Brainscape's Knowledge GenomeTM

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


See full index

STEP > Urology/Nephrology > Flashcards

Urology/Nephrology Flashcards

1
Q

Name the three types of incontinence?

A
  • Stress, Urge and Overflow

- There is also mixed

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

Stress incontinence

A
  • Outlet incompetence (urethral hyper mobility or intrinsic sphincter deficiency)
  • Also due to weak pelvic floor muscles
  • Leak with increase in intra-abdominal pressure
  • Increased risk with obesity, vaginal delivery, prostate surgery
  • Positive bladder stress test (observed leakage with cough or Vasalva)
  • Treat with pelvic floor muscle strengthening such as Kegel exercises or weight loss
  • Pseudophedrine (alpha-1-agonist) tightens up sphincter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Urgency Incontinence

A
  • Overactive bladder such as detrussor instability or spastic
  • Leads to leak with urge to void immediately
  • Treat with Kegel exercises, or bladder training such as timed voiding, distraction or relaxation techniques.
  • May treat with antimuscarinics such as Oxybutynin
    5,15 and 15mg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Overflow incontinence

A
  • Incomplete emptying (detrusor under activity or outlet obstruction)
  • Leads to leak with overfilling bladder
  • Diabetics and patients with spinal cord injuries due to damaged nerves
  • Increased post void urinary retention on catheterization or ultrasound
  • Treat with catheterization or relieving obstruction such as alpha-blockers for BPH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Vesicourethral Reflux

A
  • Retrograde flow of urine from the bladder to the kidneys
  • May be associated with UTIs, hydronephrosis or renal dysplasia (abnormal kidney development).
  • Increase risks of pyelonephritis, hypertension or progressive renal failure
  • Diagnosed with voiding cystourethrography
  • Treat with prophylactic antibiotics to avoid infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define Hydronephrosis

A
  • Distension of the renal calyces and pelvis with urine as a result of obstruction of the outflow of urine distal to the renal pelvis
  • Can be physiologic or pathologic, acute or chronic, unilateral or bilateral
  • Can be secondary to obstruction or can present without obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define Hydroureter

A
  • Dilation of the ureter
  • Can be physiologic or pathologic, acute or chronic, unilateral or bilateral
  • Can be secondary to obstruction or can be present without obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define obstructive uropathy

A
  • Functional or anatomic obstruction of urinary flow at any level of the urinary tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define obstructive nephropathy

A
  • When the obstruction causes functional or anatomic renal damage
  • Rarely does it occur without the presence of hydronephrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does hydronephrosis and/or hydroureter typically present in children?

A

-Anatomical abnormalities such as posterior urethral valves or stricture and stenosis at the uterovesical or uteropelvic junction

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

How does hydronephrosis and/or hydroureter typically present in adults young and old?

A
  • Calculi in young adults
  • Prostatic hypertrophy or carcinoma, retroperitoneal or pelvic neoplasms and calculi in older adults
  • Common during pregnancy in women, progesterone causes dilation of the pelvises and caliceal system or ureters may be compressed at the pelvic brim
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe testicular torsion and its management

A
  • Seen in young adolescents
  • Present with severe testicular pain, no fever, pyuria, or history of recent mumps.
  • On exam, testis may be swollen, tender, high riding and with a horizontal line, the spermatic cord is not tender.
  • Immediate surgical untwisting and orchipexi, contralateral orchipexi is also indicated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe acute epididymitis

A
  • Can be confused with testicular torsion
  • Seen in sexually active men
  • Starts with severe testicular pain, fever and pyuria
  • Testis are swollen and tender but in normal position
  • Spermatic cord is also very tender
  • Most common causes are E. coli, Chlamydia and Gonorrhea
  • Histology shows neutrophil infiltration
  • Treat with antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What medications are used to treat acute epididymitis based on age group?

A
  • Sexually active males 14 to 35 years of age, ceftriaxone IM 250 mg with 10 days of oral doxycycline 100 mg BID
  • Men who have anal intercourse, ceftriaxone 250 mg IM with 10 days of oral levofloxacin 500 mg QD or ofloxacin 300 mg BID
  • Men older than 35 years, epididymitis is usually caused by enteric bacteria in the ejaculatory ducts caused by reflux of urine secondary to bladder outlet obstruction. In such cases, levofloxacin 500 mg QD or ofloxacin 300 mg BID
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Patient whom is being allowed to pass a ureteral stone spontaneously develops chills, fever spike and flank pain, how do you manage?

A
  • IV antibiotics if not already on
  • Immediate decompression of the urinary tract above the obstruction.
  • Ureteral stent placement or percutaneous nephrostomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define nephrolithiasis and its presentation

A
  • Calculi in the kidneys or the ureters (ureterolithiasis) that cause pain
  • Pain generated by renal colic is caused by dilation, stretching and spasm due to acute uterus obstruction
  • Presents as sudden, severe pain in the flank that radiates inferiorly and anteriorly
  • May present with nausea and vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Characteristic pain of stones obstructing the utero pelvic junction

A
  • Mild to severe deep flank pain without radiation to the groin
  • Irritative voiding symptoms
  • Suprapubic pain, urinary frequency, dysuria, stranguria or bowel symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Characteristic pain of stones within ureter

A
  • Abrupt, severe, colicky pain in the flank and ipsilateral lower abdomen
  • Radiation to testicles or vulvar area
  • Intense nausea with or without vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Characteristic pain of upper ureteral stones

A
  • Radiate to flank or lumbar areas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Characteristic pain of midureteral calculi

A
  • Radiate anteriorly and caudally
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Characteristic pain of distal ureteral stones

A
  • Radiate into groin or testicle (men) or labia majora (women)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Characteristic pain of stones passed into bladder

A
  • Mostly asymptomatic; rarely, positional urinary retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which labs and imaging tests are done to asses and diagnose nephrolithiasis?

A
  • Urinary dipstick
  • Serum creatinine
  • CBC with differential for febrile patients
  • Serum electrolyte for vomiting patients
  • Serum and urinary pH level for type of calculus
  • Microscopic UA
  • Urine culture if infection
  • Non-contrast abdominopelvic CT (image of choice)
  • Renal ultrasound ( to determine presence of renal stone, hydronephrosis or Urethral dilation)
  • Abdominal radiograph (to asses total stone burden, size, shape, composition and location)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Kidney proper develops from what and what structures and what does it include?

A
  • Develops from the metanephros

- All the kidney structures up to the distal convoluted tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What forms from the Ureteric bud?

A

The entire collecting system

  • Collecting ducts
  • Major and minor calyces
  • Papilla
  • Hilum
  • Ureters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What must make contact with the metanephros for the kidney to develop?

A

The ureteric bud

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the mesonephros and what does it give rise to?

A
  • Appears late in the 4th week
  • Functions as the interim kidney for 5-6 weeks
  • Regresses and gives rise to the male genitalia (testis, seminal vesicles, vas deferrals and epididymis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What must happen in order to form the internal half of the internal male genitalia?

A
  • Mullein Inhibiting Factor (MIF) must be secreted from the testes
  • MIF supresses the female internal mullein structures from developing.
  • Embryo requires Y chromosome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Define true hemaphrodite

A
  • Internal genitalia does not match a persons genotype
  • XY Genotype with female internal genitalia
  • Missing MIF to prevent female internal genitalia from forming
  • Deficiency in MIF is most common cause
  • Could be due to Sertoli cell disfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Define pseudohermaphroditism

A
  • External genitalia does not match persons genotype
  • Only concentrate on external exam
  • Females with excess androgens is number 1 cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the paramesonephros and what does it give rise to?

A
  • The mullerian ducts
  • Give rise to female genitalia
  • Ovaries, fallopian tubes, uterus and upper vagina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the two ways females can be developed?

A
  • By design XX

- By default XY missing MIF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What does the urogenital sinus give rise to?

A

Males: Prostate, prostatic urethra and bulbourethral glands (Cowpers glands)
Females: Lower vagina and labia minor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does the urogenital tubercle give rise to?

A

Males: Penis
Females: Clitoris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does the labia-scrotal swellings five rise to?

A

Males: Scrotum
Females: Labia majora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the 2 types of congenital adrenal hyperplasia?

A

21- Hydroxylase deficiency

11Beta- Hydroxylase deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

21- Hydroxylase deficiency

A

Missing 21-hydroxylase enzyme
Lack aldosterone
- Low sodium, high potassium and hypovolemia
Lack cortisol
- Hypoglycemia
Excess androgens
- Ambiguous genitalia in females
Increases ACTH
- No feedback inhibition from Aldosterone or Cortisol
- Pro-opio-melano-cortin is produced causing melanocyte production and hyper pigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

11Beta-Hydroxylase deficiency

A
  • Missing 11-hydroxylase
    causes build up of 11-deoxycorticosterone
  • Weak mineralocorticoid that acts like aldosterone
  • High sodium, low potassium and hypertension
  • Leads to excess androgen production, ambiguous genitalia and hyper pigmentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Leydig cells

A
  • Adjacent to the seminaphorus tubules of the testes
  • Pre-leydig cells produce testosterone for masculinization of inner genitalia in fetus weeks 8-20
  • Leydig cells are then not activated until puberty
  • Produce testosterone when stimulated by LH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Sertoli cells

A
  • Located in the seminaphorus tubules
  • Stimulated by FSH
  • Secrete MIF in fetal life
  • Secretes inhibin to counteract FSH
  • Secrete androgen binding protein increasing testosterone concentration in the seminaphorus tubules stimulating spermatogenesis
  • Secrete estradiol aromatase converts testosterone to 17-beta estradiol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Medications for urge incontinence

A

Oxybutynin 2.5-5 mg bid-tif

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Effects of Hypercalcemia on the kidneys?

A
  • Polyuria and Polydipsia because of induction of nephrogenic diabetes insipidus
  • Calcium also precipitates in the kidney resulting in kidney stones and nephrolithiasis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Carbonic anhydrase inhibitors work on the?

A

Proximal convoluted tubule

Ex. Acetazolamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Osmotic diuretics work on the?

A

Descending limb of the loop of Henle and on the proximal convoluted tubule
Ex. Mannitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Loop diuretics work on the?

A

Thick ascending limb of the loop of Henle

Ex Furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Thiazide diuretics work on the?

A

Distal convoluted tubule

Ex. Hydrochlorothiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Potassium sparing diuretics work on the?

A

Collecting duct

Ex. Amiloride and Spironolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Spironolactone

A
  • Inhibits the effects of aldosterone and reduces secretion of K+ and H+ by the collecting tubule
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Poststreptococcal Glomerulonephritis

A
  • Nonsuppurative complication of pharyngeal or skin infections with nephrotic strains of Group A Strep (S. Progenes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Presentation of Poststreptococcal Glomerulonephritis

A
  • Presents in children with gross hematuria (cola/tea colored urine), periorbital edema and hypertension.
  • Urine studies reveal RBCs, protein and RBC casts
  • Serum studies show elevated creatinine (renal insufficiency), streptococcal antibodies (from recent infection) and decreased C3 (glomerular complement deposition)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Hyperacute transplant rejection

A

Onset time
- Occurs minutes to hours
Etiology
- Do to preformed antibodies against graft in recipients circulation
Morphology
- Gross mottling and cyanosis
- Arterial fibrinoid necrosis and capillary thrombotic occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Acute transplant rejection

A

Onset time
- Usually < 6 months
Etiology
- Exposure to donor antigen induces humoral/cellular activation of naive immune cells
Morphology
- Humoral: C4d deposition, neutrophilic infiltrate, necrotizing vasculitis
- Cellular: Lymphocytic interstitial infiltrate and endotheliitis
Symptoms
- Usually asymptomatic
- Can experience fever, chills, malaise and arthralgia
Labs
- Increased serum creatinine, hypertension, and reduced uric output
Treatment
- Mycophenolate and tacrolimus are immunosuppressants that reduce risk of acute rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Chronic transplant rejection

A

Onset time
- Months to years
Etiology
- Chronic low grade immune response refractory to immunosuppressants
Morphology
- Vascular wall thickening and luminal narrowing
- Interstitial fibrosis and parenchyma atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Effects of ACE inhibitors on the kidney?

A
  • Reduce the amount of Angiotensin II, therefore they prevent it from constricting the efferent arteriole and cause efferent vasodilation reducing GFR.
  • Lowers the intraglomerular pressure and prevent the kidney from maintaining GFR thereby may increase creatinine in and cause acute renal failure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Autosomal Dominant Polycystic Kidney Disease

A
  • Manifests in patients 40-50 years old
  • Presents as enlarged kidneys, hypertension and renal failure
  • In newborns kidneys are of normal size and cysts are too small to be detected on ultrasound ultrasonography
  • As cyst enlarge they compress the renal parenchyma and cause symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Which nerve may be injured in prostectomy and what may it cause?

A
  • The prostatic plexus lying within the fascia of the prostate which innervates the corpus cavernosa of the penis and facilitates erection.
  • Injury may cause erectile dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the cremasteric reflex, what nerve mediates it and when may it be injured?

A
  • Elicited by light stroking of the medial upper thigh.
  • Causes contraction of the cremaster muscle pulling up the ipsilateral testis.
  • Mediated by the genitofemoral nerve which originates from L1-L2 in the spine
  • Injury may occur with injury to L1-L2 or in testicular torsion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Cystinuria

A
  • Autosomal recessive
  • Caused by defective transportation of cystine, ornithine, lysine and arginine across the intestinal and renal tubular epithelium
  • Recurrent nephrolithiasis is the only clinical manifestation
  • Leads to high urinary cystine concentration, resulting in the formation of cystine kidney stones
  • Leads to aminoaciduria due to elevated cysteine levels.
  • Cyanide nitroprusside test used to diagnose (red-purple discoloration is positive test)
  • Flat yellow hexagonal stones may be seen
  • Treat with hydration and urinary alkalinization with acetazolamide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Increased bladder capacity
Increased sphincter pressure
Decreased detrusor muscle activity

A

Overflow incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Decreased bladder capacity
Normal sphincter pressure
Increased detrusor muscle activity

A

Urge incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Normal bladder capacity
Decreased sphincter pressure
Normal detrusor muscle activity

A

Stress incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Hypospadia

A
  • Opening in the base of the ventral penis
  • Penis fails to fuse properly
  • Usually near the anus, may lead to UTIs
  • Most common congenital genital-urinary abnormality
  • Treat surgically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Phimosis

A
  • Scarred foreskin adheres to the head of the penis
  • Occurs when foreskin is not retracted and cleaned properly
  • Treat with circumcision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Paraphimosis

A
  • Scarred foreskin at the base of the penis

- Treat with circumcision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Ballantis

A
  • Infection of the head of the penis (cellulitis)
  • Caused by S. aureus
  • Occurs with zipper injuries
  • More common in uncircumcised men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Urethritis

A
  • Inflammation of the urethra
  • Causes dysuria
  • MCC Chlamydia and Gonorrhea
  • If gonorrhea + then you treat for both with 250 ceftriaxone and 1 gm azithromycin
  • If chlamydia only, treat with 1 gm azythromycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Cystitis

A
  • Bladder infection
  • Urgency, frequency and dysuria
  • Most commonly caused by E. coli
  • Treat with Nitrofurantoin, TMP-SMX or Fosfomycin IM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Pyelonephritis

A
  • Ascending infection to the kidney
  • Urinary urgency, frequency, dysuria and flank pain
  • Can spread into blood and cause sepsis
  • WBC casts on urine microscopy, indicates nephritis or inflammation of the nephron
  • MCC by bacteria that are nitrite + are E. Coli, Proteus and Klebsiella
  • MCC by cater that are nitrite - is Enterococcus
  • MCC virus is adenovirus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Mechanism of action of Thiazide diuretics?

A

Inhibit Na-Cl cotransporter in the early distal convoluted tubule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Electrolyte abnormalities of Thiazide Diuretics?

A
  • Hyponatremia
  • Hypokalemia
  • Metabolic alkalosis
  • Hypercalcemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Clinical indications for Thiazide Diuretics?

A
  • Hypertension

- Calcium nephrolithiasis prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Name 4 Thiazide Diuretics

A
  • Hydrochlorothiazide
  • Chlorthalidone
  • Indapamide
  • Metolazone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Mechanism of action of Loop Diuretics?

A

Inhibit the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Electrolyte abnormalities of loop Diuretics?

A
  • Hypokalemia
  • Metabolic alkalosis
  • Hypocalcemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Clinical indications for Loop Diuretics?

A
  • Volume overload states such as congestive heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Name 4 Loop diuretics

A
  • Furosemide
  • Torsemide
  • Bumetanide
  • Ethacrynic acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Mechanism of action of carbonic anhydrase inhibitors?

A

Inhibits carbonic anhydrase enzyme in the proximal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Electrolyte abnormalities caused by Carbonic Anhydrase inhibitors?

A
  • Hypokalemia

- Metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Clinical indications for carbonic anhydrase inhibitors?

A
  • Refractory metabolic alkalosis
  • Intracranial hypertension
  • Acute angle-closure glaucoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Name a common carbonic anhydrase inhibitor?

A

Acetazolamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Mechanism of action of Sodium Channel Blockers?

A

Inhibit the apical ENaC channel in the cortical collecting duct

82
Q

Electrolyte abnormalities seen with Sodium Channel Blockers?

A
  • Hyperkalemia

- Metabolic Acidosis

83
Q

Indications for Sodium Channel Blockers?

A
  • Used in synergy with loop and thiazide diuretics to limit potassium loss.
84
Q

Mineralocorticoid receptor antagonists mechanism of actions?

A

Inhibit the apical ENaC channel and basolateral Na-K-ATPase pump in the cortical collecting tubules

85
Q

What are the electrolyte abnormalities caused by mineralocorticoid receptor antagonists?

A
  • Hyperkalemia

- Metabolic acidosis

86
Q

What are the clinical indications for mineralocorticoid receptor antagonists?

A
  • Used in synergy with loop and thiazide diuretics to limit potassium loss
87
Q

Name 2 sodium channel blockers?

A
  • Amiloride

- Triamteren

88
Q

Name a 2 Mineralocorticoid Receptor Antagonists

A
  • Spironolactone

- Eplerenone

89
Q

Patient has recurrent pneumonia, digital clubbing, azoospermia and bilateral absence of the vas deferens, most likely diagnosis?

A

Cystic fibrosis

90
Q

What is the pathogenesis for cystic fibrosis?

A

Due to mutation in the CFTR gene, causes impaired ion transport.

91
Q

Describe the respiratory tract features of patients with cystic fibrosis?

A
  • Chronic sinopulmonary infections
  • Nasal polyps
  • Bronchiectasis
  • Digital clubbing
92
Q

What extrapulmonary features are seen in cystic fibrosis?

A
  • Pancreatic insufficiency
  • Infertility due to absent vas deferens (azoospermia)
  • Failure to thrive
93
Q

How is cystic fibrosis diagnosed?

A
  • Elevated sweat chloride levels
  • Abnormal nasal transepithelial potential difference
  • Genetic testing for CFTR gene mutation
94
Q

Characteristics of acute tubular necrosis on cytology?

A
  • Patchy loss of proximal tubular epithelial cells with tubular dilation (ballooning)
  • Regenerating epithelial cells with hypo chromatic nuclei
  • Epithelial cell vacuolization
95
Q

What effects does angiotensin II have on the kidneys?

A
  • It is a powerful vasoconstrictor that dilates the afferent arteriole and constrict the efferent arteriole in order to maintain GFR
96
Q

What happens if you block ACE in the kidney?

A
  • Does not allow for afferent arteriole dilation and efferent arteriole constriction
  • Instead it causes efferent arteriole dilation, leading to increased renal bloodflow and decreased renal vascular resistance thereby dropping GFR.
97
Q

Horseshoe Kidney

A
  • Congenital abnormality where kidneys fuse sometime during development
  • Kidneys are lower in the abdomen because the inferior mesenteric artery prevents their migration upward
  • Associated with kidney stones, recurrent infections, turner syndrome, trisomy 13, 18 and 21, films tumor and carcinoid tumor
98
Q

Most common side effect with furosemide and why?

A
  • Ototoxicity (Tinnitus, Vertigo, Hearing Impairment or Deafness)
  • Due to inhibition of similar Na/Cl/K symporters in the inner ear
  • Occurs with higher dosages, pre-existing CKD, rapid intravenous administration or when used with other ototoxic agents such as ahminoglycosides, salicylate or cisplatin.
  • Hearing is reversible but may be permanent.
99
Q

What is the most effective strategy for preventing urinary tract infections after surgery?

A
  • Avoiding unnecessary catheterization
  • Using sterile technique when inserting the catheter
  • Removing the catheter as soon as possible .
100
Q

Minimal Change Disease

A
  • Most common cause of nephrotic syndrome in ages 2-6
  • Occurs after a recent upper respiratory tract infection, immunizations or atopic disorders due to immune dysregulation
  • Leads to glomerular permeability factor, a cytokine that directly damages podocytes causing foot process effacement and fusion.
  • It decreases the anionic properties of the glomerular basement membrane and a loss of negative charge leading to a loss of albumin in urine
  • Treat with corticosteroids
101
Q

What is the limiting factor for phosphate excretion in patients with CKD?

A
  • A low GFR

- Does not allow phosphate to be excreted leading to hyperphosphatemia

102
Q

Presentation of Metabolic Bone Disease due to Chronic Kidney Disease

A
  • Presents with hyperphosphatemia, secondary hyperparathyroidism and decreased calcitriol levels
  • Patients can be asymptomatic or develop weakness, bone pain and fractures.
103
Q

Pathophysiology behind metabolic bone disease due to Chronic Kidney Disease

A
  • Hyperphosphatemia develops due to decreased GFR
  • It reduces levels of calcium and stimulates osteocytes and osteoclasts to release fibroblast growth factor-23 that decreases proximal tubule phosphate reabsorption.
  • Leads to decreased calcitriol synthesis, leading to decreased calcium and phosphate absorption in the intestines
  • Hypocalcemia is due to elevated levels of phosphate, FGF
  • Hypocalcemia and hyperphosphatemia lead to increased PTH, stimulating osteoclast bone turnover.
  • Osteitis fibrous results from long term hyperparathyroidism leading to weakness, bone pain and fractures
104
Q

What converts 25-Hydroxy Vitamin D3 into 1,25 Hydroxy Vitamin D3?

A
  • 1-alpha-hydroxylase

- Stimulated by parathyroid hormone

105
Q

What are the complications of cryptorchidism?

A
  • Seminiferous tubule and sertoli cells atrophy due to high body temperatures
  • Decreased fertility and increased risk for testicular cancer and testicular torsion
106
Q

What is cryptorchidism and how it it treated?

A
  • Incomplete descent of the testis from the abdomen to the scrotum.
  • Present in 1% of males under 1 year of age
  • Treat with Orchipexi
107
Q

What is orchitis?

A
  • Acute inflammation of the testes secondary to an infection
  • Viral mumps is most common cause
  • Exam shows enlarged, indurated testis with tenderness and erythematous or edematous scrotal skin.
  • Enlarged epididymis or soft boggy prostate with epididymo-orchitis.
  • Lymphoplasmacytic inflammatory infiltrate
108
Q

What are the most common causes of epididymitis in young children and men older than 35?

109
Q

What is the most common cause of epididymitis in sexually active males between 14-35?

A
  • Gonorrhea and Chlamydia
110
Q

What causes BPH?

A

Caused by DHT which binds to androgen receptors in the prostate causing its enlargement.

  • 5-alpha reductase converts testosterone to DHT
  • Castrated males do not develop BPH due to absence of testosterone
  • Enlarged prostate constricts the urethra which restricts flow of urine from the bladder
111
Q

What are the clinical symptoms of BPH?

A
  • Increased urinary frequency
  • Nocturia
  • Difficulty starting and stopping urine
  • Dysuria
  • May lead to dissension and hypertrophy of bladder
  • Hydronephrosis
  • UTIs
  • Labs show increased PSA
112
Q

What is the treatment for BPH?

A
  1. alpha-1-antagonists which cause relaxation of the smooth muscle in the prostate and the lower urethral sphincter
    - Terazosin
    - Tamsulosin (flomax)
  2. 5-alpha reductase inhibitors which reduce the amount of DHT
    - Finasteride
  3. Phosphodiesterase-5 inhibitors
    - Tadalafil (cialis)
    - Sildenafil (viagra)
113
Q

What are the three main cell types in the testes and what do they do?

A
  1. Germ cells / spermatogonia
    - Produce primary spermatocytes
  2. Sertoli cells
    - Produce androgen binding protein that helps develop sperm
  3. Leydig cells
    - Help synthesize testosterone
114
Q

Name the germ line cell tumors in testicular cancer

A
  • Seminoma
  • Embryonal
  • Teratoma
  • Choriocarcinoma
  • Yolk sac tumore
115
Q

Name the non-germ line cell tumors in testicular carcinoma

A
  • Leydig cell tumors
  • Sertoli cell tumors
  • Lymphoma
116
Q

What are the Germ line cell tumor facts

A
  • Make up 95% of all testicular tumors
  • Almost always malignant
  • Age: 15-35
  • Cryptorchidism is a risk factor
  • They do not transilluminate (when light is shined behind the scrotum, it will not shine through)
117
Q

Seminoma

A
  • Most common germ line cell tumor
  • Young men between 15-35
  • Never occurs in children
  • Histology: “Fried egg appearance” nests of large cells with central nuclei
  • Appearance: Homogenus mass
  • Tumor markers: may see elevated ALP and BHCG
  • Presents as painless unilateral mass
118
Q

Yolk sac tumor

A
  • Most common in children under 3 years old males
  • Histology: Schiller duval bodies, resemble primitive glomeruli
  • Tumor marker: Increased AFP
119
Q

What other type of tumor has elevated AFP?

A

Hepatocellular carcinoma (HCC)

120
Q

Choriocarcinoma

A
  • Malignant tumor of placental like tissue
  • Histology: Syncytiotrophoblast and cytotrophoblasts
  • Tumor marker: Beta-hCG
  • Presentation: Testicular mass with gynecomastia or hyperthyroid (Beta-HcG mimics LH, FSH and TSH)
  • May metastasize hematogenously to the lungs described as cannon ball lesions
121
Q

Teratoma

A
  • Tumors containing cell types from all three germ layers (Endoderm, Mesoderm and Ectoderm)
  • Unlike females however, teratomas in adult males are always malignant
  • Histology: Squamous epithelium in the mass or any cell type from all three layers
  • Appearance: Large mass with hair, muscle or neural tissue
  • No tumor markers
122
Q

Embryonal Carcinoma

A
  • Painful unilateral mass
  • Occurs in young men
  • Histology: hemorrhagic mass with necrosis
  • May see elevated Beta-HCG and AFP
  • The necrosis and hemorrhage cause the pain
123
Q

Lydia Cell Tumors

A
  • Androgen and estrogen producing tumors
  • Occur in young men
  • Histology: Reinke crystals (eosinophilic cytoplasmic inclusions)
  • Appearance: Golden brown color
  • No tumor markers
  • In older men may present with gynecomastia, in younger children may present with precocious puberty
124
Q

Sertoli Cell Tumors

A
  • Benign, don’t produce hormones
125
Q

Testicular Lymphoma

A
  • Testicular tumor in men >60

- Usually bilateral and may be NHL that has metastasized

126
Q

Which medication is used to treat acute angle-closure glaucoma, how does it do this and where does it act on the kidney?

A
  • Acetazolamide
  • Acts on the proximal convoluted tubule
  • Blocks carbonic anhydrase and prevents reabsorption of bicarbonate
  • Also acts on carbonic anhydrase in the eye which modulates bicarbonate formation in the aqueous humor, thereby decreasing its formation
127
Q

What does renal biopsy for Poststreptococcal Glomerulonephritis show in for light microscopy, electron microscopy and immunofluorescence?

A
  1. Light Microscopy
    - Glomeruli are enlarged and hyper cellular due to leukocyte infiltration and proliferation of endothelial and mesangial cells
  2. Electron Microscopy
    - Electron dense deposits (humps) on the epithelial side of the basement membrane
  3. Immunofluorescence
    - Coarse granular deposits of IgG and C3 that have lumpy-bumpy appearance
128
Q

Describe the filtration of PAH (Para-aminohippuric acid)

A
  • Primarily secreted in the proximal tubule
  • Only some is freely filtered in the glomerulus
  • It is not reabsorbed in any portion of the nephron
  • Therefore its concentration is lowest in bowman space
129
Q

What are the effects of clamping one renal artery, simulating renal artery stenosis?

A
  • Causes significant renal hypo perfusion
  • Results in decreased GFR in that kidney
  • Activates Renin-Angiotensin-Aldosterone system
  • Modified smooth muscle cells (juxtaglomerular) within the afferent glomerular arterioles release the renin
  • Leads to hyperplasia of these cells and the juxtaglomerular apparatus
130
Q

Which cells make up the juxtaglomerular apparatus?

A

Macula densa
- Sense low levels of sodium and chloride
Juxtaglomerular cells
- Receive signal from macula dense, sense low blood pressure and secrete renin
Extraglomerular mesangial cells
- Help send signal from macula dense to juxtaglomerular cells

131
Q

Where is more than 60% of water reabsorbed by the glomeruli regardless of the patients hydration state?

A

In the proximal tubule

132
Q

What happens in the kidneys during the dehydrated state?

A
  • Plasma osmolarity increases, stimulating osmoreceptors in the anterior hypothalamus
  • Triggers ADH to be released
  • ADH improves water permeability on the collecting ducts
  • Allows production of maximally concentrated urine (Osm of 1200)
  • Reflects kidneys acting properly
  • Without fluid replenishment, will lead to death because kidney still puts out about .5 L of urine per day
133
Q

Uric acid stones

A
  • Appear as yellow/brown, diamond or rhomboid shaped crystals that are radiolucent on x ray
  • Caused by low urinary pH (acidic urine) and low urine volume with high uric acid concentration which may occur in chronic diarrhea
134
Q

Effects of acute ureteral obstruction

A
  • Leads to increased hydrostatic pressure proximal to the constriction
  • Pressure rise is transmitted back to the Bowmans space resulting in decreased GFR
  • Leads to a decreased filtration fraction (FF= GFR/RPF)
135
Q

Anti- Glomerular Basement Membrane Antibodies

A
  • Goodpasteurs Syndrome
  • Anti Glomerular Basement Membrane Nephritis
  • React to GBM and Alveolar Basement Membrane
  • Leads to hematuria and hemoptysis
136
Q

Hereditary Nephritis

A
  • Mutation of the alpha chains, unable to make the proper helix in the collagen type IV of the basement membrane
  • Causes weak basement membrane
  • Patients have hematuria and glomerular injury early in life
137
Q

Polyanionic Proteoglycans

A
  • Have multiple negatively charged negative molecules

- Makes glomerular basement membrane electronegative

138
Q

Minimal Change Glomerulopathy

A

Don’t see any change in the glomeruli

  • Under microscopy you see no change
  • Under electron microscopy you see that podocytes have been flattened, swollen and lost some podocytes
  • Leads to excess albuminuria
  • Negative charges of the glomerular basement membrane lose their charge
  • Thereby albumin cases through
139
Q

Mesangial Cells

A
  1. Can contract
  2. Can phagocytose
  3. Can proliferate and deposit mesangium and collagen
140
Q

How does renal blood flow?

A
  1. Renal artery
  2. Segmental artery
  3. Interlobar artery
  4. Arcuate artery
  5. Interlobular artery
  6. Afferent arterial
  7. Glomerulus
  8. Efferent arteriole
  9. Vasa recta/peritubular capillaries
  10. Venous outflow
141
Q

What anatomic structures are above the ureters?

A
  • In males, the vas deferent
  • In females, the uterine artery
  • Gynecologic procedures that ligate the uterine or ovarian vessels may damage the ureter and lead to obstruction or leakage
142
Q

Contraction Alkalosis

A
  • Volume contraction leads to alkalosis
  • During dehydration, the RAAs leads to increased ATII which acts on the Na+/H+ exchanger increasing the reabsorption of Na+, H2O and HCO3
143
Q

Proximal Convoluted Tubules

A
  • Located in the renal cortex (Isotonic)
  • Reabsorbs all glucose and amino acids, most HCO3-, Na+ (60-80%), Cl-, PO43-, K+, H2O and Uric Acid
  • Generates and secretes NH3 which allows kidney to secrete more H+
  • PTH inhibits Na+/PO43- cotransport which leads to PO43- excretion
  • ATII stimulates Na+/H+ exchanger, leads to increased Na+, H2O and HCO3- reabsorption (contraction alkalosis)
  • Carbonic anhydrase breaks down carbonic acid into H2O and CO2
  • Carbonic anhydrase inhibitors prevent breakdown of carbonic acid leading to acid urine
144
Q

Thin Descending Loop of Henle

A
  • Passively reabsorbs H2O via medullary hypertonicity
  • Impermeable to Na+
  • Concentrates urine and makes it Hypertonic
145
Q

Thick Ascending Loop of Henle

A
  • Reabsorbs Na+, K+ and Cl-
  • Indirectly induces paracellular reabsorption of Mg+ and Ca2+ via + lumen from K+ backleaks
  • Impermeable to H2O
  • Make urine less concentrated as it ascends
  • 10-20% Na+ reabsorbed
  • Loop diuretics block the luminal Na+, K+, 2Cl- cotransporter leading to hypokalemia, metabolic akalosis and hypocalcemia
  • Hypocalcemia results from no K+ backleak
146
Q

Early Distal Convoluted Tubule

A
  • Reabsorbs Na+ and Cl- via cotransporter
  • Makes urine fully hypotonic (dilute)
  • PTH causes increased Ca2+/Na+ exchange which leads to Ca2+ reabsorption
  • 5-10% of Na+ reabsorbed
  • Thiazide diuretics block the luminal Na2+/Cl- cotransporter here
147
Q

Collecting ducts

A
  • Aldosterone causes reabsorption of Na+ in exchange for K+
  • In principal cells, aldosterone increases K+ conductance, increased Na+/K+ pump, increases epithelial Na+ channel (ENaC) activity which leads to negativity and K+ secretion
  • In alpha-intercalated cells: lumen negativity leads to increased H+ ATPase activity which leads to H+ secretion and increased luminal HCO3-/Cl- exchanger activity
  • ADH acts on V2 receptor which inserts aquaporin H2O channels on apical side leading to water and urea reabsorption
  • 3-5% of Na+ is reabsorbed
148
Q

Renal Tubular Acidosis Type 2

A
  • Deficient/defective carbonic anhydrase enzyme
  • Kidney can not reabsorb bicarbonate and it is lost in urine
  • HCO3- is negatively charged and will pull K+ into the lumen
  • Patients are acidotic, hypokalemic, hypochloremic and hyponatremic
149
Q

What other substances does sodium help reabsorb in the proximal convoluted tubule and how?

A 
Amino acids
Glucose
Phosphorus
Magnesium
Calcium
- With the "Fanconi" protein
150
Q

What is Fanconi Syndrome?

A
  • Generalized reabsorptive defect in the PCT
  • Increased excretion of all amino acids, glucose, bicarb and phosphate
  • May result in proximal tubule renal acidosis
  • Low glucose leads to low energy state
    Caused by:
    1. Hereditary defects such as Wilson’s disease, tyrosinemia, glycogen storage disease, cystinosis
    2. Ischemia
    3. Multiple myeloma
    4. Nephrotoxicity/Drugs such as ifosfamide, cisplatin, tenofovir and expired tetracyclines
    5. Lead poisoning
151
Q

Characteristics of the medullary interstitium

A
  • Is hypertonic, has a high osmolarity
  • Allows it to reabsorb water easily from the collecting duct
  • Countercurrent multiplier allows it to have 5X concentration (1200-1500 mOsm)
  • ADH initiates reabsorption of water as it responds to elevated osmolarity
152
Q

Afferent arteriole constriction effects on GFR, RPF and FF (GFR/RPF)?

A

GFR: Decreased
RPF: Decreased
FF: No change

153
Q

Efferent arteriole constriction effects on GFR, RPF and FF?

A

GFR: Increased
RPF: Decreased
FF: Increased

154
Q

Increased plasma protein concentration on GFR, RPF and FF?

A

GFR: Decreased
RPF: No change
FF: Decreased

155
Q

Decreased plasma protein concentration on GFR, RPF and FF?

A

GFR: Increased
RPF: No change
FF: Increased

156
Q

Constriction of ureter effect on GFR, RPF and FF?

A

GFR: Decreased
RPF: No change
FF: Decreased

157
Q

Dehydration effect on GFR, RPF and FF?

A

GFR: Decreased
RPF: Decreased Dramatically
FF: Increased

158
Q

What effect do NSAIDs have on the nephron?

A
  • They prevent prostaglandins from dilating the afferent arteriole
  • Decrease GFR, Decrease RPF, no change to FF
159
Q

What effect do ACE inhibitors have on the nephron?

A
  • They prevent the efferent arteriole from constricting

- Decreased GFR, Increase RPF, Decrease FF

160
Q

Loop diuretics inhibit which electrolyte and what are the effects of that?

A
  • Inhibit chloride in the Na+, K+, 2Cl cotransporter
  • Affects the reabsorption of Na+, K+ and 2Cl
  • Also affects the reabsorption of Ca2+ and Mg+
  • Leads to low volume state, can lead to alkalosis, uric a cid rises, can lead to gout
161
Q

What is the macula dense and what does it do?

A
  • Located at the distal convoluted tubule
  • Measures osmolarity of plasma and urine
  • If osmolarity is high, ADH is released
  • If osmolarity is low, ADH is inhibited
  • ADH brings aquaphorins to reabsorb water and urea
162
Q

What is post obstructive diuresis?

A
  • If there is a urinary tract obstruction, it backs up urine into the collecting ducts
  • Urine will flow into the medullary interstitium and dilute its concentration.
  • Prevents the medullary interstitium from concentrating urine
  • When the obstruction is relieved, unable to concentrate the urinary flow, there will be excess fluid in the collecting duct leading to excess urination
  • Treat with normal saline replacement for every CC of urine lost
163
Q

What is Bartter Syndrome?

A
  • Autosomal recessive disorder
  • Reabsorptive defect in the thick ascending loop of Henle
  • Affects the Na+, K+, 2Cl- con transporter
  • Results in hypokalemia and metabolic alkalosis with hypercalciuria
  • Similar to chronic loop diuretic use
164
Q

Gitelman Syndrome

A
  • Autosomal recessive disorder
  • Reabsorptive defect of NaCl in distal convoluted tubule
  • Leads to hypokalemia, hypomagnesemia, metabolic alkalosis, hypercalciuria
  • Similar to long term thiazide diuretic use
  • Less severe than Bartter
165
Q

Liddle Syndrome

A
  • Autosomal dominant
  • Gain of function mutation
  • Increased Na reabsorption in the collecting tubules
  • Results in hypertension, hypokalemia, metabolic alkalosis.
  • Presents like hyperaldosteronism but aldosterone is almost undetectable
  • Treat with amiloride (ENaC channel blocker)
166
Q

Syndrome of Apparent Mineralocorticoid Excess (SAME)

A
  • 11Beta-Hydroxysteroid dehydrogenase deficiency
  • Normally converts cortisol into cortisone (inactive form)
  • Therefore there is excess cortisol
  • Increases mineralocorticoid receptor activity
  • Leads to hypertension, hypokalemia, metabolic alkalosis, low serum aldosterone
  • Can acquire disorder from glycyrrhetinic acid (licorice)
  • Treat with corticosteroids which causes a decrease in endogenous cortisol production and decreases mineralocorticoid receptor activation
    “Cortisol tries to be the SAME as Aldosterone”
167
Q

What secretes Renin and what stimulates its secretion?

A
  • Secreted by Juxtaglomerular cells
  • Secreted when there is:
    1. Decreased arteriole pressure (BP)
    2. Decreased sodium delivery to macula dense
    3. Increased renal sympathetic discharge (Beta1 receptors)
168
Q

How is angiotensin II made and what is its main function?

A
  • Released by the liver as Angiotensinogen
  • Converted into Angiotensin I by Renin
  • Converted into Angiotensin II by ACE
  • Mainly maintains blood volume and BP, affects baroreceptor function and limits reflex bradycardia.
  • Synthesized in response to decreased BP.
  • Causes efferent arteriole constriction which eads to increased GFR and FF but with compensatory Na+ reabsorption in proximal and distal nephron.
  • It preserves renal function in the low volume state with simultaneous Na+ reabsorption to maintain blood volume. secretes aldosterone from the adrenal cortex, releases ADH from the pituitary, increases PCT Na+/H+ activity and stimulates the hypothalamus for thirst
169
Q

When is ANP and BNP released and what do they do?

A
  • ANP is released by the atria
  • BNP is released by the ventricles
  • Released when there is an increase in atrial or ventricular volume
  • They relax vascular smooth muscle via cGMP which increases GFR and decreases Renin
  • Dilate the afferent arteriole and constricts the efferent arteriole promoting natriuresis (sodium excretion)
170
Q

When is ADH secreted and what does it do?

A
  • Secreted in response to increased plasma osmolarity and decreased blood volume.
  • Binds to V2 receptors on principal cells in the collecting tubule
  • Leads to increased number of aquaporins - - - Allows for water and urea reabsorption
171
Q

Name every place where angiotensin II acts and what are its effects?

A
  1. Angiotensin II receptor on vascular smooth muscle
    - Causes vasoconstriction and increases BP
  2. Constricts efferent arteriole of the glomerulus
    - Increased FF (GFR/RPF) to preserve renal function in low volume state (Low RBF)
  3. Leads to Aldosterone secretion from adrenal cortex
    - Increases Na+ channel insertion (ENaC)
    - Increases activity of Na+/K+ pump leading to K+ excretion and Na+ reabsorption
    - Increased H+ excretion by alpha-intercalated H+ ATPases
    - Increased K+ excretion by principal cell K+ channels
    - All allows for better Na+ and H2O reabsorption
  4. ADH secretion by posterior pituitary
    - Increased aquaporin insertion in principal cells leading to increased H2O reabsorption
  5. Increased Proximal Convoluted Tubule Na+/H+ activity
    - Leads to Na+, HCO3- and H2O reabsorption
    permitting contract alkalosis
  6. Stimulates the hypothalamus to increase thirst
172
Q

Which hormone primarily regulates ECF volume and Na+ content, responds to low blood volume state and responds to hyperkalemia by K+ excretion?

A

Aldosterone

173
Q

When is parathyroid hormone secreted and what are its effects on the kidney?

A 
Secreted when: 
- Plasma Ca2+ is low
- Plasma PO43- is high
- Plasma 1,25-(OH)2 D3 is low
Causes:
- Increased Ca2+ reabsorption in DCT
- Decreased PO43- reabsorption in PCT
- Increased 1,25-(OH)2 D3 production leading to increased Ca2+ and PO43- absorption from gut
174
Q

When is erythropoietin released and what does it do?

A
  • Released by interstitial cells in peritubular capillaries in response to hypoxia
  • Stimulates RBC proliferation in the bone marrow
175
Q

How is 1,25-OH Vitamin D3 made and what does it do?

A
  • PCT cells convert 25-OH vitamin D3 to 1,25-(OH)2 Vitamin D 3 (Calcitriol) via 1alpha-hydroxylase
  • PTH stimulates this conversion
176
Q

What effect do prostaglandins have on the kidney?

A
  • Paracrine secretion of prostaglandins vasodilator the afferent arteriole leading to increased RBF
  • NSAIDs block this mechanism and lead to constriction of the afferent arteriole decreasing GFR which may result in Acute Renal Failure
177
Q

What effects does dopamine have on the kidneys?

A
  • Secreted by PCT cells
  • At low doses, it dilates interlobular arteries, afferent arterioles and efferent arterioles leading to increased RBF with almost no change on GFR
  • At higher doses it vasoconstrictor
178
Q

What causes K+ to shift into cells (Hypokalemia)?

A
  • Hypo-osmolarity
  • Alkalosis
  • Beta-adrenergic agonist (Increased Na+/K+ ATPase)
  • Insulin (Increased Na+/K+ ATPase)
  • Insulin shifts K+ into cells
179
Q

What causes K+ to shift out of cells (Hyperkalemia)?

A

DO LABSS

  • Digitalis (blocks Na+/K+ ATPase)
  • HyperOsmolarity
  • Lysis of cells (crush injury, rhabdomyolysis, tumor lysis syndrome)
  • Acidosis
  • Beta-blockers
  • High blood Sugar (Hyperglycemia)
  • Succinylcholine (increased risk in burn/muscle trauma)
180
Q

What are the side effects of ACE inhibitors?

A
  • They prevent the efferent arteriole from constricting more than the afferent arteriole which leads to decreased GFR
  • Ok unless creatinine increases greater than 30% because of the long term benefits of ACE
  • Hyperkalemia due to decreased aldosterone effects on K+ excretion
  • Cough due to bradykinin accumulation
  • Angioedema is a rare but life threatherning side effect
181
Q

What is a characteristic of clear cell renal carcinoma?

A

Renal biopsy shows rounded/polygonal cells with abundant clear cytoplasm

182
Q

Clear cell carcinoma arises from?

A

Proximal tubule cells and contains copious amounts of intracellular glycogen and lipids

183
Q

What is the most common site of metastasis from renal cell carcinoma?

A
  • The lungs
  • It invades the renal vein (may cause varicocele if left sided), then IVC and spreads hematogenously; then metastasizes to lungs and bone
184
Q

Vesicoureteral Reflux

A
  • Caused by retrograde urine flow from bladder into ureter
  • Hydrostatic pressure of refluxing urine and infections due to ascending bacteria cause inflammation
  • Compound papillae in upper/lower poles are most susceptible to reflux induced damage
  • Appears as dilated calyces with overlying renal cortical scarring
185
Q

Mechanism of action of Sirolimus and when is it used?

A
  • Binds the immunophilin FK-506 binding protein (FKBP) in the cytoplasm, forming a complex that binds and inhibits mTOR.
  • Inhibition of mTOR signaling blocks interleukin-2 signal transduction and prevents cell cycle G1 to S phase progression and lymphocyte proliferation.
186
Q

Bartter syndrome effects on:

  • Blood pressure
  • Plasma renin
  • Aldosterone
  • Serum Mg2+
  • Urine Ca2+
A
  • Blood pressure: no change
  • Plasma renin: Increased
  • Aldosterone: Increased
  • Serum Mg2+: no change
  • Urine Ca2+: increased (primary disturbance)
187
Q

Gitelman Syndrome effects on:

  • Blood pressure
  • Plasma renin
  • Aldosterone
  • Serum Mg2+
  • Urine Ca2+
A
  • Blood pressure: no change
  • Plasma renin: Increased
  • Aldosterone: Increased
  • Serum Mg2+: Decreased
  • Urine Ca2+: Decreased (Primary disturbance)
188
Q

Liddle Syndrome effects on:

  • Blood pressure
  • Plasma renin
  • Aldosterone
  • Serum Mg2+
  • Urine Ca2+
A
  • Blood pressure: Increased
  • Plasma renin: Decreased
  • Aldosterone: Decreased (Primary disturbance)
  • Serum Mg2+: No change
  • Urine Ca2+: No change
189
Q

SIADH effects on:

  • Blood pressure
  • Plasma renin
  • Aldosterone
  • Serum Mg2+
  • Urine Ca2+
A
  • Blood pressure: No change or increased
  • Plasma renin: Decreased
  • Aldosterone: Decreased
  • Serum Mg2+: No change
  • Urine Ca2+: No change
190
Q

Primary aldosteronism (Conn syndrome) effects on:

  • Blood pressure
  • Plasma renin
  • Aldosterone
  • Serum Mg2+
  • Urine Ca2+
A
  • Blood pressure: Increased
  • Plasma renin: Decreased
  • Aldosterone: Increased (Primary disturbance)
  • Serum Mg2+
  • Urine Ca2+
191
Q

Renin-secreting tumor effects on:

  • Blood pressure
  • Plasma renin
  • Aldosterone
  • Serum Mg2+
  • Urine Ca2+
A
  • Blood pressure: Increased
  • Plasma renin: Increased (Primary disturbance)
  • Aldosterone: Increased
  • Serum Mg2+: No change
  • Urine Ca2+ No change
192
Q

Distal Renal Tubular Acidosis (Type 1)

A
  • Urine pH >5.5
  • Alpha intercalated cells inability to secrete H+
  • No new bicarb is generated
  • Leads to metabolic alkalosis
  • Associated with hypokalemia
  • Increases risk of calcium phosphate stones
    due to
193
Q

What is the most common type of incontinence in diabetics?

How is it diagnosed?

A
  • Diabetic autonomic neuropathy
  • Leads to overflow incontinence due to inability to sense a full bladder and incomplete emptying
  • Diagnosed via postvoid residual (PVR) testing with ultrasound or catheterization can confirm inadequate bladder emptying
194
Q

Which part of the kidney secretes erythropoietin?

A
  • Peritubular interstitial cells
195
Q

What disease usually causes decreased production of erythropoietin?

A
  • Chronic kidney disease
196
Q

When decreased renal perfusion and decreased GFR are sensed, which cells secrete renin in the kidney?

A
  • Juxtaglomerular cells of the juxtaglomerular apparatus
197
Q

Painless, enlarged fluctuant hemi-scrotum that transilluminates brightly on physical exam is most likely?

A

Communicating hydrocele

198
Q

When does a communicating hydrocele result?

A

When serous fluid accumulates within the tunica vaginalis in the setting of patent processus vaginalis.

199
Q

The uteric bud gives rise to the?

A

Collecting system of the kidney

200
Q

What consists of the collecting system?

A

Collecting tubules, ducts, major and minor calyces, renal pelvis and ureters

201
Q

The metanephric mesoderm (blastema) gives rise to the?

A

Glomeruli, bowmans space, proximal tubules, loop of henle and distal convoluted tubule.

STEP (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions