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Patho > Week 9: Renal > Flashcards

Week 9: Renal Flashcards

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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
What are two possible causes of chronic tubulointerstitial disease
Kidney infection (pyelonephritis), acute tubular necrosis
26
Define pyelonephritis
infection of kidney tissue and pelvis
27
What is acute pyelonephritis? S/S (5) Complications (3)
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
28
What is chronic pyelonephritis?
Progressive disease characterized by scarring and deformation of renal calyces (drain kidney of urine and pass it)
29
Risk factors of chronic pyelonephritis (4)
Increased risk with obstructive uropathy, glomerulonephritis, polycystic kidney disease and renal calculi
30
Complication of chronic pyelonephritis
Abscess formation around the kidney can occur
31
Possible causes of chronic pyelonephritis (3)
May be due to kidney stones, neurogenic or congenital such as strictures
32
What is acute tubular necrosis the common cause of (2)?
acute kidney injury, acute kidney failure
33
What changes in acute tubular necrosis?
elevations in BUN and creatinine, decline in urine output
34
Types of acute tubular necrosis
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
Risks for acute tubular necrosis (4)
Blood transfusion reactions Injury or trauma to the muscles (rhabdomyolysis) Hypotension or shock Recent surgery or exposure to nephrotoxic substances
36
Phases of acute tubular necrosis, include how long they last
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
Which stage of acute tubular necrosis do fatalities commonly occur in
Maintenance phase
38
What is the goal of treatment for acute tubular necrosis?
treatment is aggressive and usually requires dialysis to maintain kidney function, reduce damage and recover functional tissues
39
Define polycystic kidney disease
cystic genetic disorder of the kidneys
40
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?
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
Characteristics of polycystic kidney disease (3)
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
What are s/s of polycystic kidney disease (5)?
HTN, increased abdominal size, hematuria, flank pain, renal calculi
43
How does adult autosomal dominant polycystic kidney disease (ADPKD) progress? What is the prevalence in end stage renal disease patients?
Insidious onset - does not usually present until 30-50 years, renal deterioration is gradual 10% of ESRD patients are affected by ADPKD
44
What is the mortality rate of autosomal recessive polycystic kidney disease (ARPKD), and what population does it affect?
Mortality rates: 30% of neonates | Infants
45
Secondary effects of polycystic kidney disease
Damage to and possible formation of cysts in the liver and pancreas, rarely the heart and brain
46
Define obstructive uropathy
obstruction of urine flow as it exits from the kidney toward the bladder
47
What are causes of obstructive uropathy? (3)
Renal calculi Congenital disorders of ureters - strictures or tumors infection
48
What are renal calculi?
form when substances that normally dissolve in urine precipitate, most common in renal pelvis, calyces of the kidney
49
Which population are renal calculi most common in, and which population are they the most rare in?
Common: Men Rare: Children
50
What are the factors that can lead to renal calculi? (7)
change in pH, dehydration, gout, immobilization, infection, obstruction, family history
51
What causes calcium stones, prevalence and treatment
Cause: excess calcium Prevalence: 80% of renal calculi Tx: dietary restriction of foods containing oxalate
52
What causes struvite stones, prevalence and treatment
Cause: urea-splitting UTI Prevalence: 10-15% of renal calculi Tx: treat underlying UTI
53
What causes uric acid stones, prevalence and treatment
Cause: gout Prevalence: 5-10% of renal calculi Tx: dietary restriction of foods containing purine
54
What causes cystine stones?
rare inherited disorder of cystine metabolism
55
What is ADH's normal role and what is it's feedback loop?
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
Define SIADH
characterized by high than normal levels of ADH, results in fluid overload or dilutional hyponatremia
57
Causes of SIADH (5)
Excess ADH released from posterior pituitary Ectopic source releases ADH (lung cancer cells) Infections Head injury Drugs
58
Consequences of SIADH (4)
water retention occurs, BV increases, extracellular fluid volume increases; fluid overload/dilutional hyponatremia
59
Sx (6) and Tx (3) of SIADH
Sx: headaches, nausea, vomiting, confusion, convulsions, coma Treatment: water restriction, demeclocycline, management of underlying cause
60
Define diabetes insipidus
lower than normal levels of ADH
61
Define prerenal disease, causes, reversibility, s/s (2)
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
Define intrarenal disease, causes (4), treatment
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
Define postrenal disease, causes (4)
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
Characteristics of chronic kidney disease (4)
○ 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
S/S of CKD (8)
Azotemia, acidosis, hyperkalemia, hypertension, anemia, hypocalcemia, fluid overload, elevated phosphate
66
Progression/staging of CKD (5)
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
Causes of CKD (3)
DM, hypertension, glomerulonephritis
68
Treatment of CKD
causes of manifestations, slow/halt disease progression, dialysis, transplant
69
Define azotemia
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
Define uremia
clinical syndrome of renal failure with azotemia
71
Define uremic syndrome
accumulation of urea that causes symptoms related to renal failure
72
S/S of uremic syndrome (10)
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
Treatment of uremic syndrome
dialysis, possible restricted protein intake
74
Define neurogenic bladder
lack of bladder control d/t neurologic condition
75
Distinguish between spastic vs. flaccid neurogenic bladder
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
Define urinary incontinence
uncontrollable and involuntary expulsion of urine that may result from both physiological and psychological factors
77
3 types of urinary incontinence
Stress Urge Overflow
78
Define Wilms’ Tumor and identify the population at risk
Wilms' tumor: kidney cancer found in children usually between 3 and 5
79
Underlying genetic mutation of Wilm's tumor, s/s (2), prognosis
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
Define renal cell carcinoma, risk factors, treatment
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
Cells that may give rise to bladder cancer
transitional cell carcinoma (mostly), may include squamous cell carcinoma or adenocarcinoma
82
S/S of bladder cancer (3), risk factors (3), prognosis
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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