
Q

Define chronic glomerulonephritis

A

persistent proteinuria with or without hematuria and slowly progresses to chronic renal failure

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23
Q

Define tubulointerstitial disease

A

disorders that affect interstitial space surrounding renal tubules

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24
Q

Distinguish between acute vs. chronic tubulointerstitial disease

A

Acute: rapid onset characterized by edema
Chronic: fibrosis and atrophy, may be characterized by absence of symptoms until late in course of disease

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25
Q

What are two possible causes of chronic tubulointerstitial disease

A

Kidney infection (pyelonephritis), acute tubular necrosis

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26
Q

Define pyelonephritis

A

infection of kidney tissue and pelvis

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27
Q

What is acute pyelonephritis?
S/S (5)
Complications (3)

A

result of hematogenous spread of gram negative bacteria or infection via the urethra or instrumentation (placing catheters)
S/S: fever, chills, groin or flank pain, urinary frequency, dysuria
Complications: septic shock, chronic pyelonephritis, chronic renal insufficiency

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28
Q

What is chronic pyelonephritis?

A

Progressive disease characterized by scarring and deformation of renal calyces (drain kidney of urine and pass it)

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29
Q

Risk factors of chronic pyelonephritis (4)

A

Increased risk with obstructive uropathy, glomerulonephritis, polycystic kidney disease and renal calculi

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30
Q

Complication of chronic pyelonephritis

A

Abscess formation around the kidney can occur

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31
Q

Possible causes of chronic pyelonephritis (3)

A

May be due to kidney stones, neurogenic or congenital such as strictures

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32
Q

What is acute tubular necrosis the common cause of (2)?

A

acute kidney injury, acute kidney failure

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33
Q

What changes in acute tubular necrosis?

A

elevations in BUN and creatinine, decline in urine output

34
Q

Types of acute tubular necrosis

A

Ischemic: results from decreased perfusion or inadequate oxygenation to renal tubules
Nephrotoxic: results from number of agents that directly and specifically damage the renal tubules

35
Q

Risks for acute tubular necrosis (4)

A

Blood transfusion reactions
Injury or trauma to the muscles (rhabdomyolysis)
Hypotension or shock
Recent surgery or exposure to nephrotoxic substances

36
Q

Phases of acute tubular necrosis, include how long they last

A

Initiation phase: dominated by the initiating cause of ATN and azotemia - several hours
Maintenance phase: characterized by oliguria, profound systemic effects and significant morbidity and mortality due to retention of waste products, fluid retention and development of hypertension - lasts for a week
Recovery: characterized by profuse diuresis with recovery of renal function, may take years and some kidney damage may persist

37
Q

Which stage of acute tubular necrosis do fatalities commonly occur in

A

Maintenance phase

38
Q

What is the goal of treatment for acute tubular necrosis?

A

treatment is aggressive and usually requires dialysis to maintain kidney function, reduce damage and recover functional tissues

39
Q

Define polycystic kidney disease

A

cystic genetic disorder of the kidneys

40
Q

What are the affected genes that lead to polycystic kidney disease? Which gene accounts for the majority of cases and what does it normally do?

A

Affected genes: 3 mutations in PKD-1, 2 or 3 genes

PKD-1 gene accounts for 85% of all ADPKD - involved in cell cycle regulation and calcium transport in epithelial cells

41
Q

Characteristics of polycystic kidney disease (3)

A

Multiple cysts in kidneys - may be one affected kidney and typically progresses to bilateral

Cysts are numerous and fluid filled which enlarges the kidney, compresses and replaces functional renal tissue

Renal deterioration which progresses to fatal anemia

42
Q

What are s/s of polycystic kidney disease (5)?

A

HTN, increased abdominal size, hematuria, flank pain, renal calculi

43
Q

How does adult autosomal dominant polycystic kidney disease (ADPKD) progress? What is the prevalence in end stage renal disease patients?

A

Insidious onset - does not usually present until 30-50 years, renal deterioration is gradual
10% of ESRD patients are affected by ADPKD

44
Q

What is the mortality rate of autosomal recessive polycystic kidney disease (ARPKD), and what population does it affect?

A

Mortality rates: 30% of neonates

Infants

45
Q

Secondary effects of polycystic kidney disease

A

Damage to and possible formation of cysts in the liver and pancreas, rarely the heart and brain

46
Q

Define obstructive uropathy

A

obstruction of urine flow as it exits from the kidney toward the bladder

47
Q

What are causes of obstructive uropathy? (3)

A

Renal calculi
Congenital disorders of ureters - strictures or tumors
infection

48
Q

What are renal calculi?

A

form when substances that normally dissolve in urine precipitate, most common in renal pelvis, calyces of the kidney

49
Q

Which population are renal calculi most common in, and which population are they the most rare in?

A

Common: Men
Rare: Children

50
Q

What are the factors that can lead to renal calculi? (7)

A

change in pH, dehydration, gout, immobilization, infection, obstruction, family history

51
Q

What causes calcium stones, prevalence and treatment

A

Cause: excess calcium
Prevalence: 80% of renal calculi
Tx: dietary restriction of foods containing oxalate

52
Q

What causes struvite stones, prevalence and treatment

A

Cause: urea-splitting UTI
Prevalence: 10-15% of renal calculi
Tx: treat underlying UTI

53
Q

What causes uric acid stones, prevalence and treatment

A

Cause: gout
Prevalence: 5-10% of renal calculi
Tx: dietary restriction of foods containing purine

54
Q

What causes cystine stones?

A

rare inherited disorder of cystine metabolism

55
Q

What is ADH’s normal role and what is it’s feedback loop?

A

normal role: increases water reabsorption from renal tubules that increases BP by increasing BV
Feedback loop: Released from posterior pituitary in response to low BP or increased blood osmolarity

56
Q

Define SIADH

A

characterized by high than normal levels of ADH, results in fluid overload or dilutional hyponatremia

57
Q

Causes of SIADH (5)

A

Excess ADH released from posterior pituitary
Ectopic source releases ADH (lung cancer cells)
Infections
Head injury
Drugs

58
Q

Consequences of SIADH (4)

A

water retention occurs, BV increases, extracellular fluid volume increases; fluid overload/dilutional hyponatremia

59
Q

Sx (6) and Tx (3) of SIADH

A

Sx: headaches, nausea, vomiting, confusion, convulsions, coma
Treatment: water restriction, demeclocycline, management of underlying cause

60
Q

Define diabetes insipidus

A

lower than normal levels of ADH

61
Q

Define prerenal disease, causes, reversibility, s/s (2)

A

underlying cause d/t blood supply to kidney
Causes: systemic hypotension, shock, substances that promote vasoconstriction
Reversible if detected before damage has occurred
s/s: oliguria, disproportionate elevation of BUN relative to creatinine (20:1, normal 10:1)

62
Q

Define intrarenal disease, causes (4), treatment

A

underlying cause within the kidney itself
Causes: disease that injures or damages structures within kidney, associated with ischemia or toxicity - ATN, glomerulonephritis, pyelonephritis, rhabdomyolysis
Tx: identify and correct underlying cause

63
Q

Define postrenal disease, causes (4)

A

underlying cause in the urinary tract or issue with outflow from the kidney, depends on cause and severity of obstruction, back pressure can damage the kidneys
Causes: calculi or strictures in the ureter, bladder tumor, neurogenic bladder, prostatic hyperplasia

64
Q

Characteristics of chronic kidney disease (4)

A

○ Slow, insidious, irreversible impairment of renal function
○ Destruction of renal tissue with irreversible sclerosis and loss of nephron function
○ Results from chronic illness or rapidly progressing disease
○ Symptoms generally nonspecific and might include reduced appetite or generally feeling unwell

65
Q

S/S of CKD (8)

A

Azotemia, acidosis, hyperkalemia, hypertension, anemia, hypocalcemia, fluid overload, elevated phosphate

66
Q

Progression/staging of CKD (5)

A
  1. Kidney damage with normal or increased GFR
  2. Kidney damage with mild decrease in GFR
  3. Moderate decrease in GFR
  4. Severe decrease in GFR
  5. Kidney failure
67
Q

Causes of CKD (3)

A

DM, hypertension, glomerulonephritis

68
Q

Treatment of CKD

A

causes of manifestations, slow/halt disease progression, dialysis, transplant

69
Q

Define azotemia

A

general condition of elevated serum levels of nitrogen-containing substances including urea, creatinine and uric acid, causes may not all be renal, treat underlying condition; does not affect other systems

70
Q

Define uremia

A

clinical syndrome of renal failure with azotemia

71
Q

Define uremic syndrome

A

accumulation of urea that causes symptoms related to renal failure

72
Q

S/S of uremic syndrome (10)

A

Altered CNS function, neuropathy of lower extremities, ulceration of GI tract, N/V, hypertension, pruritis/altered skin coloration, acid-base/fluid and electrolyte imbalances, poor blood clotting, immunosuppression, pericarditis

73
Q

Treatment of uremic syndrome

A

dialysis, possible restricted protein intake

74
Q

Define neurogenic bladder

A

lack of bladder control d/t neurologic condition

75
Q

Distinguish between spastic vs. flaccid neurogenic bladder

A

Spastic: failure to store urine and results from neural lesions above the level of the sacral cord, neurons in the micturition center function reflexively

Flaccid: failure to empty the bladder results from neural disorders affecting the motor neurons in the sacral cord or peripheral nerves

76
Q

Define urinary incontinence

A

uncontrollable and involuntary expulsion of urine that may result from both physiological and psychological factors

77
Q

3 types of urinary incontinence

A

Stress
Urge
Overflow

78
Q

Define Wilms’ Tumor and identify the population at risk

A

Wilms’ tumor: kidney cancer found in children usually between 3 and 5

79
Q

Underlying genetic mutation of Wilm’s tumor, s/s (2), prognosis

A

Genetic mutations: WT1 gene associated with mutations in the CTNNB1 gene encoding a proto-oncogene
S/S: large abdominal mass, hypertension
Prognosis: 90% of patients survive for 5 years

80
Q

Define renal cell carcinoma, risk factors, treatment

A

Originates in the lining of the proximal convoluted tubule, tumor mass may cause ischemia, necrosis or hemorrhage, metastasis may occur at any stage often to: lungs, liver, lymph nodes, bones

Risk factors: heavy smoking, obesity, occupational exposure to substances like asbestos

Treatment: depends on stage - surgery or chemo

81
Q

Cells that may give rise to bladder cancer

A

transitional cell carcinoma (mostly), may include squamous cell carcinoma or adenocarcinoma

82
Q

S/S of bladder cancer (3), risk factors (3), prognosis

A

S/S: hematuria, frequent/painful urination, back/pelvic pain

Risk factors: smoking, radiation, chemical exposure

Prognosis: high survival rate - usually diagnosed early, but has high risk of recurrence

Patho (14 decks)

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