Unit 8 - General Review

Front 1

blunting of the calyces

Back 1

pyelonephritis; get blunted under the scarred/contracted tissue

Front 2

fever, rash, oliguria, pyuria (esosinophils) after a pt is put on a drug (methicillin)

Back 2

acute drug induced interstitial nephritis

stop the drug (combo type I and IV hypersensitivity)

Front 3

nephrosclerosis

Back 3

caused by chronic hypertension which causes hyaline arteriosclerosis in the kidney

Front 4

pt w headache, blurry vision,

paiplladema, malignant htn

Back 4

"flea bitten kidney" red and black

This is called a flea-bitten kidney and is associated with glomerular damage, glomerulitis, arteriolitis and hemorrhage in a case of malignant hypertension.

onion skinning arteriosclerosis, petechiae (ruptured blood vesels); petechial lesions on cortex

Front 5

in a pt w irregular irregular pulse

Back 5

Multiple pale renal infarcts
Note the irregular white areas on the cortical surface. Most infarcts occur from embolic disease from the left heart.

Front 6

pt w a renal mass. Pt is a smoker and obese.

labs show polycythemia and hypercalcemia

Back 6

renal cell carcinoma (VHL on chromosome 3, polyognal clear cells full of glycogen, paraneoplastic syndromes (ectopic EPO = polycythemia, PTHrP = hypercalcemia)

Front 7

kid with unilateral flank mass and hypertension

Back 7

wilms tumor

htn bc tumor is making renin

chromosome 11

Front 8

aniridia (absent iris) and one limb greater than the other

Back 8

wilms tumor; chromosome 11

Front 9

painless hematuria

Back 9

bladder cancer (transitional cell)

Front 10

baby w potters facies (flattened nose, low-set ears, and recessed chin)

Back 10

ARPKD

Front 11

hx of HTN, abnormality of ultrasound in the renal pelvis,
and had click murmur (therefore MVP) – dx?

Back 11

ADPKD

Front 12

pt with HTN, abnormality on ultrasound in renal
area, lost 600 mls of blood all of a sudden, leading to hematochezia (MCC hematochezia =
diverticulosis).

Back 12

Diverticulosis

associated w ADPKD

Front 13

how does an increase or decrease in capillary oncotic pressure affect GFR

Back 13

increase = decreases GFR (reaches equilibrium faster)
decrease = increases GFR (takes longer to reach equilibrium)

Front 14

how does an increase or decresae in Kf affect GFR

Back 14

increase Kf = increseased GFR (more can filter across bc o fincreased permeability)
decreased Kf = decreased GFR (less can filter across)

Front 15

how does afferent dilation or constriction affect hydrostatic pressure and renal plasma flow

Back 15

afferent dilation = increased hydrostatic pressure, increased renal plasma flow
afferent constriction = decreased hydrostatic pressure, decreased renal plasma flow

Front 16

affects of efferent constriction and dilation on cap hydrostatic pressure

Back 16

e. c. = increased hydrostatic pressure
e. d. = decresaed hydrostatic pressure

Front 17

tinnitus

Back 17

salicylate poisoning

Front 18

dense calcification of kidney

Back 18

compication of chronic pyelonephritis

Front 19

differentiate acute vs chronic pyelonephritis other than time frame

Back 19

APN = fever, spares cortex

CPN: assymetrical scarring, blunted calyces, thyroidization of kidney (eosinophilic casts)

Front 20

primary pathogen capable of causing UTI + liver abscess and pneumonia in otherwise healthy people.

Back 20

klebsiella pneumoniae

Front 21

K capsular antigen

Back 21

anti-phagocytic

Front 22

electron dense deposits composed of Ig and complemtn within the basement membrane

Back 22

MPGN II (dense deposit disease)

Front 23

does MPGN type I or II involve complement activation

Back 23

II

Front 24

subepithelial deposits

Back 24

acute GN (post streptococcal = subendothelial humps)

Front 25

Epimembranous deposits

Back 25

Membranous GN

Front 26

Subendothelial deposits

Back 26

lupus glomerulonephritis (diffiuse proliferative)

Front 27

deposits in mesangium

Back 27

IgA nephropathy/Henoch-Schonlein GN

Front 28

fibromuscular dysplasia

Back 28

stenotic renal artery; mc in YOUNG WOMEN

Front 29

embryonic glomerular structures

Back 29

Wilms tumor (deletions involving WT1 located on c11)

Front 30

enlarging abdominal mass w normal VMA

Back 30

Wilms tumor (deletions involving WT1 located on c11)

Front 31

WAGR complex

Back 31

Wilms tumor, aniridia, genitourinary malformation, mental motor retardation

Front 32

19 y/o male w dysuria and yellow green urethral discharge; play odds

Back 32

nongonococcal urethritis (more common than gonococcal)

i.e. chlaymdiae (intracellular)

Front 33

High fractional excretion of sodium indicates what

Back 33

Post renal (can't reabsorb sodium)

>4%

>40 urine Na

Front 34

Low fractional excretion of sodium indicates what

Back 34

Pre-renal

<1%

<10 urine Na

Front 35

leukocytes and neutrophils

Back 35

tubulointerstitial nephritis

Front 36

pulmonary congestion

Back 36

due to fluid overload in acute glomerulonephritis

Front 37

uniformly progresses to chronic renal failure if untreated

Back 37

diffuse proliferative glomerulonephritis (SLE)

mcc of death in SLE

Front 38

why would a pt be hypocalcemic in chronic renal failure

Back 38

decreased calcitriol synthesis -> hypocalcemia
secondary hyperparathyroidism -> hypercalcemia, phosphauria

Front 39

management of hyponatremia

Back 39

water restriction

Front 40

management of hyperphosphatemia

Back 40

phosphate binders (niital)

Front 41

management of hypervolemia

Back 41

decreased salt and water intake + loop diuretics

Front 42

this dz is due to hyperparathyroidism and is associated w myopathy

Back 42

Osteitis fibrosa

Front 43

Adynamic bone disease

Back 43

oversuppression of PTH

Front 44

Suppressor of PTH production

Back 44

1,24 dihydroxyvitamin D? not sure

Front 45

hematuria time frame in APSGN vs IgA nephropathy

Back 45

IgA = fast, very close

APSGN = 10 days or more after infection (often a cutaneous infection)

Front 46

pathologic features of predominant small artery involvement w intimal proliferation and sometimes thrombosis also termed "thrombotic microangiopathy" is found in which renal dzs

Back 46

HUS, TTP, scleroderma, sickle cel nephropathy, malignnat htn

the primary process is endothelial damage

Front 47

why dont give loop diuretic sin nephrotic syndrome

Back 47

high dose loop diureics can precipitate renal failure in nephrotics bc the intravascular volume cannot be defende dby hypoalbuminemia (thus you accelerate hypoalbuminemia worsening fluid status)

Front 48

causes of euvolemic hyponatremia

Back 48

SIADH

Front 49

causes of hyponatremia w low urine sodium

Back 49

CHF (decreased renal perfusion = decreased perfusion)

Front 50

pt w hypertension, alkalosis, hypokalemia

Back 50

Hyperaldosteronism (Conns syndrome)

Front 51

diagnosis of medullar sponge kidney

Back 51

IVP

Front 52

function of the urine anion gap

Back 52

differentiates renal from nonrenal causes of nongap acidosis

Front 53

Pseudohyponatremia

Back 53

associated w elevated lipids, glucose or plasma proteins

Front 54

causes of hypervolemic hyponatremia

Back 54

CHF, cirrhosis and nephrotic syndrome, massive edema of any cause

Front 55

causes of isovolemic hyponatremia

Back 55

SIADH, cerebral trauma

Front 56

selective proteinuria

Back 56

minimal change dz

Front 57

prognosis of minimal change

Back 57

good; responds to steroids

Front 58

prognosis of ASGN

Back 58

often resolves spontaneously

Front 59

prognosis of RPGN

Back 59

bad

Front 60

prognosis of DPGN

Back 60

bad (lupus)

Front 61

what should you not use to tx malignant htn

Back 61

ACe inhibitor (can bottom out GFR = renal failure)

Front 62

stones in alkaline urine

Back 62

ammonium magnesium phosphate (struvite)

Front 63

lithium association

Back 63

nephrogenic diabetes insipudus

Front 64

how to differentiate nephrogenic diabetes insipudus from central diabetes isnipudus?

Back 64

desmopressin injection

if central, will increase urine conc
if nephrogenic, no effect

Front 65

ADH MAO

Back 65

sitmulates production of cAMP -> insertion of aquaporins on apical surface of collecting ducts

Front 66

waxy casts w very low urine flow

Back 66

CESRD

Front 67

WBC casts in urine

Back 67

acute pyelonephritis or cystitis

Front 68

vasculitis from exposure to endotoxin causing glomerular thrombosis

Back 68

Schwartzman reaction (following second exposure to endotoxin)

Front 69

Urethritis, conjunctivitis, arthritis in a male

Back 69

Reiter's syndrome (reactive arthritis associated w HLA-B27)

Front 70

Streak ovaries, congenital heart disease, horseshoe kidney

Back 70

Turner syndrome (XO, short stature, webbed neck, lymphedema)

Front 71

renal cell carcinoma, hemangioblastomas, angiomatosis, pheochromocytoma

Back 71

VHL disease (dominant tumor suppressor gene mutation)

Front 72

Red urine in the morning

Back 72

paroxysmal nocturnal hemoglobinuria

Front 73

Polyuria, acidosis, growth failure, electrolye imbalances

Back 73

Faconi's syndrome (proximal tubular reabsorption defect)

Front 74

Palpable purpura, joint pain, abdominal pain (child)

Back 74

Henoch-Shonlein purpura (IgA vasclitis affecting skin and kidneys)

Front 75

Hypertension, hypokalemia, metabolic acidosis

Back 75

Conn's syndroem (primary hyperaldosteronism)

Front 76

deep, labored breathing/hyperventilation

Back 76

Jussmaul breathing (diabetic ketoacidosis)

Front 77

free water clearance

Back 77

Defined as the volume of distilled water that would have to be added to or subtracted from the volume of urine produced in one minute so as to make that urine isomotic with plasma.

(-) free water clearance = concentrated urine
(+) free water clearance = dilute urine
(0) free water clearance = isomotic urine

Front 78

Cockcroft-Gault Prediction of Creatinine Clearance

Back 78

CCr = 140 - AgxWt/Plasma creatinine x 72

for women multiply by .85

Front 79

clinical examples of neurogenic flaccid bladder

Back 79

CONUS MEDULLARIS OR CAUDA EQUINA SYNDROMES; NEOPLASM;
HERNIATED (EXTRUDED) DISC; DIABETES MELLITUS; MOTOR RADICULOPATHY

Front 80

The bladder frequently becomes distended,
the wall thins, and bladder tone decreases. However, some residual contractions remain
because of the intrinsic contractile response of smooth muscle to stretch. As a rule,
residual volume is present after urination. Incontinence is present, and urinary retention
occurs. Perianal sensation, and the anal and bulbocavernous reflexes are abolished. Bladder
volume is increased, but bladder pressure is decreased

Back 80

flaccid neurogenic bladder

Front 81

Bladder volume is often
reduced and reflex hyperactivity may lead to a state of spastic neurogenic bladder,
in which the bladder fills to a set point, and then spontaneously empties whether it is
convenient for the patient or not. Perianal sensation is preserved, and the anal and bulbo-
cavernous reflexes are normal. Bladder intravesical pressure is increased but bladder volume is decreased.

Back 81

spastic neurogenic bladder; frequent UTis bc of residual volume


In addition, during the
period of overflow incontinence before the voiding reflex is re-established, these patients
must be catheterized frequently, further predisposing them to urinary tract infections.
The level of the lesion is between the lower brainstem or spinal cord above the level of the conus medullaris.

Front 82

what do the anal or bulbocavernous reflex measure

Back 82

These reflexes measure the integrity of S2, 3, and 4.