Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HS 401 - SU 16 @ OU > Exam 4 - Chapter 16 > Flashcards

Exam 4 - Chapter 16 Flashcards

1
Q

Diagnostic Testing

A

BUN: Blood Urea Nitrogen
Creatinine levels in blood/urine
GFR: Glomerular filtration rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Polyuria

A

Increased amount of urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Oliguria

A

Decreased daily output of urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Anuria

A

No urine produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Proteinuria

A

Increased protein in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Glucosuria

A

Increased glucose in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hematuria

A

Blood in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pyuria

A

Pus in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Dysuria

A

Painful and burning urination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Developmental Disorders of the Kidney

A

Renal Agenesis (not formed): Bilateral (Potter syndrome: deadly) or unilateral (Unilateral agenesis: leads to hypertrophy of the existing kidney and hyper filtration increases risk of renal failure later in life)
Horseshoe Kidney: fusion of kidneys at the lower pole
Multi-cystic Renal Dysplasia: Usually unilateral. Cysts are
embedded in the connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Adult Polycystic Kidney Disease (APKD)

A

Renal parenchyma is replaced with multiple, large cysts. Results in renal failure in adults

Causes: Autosomal dominant. 90% from mutation of APKD1 gene
Symptoms: Hypertension (due to increased renin), hematuria, palpable renal masses, worsening renal failure, Berry aneurysms of the cerebral circulation, hepatic cysts, mitral valve prolapse
Treatment: Can’t prevent renal failure, but HTN treatment with ACE inhibitors may slow progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Infantile Polycystic Kidney Disease (IPKD)

A

Closed, small cysts that are not in continuity with the collecting system. Very rare, results in renal failure and death in infants

Causes: Autosomal recessive
Symptoms: CT scan shows multiple cysts
Treatment: None

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Nephrotic Syndrome

A

Massive proteinuria is generally characterized by excretion of more than 4 grams of protein per day

Causes: Membranous Nephropathy (immune molecules form harmful deposits in glomeruli)
Pathology: Unlike disorders with greater disruption of glomerular structure, proteinuria in the nephrotic syndrome is unaccompanied by increased urinary red cells or white cells
Symptoms: Hypoalbuminemia (low alubumin) results from proteinuria and is often marked by a serum concentration of less than 3 g/100 mL, edema results from decreased plasma colloid oncotic pressure
Treatment: Treating underlying causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Membranous Nephropathy

A

Immune complexes deposit in glomeruli

Causes: Idiopathic, autoimmune, lupus, infections, drugs
Pathology: IgG deposits in subepithelial locations, spike-and-dome appearance (basically crevices) best seen with silver stain, GBM thickeningType I (subendothelial deposits): Associated with HBV and HCV. Type II (dense deposit disease): Associated with overactivation of complement system
Symptoms: Nephrotic syndrome, edema, proteinuria, azotemia, hematuria, renal vein thrombosis
Treatment: Spontaneous remission, ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Berger’s Disease (IgA Nephropathy)

A

Most common nephropathy in the world. IgA deposits in mesangium of glomeruli

Causes: Idiopathic, bacterial/viral infections. NOT autoimmune
Pathology: Mesangial deposits of IgA, increased serum IgA
Symptoms: Hematuria 1-2 days after infection, proteinuria, hypertension, fatigue
Treatment: ACE inihibitors, steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Goodpasture Syndrome

A

Autoimmune disease

Causes: Antiglomerular basement membrane (anti-GBM).
Pathology: IgG antibodies attack alveolar and GBM
Symptoms: Pulmonary hemorrhage and glomerulonephritis
Treatment: Immunosuppressive drugs, corticosteroids

17
Q

Rapidly Progressive (Crescentic) Glomerulonephritis (RPGN)

A

Severe and progressive glomerular injury

Causes: Idiopathic, Goodpasture syndrome, Lupus, Berger’s Disease, Wegener granulomatosis
Pathology: Crescent-moon shape between Bowman’s capsule and glomerular tuft
Symptoms: NePHRITic syndrome, hematuria, hypertension, azotemia, and symptoms of the causes
Treatment: Diuretics, ACE inhibitors, immunosuppressive drugs, steroids

18
Q

Poststreptococcal Glomerulonephritis (Acute Proliferative Glomerulonephritis)

A

Prototype of nephritic syndrome. Immune complex disease with the antigen of streptococcal origin

Causes: Nephritogenic strains of group A
β-hemolytic streptococci. Unlike rheumatic fever, which chiefly follows streptococcal tonsillitis, it can also occur after skin infections
Pathology: Urinary RBCs, decreased serum C3, azotemia, elevated ASO antibody titer
Symptoms: Hematuria, oliguria, hypertension, nephritic syndrome, and periorbital edema
Treatment: Spontaneous recovery. Complete recovery in almost all children and many adults follows. A very small minority develops rapidly progressive glomerulonephritis

19
Q

Alport Syndrome

A

Hereditary nephritis associated with nerve deafness and ocular disorders, such as lens dislocation and cataracts

Causes: Genetic (usually X-linked dominant) results in mutation in the gene for the α5 chain of type IV collagen
Pathology: Thinning and splitting of GBM
Symptoms: Nephritic syndrome, often progressing to end-stage renal disease by 30 years of age, hematuria, erythrocyte cysts, nerve deafness, cataracts, ectopia lentis, corneal dystrophy
Treatment: ACE inhibitors, renal transplant in severe cases

20
Q

Focal Segmental Glomerulosclerosis

A

Sclerosis of glomeruli that involves some but not all glomeruli and only a part of those some. Clinically similar to minimal change disease, although it occurs in both children and older patients. More common in African Americans

Causes: Idiopathic, heroin use, morbid obesity, reflux nephropathy, HIV infection, untreated minimal change disease
Pathology: IgM and C3 seen in secrotic lesions, hyalinosis, sclerosis of glomeruli with focal and segmental distribution
Symptoms: Nephrotic syndrome, edema, proteinuria, hematuria
Treatment: Poor prognosis to steroids and resulting in chronic renal failure. Corticosteroids, cyclosporine, ACE inihibitors

21
Q

Diabetic Nephropathy

A 
Nodular and diffuse thickening of glomerular
basement membranes (GBM)

Pathology: Electron microscopy demonstrates a striking increase in thickness of the glomerular basement membrane. Thickening of vascular basement membranes
observable by electron microscopy is one of the earliest morphologic changes in diabetes mellitus.
Symptoms: An increase in mesangial matrix results in two characteristic morphologic patterns: a) Diffuse glomerulosclerosis is marked by a diffusely distributed increase in mesangial matrix, b) Nodular glomerulosclerosis is marked by nodular accumulations of mesangial matrix material (Kimmelstiel-Wilson nodules)

22
Q

Urinary Stones

A

Calcium stones (75%): Calcium phosphate or calcium oxalate stones - Increase of Ca concentration

Struvite stones (15%): Staghorn calculi are magnesium phosphate stones that form in alkaline urine, which is commonly found in patients with persistent UTIs

Uric acid stones (5%): Found in gout

Cystine stones (1%): Occur in patients with cystinosis, an inborn error of metabolism

23
Q

Urolithiasis (Kidney Stones)

A

Pathology: Increased concentration of salts in urine. Gout will increase the uric acid production due to defective purine metabolism. Increase of Ca ions due to hyperparathyroidism
Urinary tract infection: a) Decrease solubility of salts. b) Bacteria (UTI) are responsible for crystalizing the salts.
Symptoms: High intensity of pain in the back radiating to the right shoulder and groin, hematuria
Treatment: Surgery/wave therapy, drugs which will pass the stone

24
Q

Urinary Tract Infection (Cystitis)

A

Bacterial infection in the bladder. Common in young sexually active women and in older men due to BPH

Causes: Most frequently Escherichia coli (normal flora). The most common pathogen in young, sexually active women is Staphylococcus saprophyticus. Klebsiella pneumoniae & Proteus mirabilis (alkaline urine with ammonia scent). BPH (males). Catheter that may carry bacteria. Injury to mucosa by kidney stone which disrupts
protective epithelium allowing bacteria to invade deeper tissue
Pathology: Urinalysis - cloudy urine with > 10 WBCs/high power field (hpf). Dipstick - Positive leukocyte esterase (due to pyuria) and nitrites (bacteria convert nitrates to nitrites). Culture - greater than 100,000 colony forming units (gold standard)
Symptoms: Frequent urination, dysuria, pyuria, hematuria, bacteriuria. No urinary white cell casts

25
Q

Urinary Tract Infection (Pyelonephritis)

A

Bacterial infection in the kidney. Can be acute or chronic. More frequent in women, especially during pregnancy

Causes: Hematogenous bacterial dissemination to the kidney or by external entry of organisms via urethra into the bladder and then spread upward from the bladder into the ureters (vesicoureteral reflux) and through the ureters to the kidney (ascending infection)
Pathology: Acute - affects renal cortex with sparing of glomeruli. Chronic - assymetric corticomedullary scarring, thyroidization of kidneys
Symptoms: Acute - fever, flank pain, CVA tenderness, WBC casts, leukocytosis, polyuria, dysuria, nauseau, vomiting, diarrhea. Chronic - renal hypertension, ESRD
Treatment: Acute - antibiotics and fluid. Chronic - renal transplant

26
Q

Acute Renal Failure (Prerenal)

A

Kidneys can’t filter waste from the blood

Causes: Decreased effective arterial volume (decreased cardiac output, systemic hypovolemia (as in massive burns), or peripheral pooling of blood due to marked vasodilation (as in gram-negative sepsis)), renal vasoconstriction.
Pathology: Renal hypoperfusion leads to decreased GFR, sodium and water retention, concentrated urine, oliguria. Measurement of urinary sodium is diagnostically significant in addition to oliguria. The BUN:creatinine ratio is characteristically greater than 20 due to a combination of both decreased glomerular filtration and increased tubular reabsorption of urea
Symptoms: Oliguria, azotemia, hyperkalemia, urinary Na+ 500, BUN/Cr > 20
Treatment: Fluid/electrolyte management, reversal of underlying cause

27
Q

Acute Renal Failure (Intrarenal)

A

Kidneys can’t filter waste from the blood

Causes: Acute tubular necrosis, acute interstitial nephritis, glomerulonephritis, thrombotic microangiopathy
Pathology: Patchy tubular necrosis, tubule obstruction, fluid backflow, decrease in GFR
Symptoms: Oliguria, azotemia, hyperkalemia, urine osmolality

28
Q

Acute Renal Failure (Postrenal)

A

Kidneys can’t filter waste in the blood

Causes: Mechanical blockage of urinary flow, BPH, neurogenic bladder, neoplasia
Pathology: Bilateral outflow obstruction, elevated uretal pressure, decreased GFR
Symptoms: Oliguria, azotemia, hyperkalemia, urinary Na+ > 40, BUN/Cr > 20
Treatment: Treatment of obstruction

29
Q

Acute Tubular Necrosis

A

Injury and necrosis of tubular epithelial cells which can lead to acute renal failure (intrarenal azotemia)

Causes: Necrotic cells plug tubules; obstruction decreases GFR, renal ischemia (decreased blood supply from prolonged hypotension or shock), crush injury, nephrotoxic drugs (NSAIDs, lead, chemo, post-operative antiobiotics, ethylene glycol
Pathology: Brown, granular casts are seen in the urine, BUN/Cr

30
Q

Hemodialysis

A

It substitutes for the functions of the kidneys, which removes waste products from the patient’s blood

Waste products from the patient’s blood diffuse across a semipermeable membrane into a solution (the dialysate) on the other side of the membrane

Two Types:
Extracorporeal (more common): Patient’s circulation connected to artificial kidney machine
Peritoneal (less common): Patient’s own peritoneum used as dialyzing membrane

31
Q

Renal Transplantation

A

When kidneys fail, renal transplantation may be attempted
• The kidney is obtained from a close relative or cadaver donor
• The survival of the transplant depends on the similarity of HLA antigens (MHC) between donor and recipient
• Only identical twins will contain identical HLA antigens in their tissues

32
Q

Hypertensive Nephrosclerosis

A

Shrunken and scarred kidneys

Causes: Poorly controlled hypertension
Pathology: Mesangial cell proliferation with shrunken glomerular tuft, sclerosis and hyanilization of afferent arterioles
Symptoms: Nephrotic syndrome, proteinuria, hypertension, hypertensive retinopathy, left ventricular hypertrophy
Treatment: ACE inhibitors, dialysis

33
Q

Wilm’s Tumor

A

Malignant tumor of infancy and childhood (2 to 4 years of age)

Causes: Deletion of WT-1 and WT-2 genes (cancer suppressor genes), familial or bilateral in 10% of cases
Pathology: Composed of immature cells resembling renal blastoma, presence of mesenchymal elements (bone, cartilage, etc.), large well-circumscribed renal mass, microscopic hematuria
Symptoms: Huge nontender palpable flank mass, fever, abdominal pain
Treatment: Good prognosis when surgery is combined with chemotherapy

34
Q

Renal Cell Carcinoma

A

Most common renal malignancy, more common in men, 50-70 years old

Causes: Von Hippel-Lindau disease, deletion on chr 3 and cigarette smoking
Pathology: Secondary polycythemia (results from erythropoietin production), polygonal clear cells (derived from tubular epithelium), invades IVC and spreads hematogenously to lungs, bones, etc.
Symptoms: Classic triad of flank pain, palpable mass, and hematuria. Paraneoplastic syndromes (ectopic EPO, ACTH, prolactin, gonadotropins, and renin) which can cause hypercalcemia
Treatment: Nephrectomy, chemo, radiation

35
Q

Transitional Cell Carcinoma

A

Most common tumor of the urinary collecting system and can occur in renalpelvis, ureter, or bladder. It is often multifocal in origin due to the field effect

Causes: Industrial exposure to benzidine or β-naphthylamine, an aniline dye, cigarette smoking
Symptoms: Hematuria, local extension to surrounding tissues
Treatment: Cyclophosphamide, likely to recur after removal

36
Q

Urinary Bladder Carcinoma

A

Most common cancer of the urinary tract. Most tumors are transitional carcinomas but may be squamous or adenocarcinomas

Causes: Infections, benign tumors, kidney stones,
Pathology: Diagnosis made on urine cytology and cystoscopic biopsy
Symptoms: Hematuria, dysuria, lower abdominal pain
Treatment: Grade I tumors localized to mucosa—98% 5-year survival but tend to recur. Grade III tumors with metastases—15% 5-year survival

HS 401 - SU 16 @ OU (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions