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UWORLD QuestionQuestions > Renal > Flashcards

Renal Flashcards

1
Q

Abs associated with Goodpastures? Where else can these Abs React on?
With what specific collagen?

A

Anti-GBM Abs- Cross react with BM of lung alveoli- Hemoptysis!

@ alpha 3 chain of Collaen Type IV-

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2
Q

GoodPastures Disease presents with what renal disease?
With what Immunoflorescent findings?
EM?

A

RPGN
IgG & C3 in Linear Deposits
GBM diruptions and fibrin deposition on EM

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3
Q

What stones can precipitate from ACIDIC urine?

A

Uric Acid, Cysteine, Calcium Oxalate stones

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4
Q

What stones can precipitate from ALKALINE urine?

A

struvite, Calcium PHOSPATE stones

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5
Q

What 2 things can dissipate Stones (specifically calcium precipitated stones)

A

Citrate (binds free Ca2+ => excretion)

High fluid intake

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6
Q

Oncotic Pressure is what?

How does it relate to Hyper/HypoProtein/Albuminemia

A

Pressure that keeps and fluid within the vessel/plasma.

Hyper= high oncotic pressure => plasma fluid retention due to high amount of albumin/protein in the blood

Hypo= low oncotic pressure => intersitial edema formation

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7
Q

MCC of ESRD in US? (renal disease)

best method for early detection?

A

Diabetic Nephropathy

Microalbuminuria detection

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8
Q

When does Autosomal Reessive Polycystic kidney disease usually present? and how

A

At birth/early childhood

enlarged kidneys with cysts >1cm visble on US

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9
Q

how long after vasectomy is sperm still viable?

A

3months

20 ejaculations

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10
Q

IV Acyclovir requires which co-administrative treatment and why?

A

aggressive IV hydration because crystalline nephropathy can occur

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11
Q

What type of endocrine disorder is caused by Chronic renal failure commonly?

A

hyperparathyrioidsm

Increase PTH
Decr. Calcitriol
Low Calcium
High Phosphate

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12
Q

What disease is an inborn defect of the transporter of cystine, ornithine, arginine & lysine? and when and which symptom is seen?

A

Cystinuria

renal colic @ 2-3rd decades of life

pathognomonic hexoganal cystine crystals

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13
Q

Where does ADH act?

A

Medullary segment of the collecting duct

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14
Q

Predisposers to post-streptococcal glomerulonephritis? hypersensitivity reaction type?

A

impetigo
cellulitis
pharyngitis
FROM STREP (GrpA B-hemolytic Strep)

TypeIII HSR

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15
Q

IL -2 actions? Which cancers can it effect and How?

A

Produced by Thelper => stimulates growth of CD4 & CD8 Tcells & BCells

activates NK cells & Monocytes

overall anti-cancer effect on metastatic melanoma & Renal Cell carcinoma

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16
Q

Fabry’s disease (deficiency?)

early manisfestations?

without enzyme replacement what will this disease lead to?

A

alpha glalactosidase A deficiency (cant metabolize ceremide trihexoside)

hypohidrosis
acroparesthesia
angiokeratomas

renal failure

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17
Q

Amphotericin B main side effect?

A

Nephrotoxicity

Hypokalemia hypomagnesmia => increase distal tubular membrane permiabilityy

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18
Q

NSAIDs do what to prostaglandin synthesis

A

inhibit it

ibuprofen, naproxen, indomethacin

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19
Q

What effect do Loop dieuretics have on prostaglandins?

what will happen with concurrent use of NSAIDs

A

Stimulate prostaglandin release.=> increased GFR and enhanced drug delivery

decreased diuretic response

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20
Q

How does Vasopressing affect the V2 reeceptor?

A

v2 receptor-mediated increase in permeability to water and urea at the luminal membrane of the inner medullary collecting duct

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21
Q

Winters Formula

PaCO2=?

A

(1.5 X HCO3-) + 8+/-2

PaCO2 > # => concurrent respiratory acidosis
PaCO2 < # => concurrent respiratory alkalosis

Use to evaluate respiratory compensation when there is metabolic ACIDOSIS

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22
Q

Histology of postreptococcal glomerulonephritis (3)

A

Enlarged hypercellular glomeruli on light microscopy

Lumpy bumbpy granular deposits of igG and C3 on immunofluorescence.

Electron dense deposits on the epithelial side of basal membrane on e- microscopy

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23
Q

Which bugs lack:
peptidoglycan within cell wall
cell wall entirely

Rx?

A

Chlamydia Trachomatis
Ureaplasma urealyticum

Antiribosomal abx= Microlides/Tetracyclinnes

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24
Q

Which portion of Kidney system is involved in acute renal colic due to nephrolithiasis?

A

Calices/Ureters

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25
Q

Pts with sickle cell, DM , analgesic nephropathy, severe acute pyelonephritis can have which type of pathologic damage of the kidney?

A

Renal papillary necrosis

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26
Q

When and how does acute interstitial nephritis present?

A

Fever maculopapular rash and Acute renal failure sx,

1-3 wks post B-lactam ABx

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27
Q

Contraindications to OCP (oral contraceptive pills)

A 
Hx of thromboemolic event/stroke
Hx of estrogen dependent tumor
>35 heavy smoker
hypertriglyceridemia
active liver disease
pregnancy
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28
Q

What happens to Creatinine as GFR decreases?

Increases?

A

Creatinine increase (when GFR halves-Creatinine doubles)

small increase in creatinine

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29
Q

Standard treatment of dysuria and/or urethral discharge in young adult?

A

ceftriaxone

AZITHROMYCIN/Doxycycline

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30
Q

Flucanozole is used to treat?

A 
candidiasis
cryptococcosis
histoplasmosis
blastomycosis
coccidiodomycosis
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31
Q

Why would prednisone and cyclosporin/Tacrolimus be used in a graft/transplant?

how do the last two achieve this action?

A

immunosuppressantt drugs that reduce risk of developing acute rejection

cyclosporin/tacrolimus inhibit calcineurin activation

which —| IL-2 activation ( aka no diffentiation of Tcells)

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32
Q

What is muromonab-CD3 (OKT3)? how does it work?

A

Anti-CD3 Monoclonal Ab that inhibit T-lymphocyes used in treatment of acute reection in kidney heart liver transplants

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33
Q

MCC of Urinary Tract obstruction in elderly male patients?

A

BPH

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34
Q

Activation of IL-2 via which protein? why would you inhibit this protein and its subsequent activation?

what does IL-2 promote?

A

Calcineurin; for immuno supression

promotes the growth and differentiation of T cells

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35
Q

MC subtype of RCC?

histology of this type?

Classical clinical triad ? (its rare to see)

MC site of metastisis

A

Clear Cell Carcinoma

large rounded/polygonal cells with clear cytoplasm.

hematuria, flankpain, palpable mass

lung

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36
Q

What is endometriosis?

Symptoms seen?

Pts have what 2 things on vaginal examination?

A

presence of endometrial glands and stroma outside the uterus

dysmenorrhea
dyspareunia= painful sex
dyschezia (due to pelvic adhesions) infertility

Nodularity of the uterosacral ligaments and fixed retroversion of the uterus!!!

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37
Q

Sexual characteristic manifestations of Turners (4)?

A

primary amenorrhea
high arched palate
widely spaced nipples
Ovarian dysgenesis + STREAK GONADS

38
Q

PCOS signs & symptoms?

6 categories with descriptions/levels/assoc. disorders

A

Menstrual irregularity = oligomenorrhea & infertility due to anovulation

Hormonal dysregulation= unopposed estrogen INCR. risk for endometrial Adenocarcinoma (progestrone def. , estrogen prod., elevated LH)

Increased insulin resistance => obesity/DM2

Hirsutism/Acne (incr. androgens)

Dyslipidemia=> atherosclerosis &CAD

bilateral ovarian enlargement (multiple enlarged sclerotic cystic follicles)

39
Q

endometrial glands within the uterine myometrium? how is this distinguishable from Endometriosis?

A

Adenomyosis

ENLARGED UTERUS

40
Q

When is basement membrane splitting scene?

A

Membranoproliferative glomerulonephritis and Alport syndrome

41
Q

Light microscopy and clinical manifestations of nephrotic syndrome?

A

Uniform diffuse thickening of glomerular capillary walls

Generalized edema, March proteinuria (> 3.5 g per day), hypoalbuminemia, hyperlipidemia and lipiduriia

42
Q 
Site of action of diuretics? name one
Carbonic anhydrase
Osmotic Diuretics
Loop diuretics
Thiazide diuretics
Potassium sparing diuretics-
A

CA-proximal tubule
Acetozolamide

OD-descending limb of Henle’s loop & proximal tubule
Mannitol

LD-Thick ascending limb of Henle’s Loop
Furosemide

TD-Distal convoluted tubule
Hydrochlorothiazide

PSD- Collecting Duct
Sodium Channel BLockers-Amiloride
Aldosterone rec. Blockers- Spirinolactone

43
Q

what is a cellular often myxoid stroma that encircles and sometimes compresses epithelium-lined glandular and cystic spaces?

A

Fibroadenoma

44
Q

Hypersensitivity of a Hyperacute rejection? describe this type? another example of this

A

Type II

mediated by preformed recipient antibodies against antigens on the host organ.

ABO blood group antibodies and anti-HLA antibodies.

45
Q

What Medium does Niesseria Gonnorrhea grow on?

Why is it selective medium?

A

Thayer-Martin VCN

Anitbiotics kill contaminants like Gm+ other Gm- (not gonorrhea) and fungi

46
Q

Purpose of Differential media?

Name 2

A

differentiate btw biochemical and metablic properties

EBM & MacConkeys

47
Q

acid base abnormalities associated with salicylate intoxication? (2)

A

FIRST: Respiratory Alkalosis-stimulate medullary respiratory center => Hyperventilation=> increased CO2 lost in expired air.

Anion Gap Metabolic Acidosis-accumulation of organic acids in the blood,

48
Q

How do Ketoacids, lactate and pyruvate accumulate in salicylate poisoning? 3

A

Increase lipolysis
Uncouple oxidative phosphorylation
Inhibit the TCA cycle

49
Q

The finding of mucopurulent cervicitis is typical for which disease in women?

2 bugs that cause this?

A

PID

N.gonorrhea, C.Trachomatis

50
Q

How is endometrial hyperplasia caused?

What are its clinical findings?

A

Caused by elevation in estrogen unopposed by progesterone acting on in the endometrial lining

  • exogenous : hormone replacement therapy
  • endogenous: estrogen secreting ovarian tumor, increase aromatization of androgens and obese women

Dysfunctional uterine bleeding

51
Q

What two things can PID potentially lead to? why?

A

Ectopic pregnancy
Infertility

Due to salpingitis leading to scarring of the fallopian tubes

52
Q

how is LPS released from bacteria?

A

During division or by bacterial lysis.

NOT actively secreted by bacteria.

53
Q

What is the toxic component of LPS?

What does it cause?

A

Lipid A

Lipid a causes activation of macrophages leading to the widespread release of IL-1 and TNF – Alpha. => septic shock: fever, hypertension, diarrhea, oliguria, vascular compromise, DIC

54
Q

how does a Competitive inhibitor change the log dose response curve?

A

Change ED 50 = shift right/L

55
Q

How does a noncompetitive inhibitor change the lock those response curve?

A

Change E Max = shift down/up

56
Q

in whom does an indirect inguinal hernia most commonly present?

where does it occur?

How does it occur?

A

Male infants

Lateral to inferior epigastric vessels

Persistent processes vaginalis, and failure of internal inguinal ring to close; covered by all 3 spermatic fascial layers

57
Q

in whom does a direct inguinal hernia most commonly present?

where does it occur?

how does it occur?

A

Older man

Medial to inferior epigastric vessels

Weakness in transversalis fascia, external spermatic fascia covering only

58
Q

in whom does a femoral hernia most commonly present?

where does it occur?

A

Women

Medial to the femoral vessels and inferior to the inguinal ligament

59
Q

ANCA– associated RPGN is also called immune glomerulonephritis because the absence of what 2 things? Which type of RPGN is this?

What presentation?

A

Ig and C3 deposits; TYPE 3

Renal failure, pulmonary symptoms, upper respiratory tract symptoms (epistaxes, mucosal ulceration, chronic sinusitis and parentheses

CRESCENTS on Light Microscopy

60
Q

Type 1 RPGN has which antibodies present and what is seen on IF microscopy?

A

Anti – GBM antibodies

Goodpastures syndrom

61
Q

Type 2 RGPN is associated with what deposits?

what is seen on IF?

What 4 diseases present with this RPGN?

A

Immune –Complex mediated

Lumpy bumpy granular pattern on IF microscopy

Post streptococcal Glomerulonephritis, SLE, IgA nephropathy, and Henoch-Schlonlein Purpura

62
Q

When would a decrease serum C4 be present? Which pathway is activated?

A

Hereditary angioedema

Classical pathway is activated secondary to a lack of C1 esterase inhibitor (breaks Down C4)

63
Q

What is the diagnosis of a patient with a positive VDRL and pleocytosis in the CSF?

A

Neurosyphilis

64
Q 
Syphilis:
primary-
secondary-
latent-
tertiary-
A

1: painless ulcerated Chancre 1-3wks after contact & resolves in 3-6wks’
2: 5-10wks bacteremic stage with diffuse macular rash in the palms and soles, condylomata lata (grey-wartlike growths)

L:asymptomatic = early latent and late latent (1yr post 2ndary symptoms)

3: syphilis years after infection includes subacute meningeal encephalitis, tabes dorsalis, Gummas

65
Q

Where does ADH act upon? how?

where would be most dilute/ concentrated portion of the nephron be?

A

Collecting ducks, increases their permit ability to water.

Collecting ducts most concentrated fluid in the nephron thick ascending limb and distal convoluted tubules are most dilute.

66
Q

Which part of the ovary can be affected by excessive hCG?

A

Theca–lutein cysts

67
Q

clearance of PAH is equal to?

A

RPF

68
Q

The secretion of PAH is through which process?

A

Carrier-enzyme mediated process

Transport maximum= secretion plateau

69
Q

What cells compose Crescents of RPGN?

A

Glomerular parietal cells, monocytes, macrophages, abundant fibrin

70
Q

Beta-Lactamase inhibitors (name 3) extend the penicilin spectrum via which mechanism?

A

Clavulanic acid
sulbactam
tazobactam

They decrease the destruction (via beta lactamase) of penicillins

71
Q

Where is the lowest concentration of PA H?

A

In Bowman space

72
Q

Acute tubular necrosis stage descriptions:
Initiation-
Maintenance-
Recovery- plus serious complication

A

I- ischemic injury due to hemorrhage, acute MI, sepsis, surgery

M-decreased urine output, fluid overload, increasing creatinine/BUN, hyperkalemia

R-gradual increase in urine output = >high-volume diuresis.
HYPOKALEMIA; decreased Mg, PO4, Ca due to slow tubular recovery

73
Q

How to diagnose the maintenance stage of acute tubular necrosis

A

24-36hours after ischemic damage

URINARY:
pathognomonic muddy brown Casts, low urinary osmolality (less than sign 350), high urinary sodium (>30), high urinary fractional sodium excretion (FeNa>1).

&&& hyperkalemia, high anion gap metabolic acidosis

74
Q

Laboratory findings of PSGN: (4)

A

Elevated antistreptolysin-O (ASO) titers
Elevated anti-DNase B titers
Decreased C3 and total complement levels (c4 normal)
Presence of cryoglobulins

75
Q

Ruptured ectopic pregnancy symptoms? Biopsy findings?

A

Abdominal pain
Vaginal bleeding
Hemorrhagic shock
History of amenorrhea

Decidual changes in endometrium but NOT chorionic villa

76
Q

(4) secondary hyperaldosteronism causes?

What symptoms will the patients have (2) and what findings will they have (2)

A

Renovascular hypertension
Malignant hypertension
Renin secreting tumor
Diuretic use

Hypertension and hypokalemia

Increase renin, increase aldosterone

77
Q

(2) primary hyperaldosteronism causes

Patient presents with (2) what symptoms and what clinical findings (2)

A

Aldosterone producing tumor
Bilateral adrenal hyperplasia

Hypertension and hypokalemia

Decreased renin, increased aldosterone

78
Q

Non-aldosterone causes of patients with hypertension and hypokalemia (4)? what clinical findings are seen (2)

A

Decrease renin decreased aldosterone

CAH
Deoxycorticosterone producing adrenal tumor
Cushing syndrome
Exoogenous mineralocorticoids

79
Q

Gross painless hematuria and older adults to be considered what until proven otherwise?

A

Urothelial cancer

80
Q

Reno clear-cell carcinomas originate from which type of cells?

A

Tubular epithelial cells

81
Q

What happened to the blood in nephrotic syndrome?

Common complication of nephrotic syndrome?

A

Hypercoagulable state
Loss of antithrombin III

Renal vein thrombosis; hematuria, left-sided varicocele or flank pain

82
Q

Description of JG Aparatus subunits and where they are located?

MOA?

A

JG cells - are modified smooth muscle cells located in the walls of the efferent and afferent arterioles

macula densa cells- are tall narrow cells located in the distal tubule

*MD cells monitor osmolarity/urine volume in DT and transmit information to JG cells where renin synthesis occurs

83
Q

VHL (3) => three clinical syndromes associated with it

Where and what are the genetic change associated with VHL gene? what type of gene is VHL

A

Cerebellar hemangioblastoma’s
Clear cell renal carcinoma (40%)
Pheochromocytomas

Deletion on chromosome 3p; tumor suppressor gene

84
Q

Where is the RB anti-oncogene located?

Mutations in this gene lead to which two disorders

A

Chromosome 13

Retinoblastoma
Osteosarcoma

85
Q

When would tubular affection with urate crystals occur? And which kind of patient is this seen?

A

Tumor lysis syndrome classically presenting as acute renal failure during chemotherapy for malignancy

86
Q

Which two toxins bind to sodium channels inhibiting sodium influx and preventing action potential conduction?

A

tetrodotoxin -pufferfish

Saxitoxin- dinoflagellates

87
Q

Which to toxins bind to sodium channels keeping them open and causing persistent depolarization?

A

Ciguatoxin- eel

Batrachotoxin (S.A. Frogs)

88
Q

When is vitamin E deficiency seeing? (3)
-lipid soluble & antioxidant

what does it present similarly to? What symptoms? (3)

A

Fat malabsorption
Abetalipoproteinemia
Low birth weight infants

Degeneration of :
spinocerebellar tracts
Dorsal column of smile cord
Peripheral nerves
==>Friedrech Ataxia (ataxia, dysarthria, loss of position & vibration)
89
Q

What Activates CPS I of the Urea cycle? what is special of this enzyme?

A

N-Acetylglutamate (NAG)

RLS

90
Q

What molecule does the Urea cycle derive its Nitrogen from?

A

Aspartate.

91
Q

Which SE of opiod use does not change with increased tolerance? (2)

A

Constipation

Miosis

92
Q

nephrotic syndrome (4)

A 
massive proteinuria
hypoalbuminemia
generalized edema
hyperlipidemia
lipiduria

UWORLD QuestionQuestions (12 decks)

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