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Study decks > Patho - Alterations in Renal Function > Flashcards

Patho - Alterations in Renal Function Flashcards

1
Q

what is renal agenesis?

A

-Failure of 1 or both kidneys to develop before birth
-Rare; associated with other congenital abnormalities.
-Total bilateral agenesis (Potter Syndrome) incompatible with life; found in stillborn infants.
-Unilateral results in compensatory hypertrophy of functional kidney.
-Single normal kidney is sufficient for renal function.

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2
Q

what is polycystic kidney disease?

A

-Congenital, genetic disorder
-growth of cysts that can expand & disrupt urine formation & flow; localized to one or both kidneys.
-Multiple dilations of collecting ducts, appearing as fluid filled cysts.
-Can lead to renal failure, requiring dialysis or transplant
-ARPKD dx ́d in infants & children—Rare anomaly
-ADPKD dx ́d in adults-more common

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3
Q

pathogenesis of polycystic kidney disease (autosomal recessive forms)

A

-Evident at birth
-Kidneys enlarged
-Respiratory distress or palpable kidneys on PE
-Severe systemic HTN
-Liver problems
-Diagnosis: inheritance pattern

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4
Q

pathogenesis of polycystic kidney disease (autosomal dominant forms)

A

-most common
-Symptoms are later in life
-Normal functioning kidney tissue slowly reduced
-Many round cysts of varying sizes
-Other organs can develop cysts, especially liver

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5
Q

polycystic kidney disease CM

A

-Decreased ability to concentrate urine
-HTN
-Pain: most common
-multiple cystic liver involvement

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6
Q

polycystic kidney disease diagnosis

A

genetic hx & ultrasonography

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7
Q

polycystic kidney disease treatment

A

primarily supportive, controlling BP & managing associated pathologies
End-stage renal disease (ESRD): dialysis initiated

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8
Q

what is benign renal neoplasm? what is the diagnosis? treatment?

A

-Non-metastasizing growths
-Symptoms depend on size; may have no symptoms until large enough to form palpable abdominal mass, hematuria, & flank pain

Diagnosis: renal ultrasound and/or CT scan

Tx: nephrectomy (treatment of choice); laparoscopic and tissue-sparing procedures also being used

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9
Q

what is renal cell carcinoma? CM? treatment?

A

Kidney cancer that originates in the cells of the kidney tubules
Often familial pattern; risk factors (smoking,obesity,HTN)

Clinical Manifestations: none until advanced
-CVA tenderness, hematuria, palpable mass

Tx: nephrectomy
-Metastases often resistant to radiation, immunotherapy, and chemotherapy

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10
Q

what is nephroblastoma? CM? treatment?

A

Most common kidney CA in children

Clinical manifestations: Palpable abd. mass; may also have abd. pain, HTN, and/or hematuria

Treatment: nephrectomy, radiation therapy, and chemotherapy

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11
Q

what is acute pyelonephritis?

A

Infection where bacteria moves from bladder to kidneys, infects renal pelvis/parenchyma usually from ascending UTI
-Major risk factor: pregnancy

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12
Q

acute pyelonephritis CM

A

CVAT with fever, N/V, chills, anorexia, fever-induced dehydration
Urosepsis: organisms in bloodstream originating from UTI

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13
Q

acute pyelonephritis diagnosis and treatment?

A

DX: WBC casts in urine indicate upper UTI

TX: prompt antimicrobial tx to avoid decreased renal function

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14
Q

what is chronic pyelonephritis?

A

-Long-term inflammation of the kidneys usually resulting from recurrent or persistent kidney infections
-Can result in chronic kidney disease
-Associated with reflux or obstruction leading to persistent urine stasis
-Chronic inflammation causes scarring & loss of functional nephrons

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15
Q

chronic pyelonephritis CM

A

Abd./flank pain, fever, malaise, anorexia

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16
Q

chronic pyelonephritis diagnosis and treatment?

A

DX: renal imaging

Tx: correct underlying processes & extend abx tx

17
Q

what is renal calculi (nephrolithiasis)

A

-Masses of crystalized minerals normally excreted in urine.
-Most composed of Ca+ crystals
-Develop & cause obstruction at any point in urinary system.
-Stationary stones usually asymptomatic; stone migration causes intense renal colic pain abrupt in onset & may radiate; N/V, diaphoresis, hematuria
-Often form in urinary tract d/t solute saturation, low urine volume & abnormal urine pH. (Dehydration favors stone formation)
-High-protein diet predisposes to stone formation in susceptible pts
-Pain d/t distention of ureter, renal pelvis, or renal capsule.
-Most pass spontaneously, but tend to recur

18
Q

renal calculi (nephrolithiasis) diagnosis and treatment?

A

Diagnosis: CT scan

TX: fluids, lithotripsy, ureteral stenting, ureteroscopy
-Pain rx needed

19
Q

what are the major complications of renal calculi (nephrolithiasis)?

A

-Hydronephrosis (dilation of renal pelvis) & permanent renal damage d/t complete obstruction of ureter, results in backup of urine & buildup of pressure.
-Infection or abscess formation behind partially or completely obstructing stone, which can rapidly destroy the involved kidney.
-Renal damage subsequent to repeated kidney stones.
-HTN results from increased renin production by obstructed kidney.

20
Q

what are glomerular abnormalities?

A

-Damage mediated by immune processes.
-Results from alterations in structure & function of glomerular capillary circulation.
-Attraction of immune cells to area of inflammation results in degradation of the basement membrane.

21
Q

glomerular abnormalities etiology

A

Autoimmune, drug exposure, vascular or systemic disease. Acute post streptococcal glomerulonephritis is most common form.

22
Q

glomerulonephritis CM (children, adults)

A

Children: abruptly develop malaise, fever, nausea, oliguria, & hematuria (smoky or cocoa-colored urine) 1-2 wks after recovery from sore throat, red cell casts in the urine, mild proteinuria, periorbital edema & mild to moderate HTN. 95% pts with eventual total recovery
Adults: onset more likely atypical with sudden appearance of HTN or edema, frequently elevated BUN. Approx. 60% recover promptly.

23
Q

glomerulonephritis treatment?

A

-Steroids
-Plasmapheresis
-dietary and fluid management
-Management of systemic and renal hypertension

24
Q

what is nephrotic syndrome?

A

-Collection of symptoms caused by glomerular disease.
-Characterized by increase in capillary wall permeability to serum proteins.
-Major loss of proteins in urine.
-Leads to hypoalbuminemia & edema d/t decreased colloid osmotic pressure.
-Tx: manage underlying process.
-Urinary loss of 3 to 3.5 g of protein per day.

25
Q

what is acute kidney injury?

A

-Broad range of kidney diseases from minor changes in renal function to complete failure requiring renal replacement tx
-Abrupt reduction in renal function causes accumulation of waste materials in blood.
-Renal function monitored by serum CR & calculated GFR
-Retention of metabolic wastes (azotemia/uremia); monitored by BUN,
widespread systemic effects (uremic syndrome)
-Pt. presents with rapidly rising BUN & CR

26
Q

acute kidney injury etiology

A

-Aging
-comorbidities
-insults to kidney

27
Q

Acute Kidney Injury-Prerenal etiology

A

Conditions that decrease perfusion to kidney
-Hypovolemia, HTN, heart failure
-Renal artery obstruction
-Fever, vomiting, diarrhea
-Burns
-Overuse of diuretics
-Edema, ascites
-Drugs: ACE inhibitors, angiotensin II blockers, NSAIDs

28
Q

what is acute tubular necrosis?

A

-Destruction of tubular cells & loss of renal function.
-Most common cause of ARF
-Rapid decrease in function & urine flow within 24hrs to <400 mL/day.
-Reversible renal lesion arises with inadequate blood flow, marked hypotension & shock

29
Q

Acute Tubular Necrosis etiology

A

-Ischemia, d/t decreased or interrupted blood flow
-Acute tubulointerstitial nephritis, commonly d/t hypersensitivity rxn to drugs
-Disseminated intravascular coagulation (DIC)
-Urinary obstruction; tumors, BPH, or blood clots

30
Q

Acute Tubular Necrosis CM

A

d/t loss of ability to excrete H20, Na+ & waste
-Early; Fatigue & malaise
-Severe: dyspnea, orthopnea, rales, prominent S3 & peripheral edema. Altered LOC reflects toxic effect of uremia on brain & elevated serum lvls of nitrogenous wastes

31
Q

Chronic Renal Failure dx

A

Dx-Elevated BUN, serum CR & GFR <60 ml/minute
-Loss of nephron function over mos to yrs with inability of kidneys to produce enough urine.
-Defined as decreased kidney function or kidney damage of 3 mos duration based on blood tests, urinalysis & imaging studies

32
Q

Chronic Renal Failure etiology

A

-glomerulonephritis
-diabetic nephropathy—most common
-HTN
-pyelonephritis (UTI)
-polycystic kidney disease
-nephrotoxic exposure
-obstructive nephropathy
-infection

33
Q

chronic renal failure pathogenesis?

A

-Chronic injury results in gradual & irreversible loss of nephrons.
-Greater functional burden by fewer nephrons
-Causes fibrosis & scarring (glomerular sclerosis).
-Progresses to uremia: group of S/S occurring when residual renal function inadequate.
-Functional capacity lost & renal mass is reduced.
-Progressive deterioration of glomerular filtration.

34
Q

chronic renal failure CM

A

-Early Stage—symptom free and BUN & CR
-Second Stage—slight rise in BUN and CR, oliguria.
-Third Stage—sharp increase in BUN and CR, oliguria, uremia, multisystem effects.
-Fourth Stage—dialysis
-Fifth Stage—transplant

35
Q

what are the complications of chronic kidney disease?

A

-HTN & CVD d/t hypervolemia, escalated atherosclerotic process, increased RAAS and SNS activity.
-Uremic syndrome: d/t retention of metabolic wastes.
-Metabolic acidosis: d/t retention of acidic waste products; kidneys lose
ability to secrete H+ ions and bicarbonate.
-Electrolyte imbalances- Retained K+, Phos., Mg+
-Bone & mineral disorders Elevated Phos. & PTH causes altered bone/mineral metabolism; unable to reabsorb Ca+
-Malnutrition-Decreased intake d/t uremic syndrome, depression, dietary limitations, changes in taste, protein-energy wasting; negative Ntg balance
-Anemia-Lack of erythropoietin; uremia shortens RBCs life; combination of worsening CKD, anemia, & heart failure Pain-Many reasons; disease itself, treatment, comorbidities
-Depression-Co-morbid conditions; disease itself; disruption of social interactions and relationships

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