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STEP1 > Renal > Flashcards

Renal Flashcards

1
Q

Varicocele

A

Scrotalenlargement
Indicates high venous pressure
“ Left more common- into L renal vein not IvC
Often sign of tumor in kidney

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2
Q

Neurons kidney

A

Renal plexus
Para from vagus
Symp from sphlanchnic-n. T10-L1 Via celiac plexu.
Pain sphlanchnic n t10-11, referred pain at T 10-11 dermatome

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3
Q

Quadratus eumborum

A

Fixes rib during inspiration, stabilizes diaphragm

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4
Q

Psoas major

A

Flex hip
Medial posterior ab wall

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5
Q

Gonadal v tributary to

A

L- L renal
R-ivc

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6
Q

Bladder a

A

Superior and inferior vesicle a
Both from internal iliac a
F- also uterine a

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7
Q

Kidney lymph tributary to

A

Para-aortic and para-caval nodes

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8
Q

Nerves bladder

A

Sump - L 1-L2 urine retention
Para- s 2-4 urine release, detrusor m.
Sensory- s 2-4 bladder dissension.’

External urethralsphineter-skeletal/voluntary,pudendal n

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9
Q

Mesangial cells

A

Debris phagocytosis, cytokine secretion,
Blood flow regulation
ECM production

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10
Q

Nephrosis nephritis

A

,osis-protein
Itis - blood

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11
Q

Macula densa-where

A

DCT

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12
Q

Bowman capsule cells

A

Podocyte= visceral epithelial cells
Parietal epithelial cells

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13
Q

Renal tubular necrosis causes

A

Drugs
-Radiology contrast
-Aminoglycosides (-mycin/micin)

Hypoxia/ischemic

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14
Q

Loop diuretics

A

E.g. Furosemide
Block NaCl reabsorption at thick ascending limb
Sodium diuresis
K wasting

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15
Q

Renal blood flow reg.

A

Macula densa @dct near glomerulus senses
Signals jg @afferent a
Jg relax, release renin
= more blood flow, more sodium retention
In response to low bp

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16
Q

Thiazide diuretics

A

@Dct
Na and k wasting

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17
Q

Ad h target

A

Principal cells @ collecting duct

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18
Q

Aldosterone tar yet

A

Principal cells @collecting duct - Na and k
Alpha intercalated cells @collecting duct- acid-base

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19
Q

Alpha intercalate cells

A

@Collecting duct
Acid-base
Hco3 reabsorb H+ out
Re: acidosis, aldosterone

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20
Q

PT H responsive element

A

Reabsorb Ca @dct

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21
Q

Urinary epithelium

A

Transitional
Stratified, impertheable to salt and water
Expands

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22
Q

Kidney embryo origin

A

Intermediate mesoderm

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23
Q

Provephros

A

Week 4
Primitiveglomeruli

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24
Q

Mesonephros

A

Week 4-8/first tri
Interimfiltration
Into mesonephire duct
MD will later become male genitals

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25
Q

Metanephros

A

Week 5 -32+
Ureticduct- me somephric duct outgrowth → collecting tubes, urinary system sans bladder
Metanephric blastema- rest of nephron

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26
Q

Kidney ascend

A

‘really rest of embryo moving down
Sacral → lumbar
Week 6-9

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27
Q

Cloaca

A

→ bladder

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28
Q

Trigone

A

Mesonephric duct → trigone → sensation of bladder distention

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29
Q

Urachal fistula

A

Failure of allantois degeneration
Fistula between bladder and umbilicus

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30
Q

Pelvic kidney

A

Umbilical arteries prevent ascent
Complications:
-Reflux, hydronephrosis
- dt ureter obstruction, urinary reflex, improper rotation

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31
Q

Horseshoe kidney

A

Fusion
Inferior mesenteric a-blocksascent
Complication:
- obstruction
- stones
-Infection

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32
Q

Amniotic fluid source late gestation

A

Fetal urine and lung secretions

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33
Q

Oligohydramnios

A

Insufficientamniotic frid ‘
Lethal if severe
Usually dt kidney agenesis or-malformation or obstruction

34
Q

Potter sequence

A

Findings related to oligohydramions
Fetal compression
Flat nose, low ears, recessed chin, limb deformities, redundant skin
Pulmonary hypoplasin

Dt:
- bilateral renal agenegis
- autosomal recessivepolycystic kidney disease
- autosomal dom”
- urinary obstruction -mostly dt posterior urethral valve in male infants
- prom - premature rupture of amniotic membrane

35
Q

Alport Syndrome

A

Hereditary nephritis
* no inflammation
Glomerulus- eye- hearing loss
Mutation in type 4 collagen- bm
X-linked ~85%

Micro hematuria → proteinuria with hypertension
Need dialysis by middle age

Anterior l enticonus ~25%, pathognomonic
= lens bulge thru pupil

36
Q

D x Alport

A

Skin biopsy for collagen

37
Q

Adpkd gene

A

Pkd1 chr. 16
~80%
Polycystin -1
cAMP → epithelial profiler
Ons-t ~50 y/o
Incomplete penetrance

38
Q

Adpkd clinical

A

Asymptomatic
Flank pain
Cyst/pyelo E coli
Uric acid stones
RAAS → hy pertenten

Liver cysts
Berry aneurysms
Mitral value prolapse

39
Q

-arpkd gene

A

Pkhd-1 most common

40
Q

Struvite_stones

A

~15%
Associated with recurrent upper UTIs with urease producing bacteria
- proteus
- staph
Urine ph>7
Coffin lid
Aka ammonium magnesium phosphate

41
Q

Stones risk factors

A

Dehydration
Recurrent UTI
Gout
Hyper-pth
Fatty malabsorption - bariatric surgery, IBD
Family Hx

42
Q

Calcium stones

A

Most common
If high serum Ca high suspicion for hyper-pth
Envelope or dumbbell appearance

43
Q

Urate stones

A

Tx with-gout agents
Mostly don’t have other gout sx
Gout, leukemia, chemo,
Rhomboi d or rosette

44
Q

Stones in type 1 RTA

A

Usually Ca dt low urine citrate dt kidney not secreting H

45
Q

Stones Tx

A

Pain plus observe
Calcium channel blockers - nifedipine
a-blockers -osin
Surgery

Prevention:
- less dietary oxalate
- oral ca supplement
-Thiazide diuretic
- citrate
- UTI prevention
- u ric acid: bicarb, allopurinol

46
Q

Allopurinol

A

Inhibits xanthine oxidase
Prevents hypoxanthine→ xanthine

47
Q

Ace inhibitors

A
  • Sartan
    Inhibit angiotensin 2 formation
    Efferent arteriole dilation
    Benefit of decreasing glomerular pressure > decreased GFR
48
Q

Jg stimuli

A
  • low bp
  • low NaCl
  • more sympathetic input
49
Q

ANP and BNP

A

Natriaresis - Na and water
Released by heart
Re: high bp

50
Q

Endotheli n

A

Made by kidney endothelium
Vasoconstrictor a fferent and efferent
Low RB F and GFR

51
Q

K sparingdiaretics site of action

A

Proximal collecting duct

52
Q

Acetazolamide

A

Pct
Carbonic anhydrase inhibitor
Na and hco3 excretion
Weak diuretic

Uses:
- open-angle glaucoma _ intraocular
- serum s ‘ ickness

53
Q

Loop diuretics

A

-emide / - nadide / ethacrynic acid
Strongest
K wasting
Na-k-2 cl @thick ascending LOH
Ca and mg loss dt membrane potential change
H wasting → alkalosis
venous vasodilation

Uses:
- chf
-Volume overload
- hyper-k crisis
- not as good for htn b/c no arterial dilation

54
Q

Thiazide diuretics

A

Na cl symporter @. Dct
Compensatory Na Ca exchanger action → hyper-ca
K wasting
H wasting → alkalosis

Uses:
- First line htn
. Calcium kidney stones

55
Q

Spironolactone

A
  • Aldosteronereceptor blocker @collecting duct
    K sparing
    H retention → acidosis

Use:
- chf
- liver failure/acites
- Maintain k
- Hyper-aldosterone
- feminizing: PCOS, trans-f

56
Q

Na channel blocker

A

.inhibit enac - @collecting duct
K sparing
H retention →acidosis

Amiloride
Triamterene

57
Q

Non renal uses CA in hibitors

A

Respiratory alkalosis _ COPD -, sleep apnea, altitude sickness
Pressure- glaucoma, ICP
Epilepsy- nerve de polarization inhibitor

58
Q

CA inhibitors c/i

A

acidosis
sulfa allergy
cirrhosis (–> hepatic encephalopathy)

59
Q

SIADH

A

excess ADH = water retention
hyponatremia
but usually euvolemic (total body water) d/t compensatory water loss by ANP/BNP
cerebral edema - potentially lethal

60
Q

SIADH tx

A

can be treated with loop diuretics + saline b/c loop diuretics interrupt formation of gradient needed to reabsorb water in collecting duct. Then we replace sodium and fluids with the saline.

61
Q

loop diuretics c/I and AEs

A

volume depletion
- liver disease -> hepatic encephalopathy d/t concentration of toxins
- prerenal AKI
- hypercoagulopathy
hypokalemia
alkalosis (H+ loss)

ototoxicity esp. ethacrynic acid
sulfa allergy except ethacrynic acid

62
Q

osmotic diuretics c/i

A

d/t transitory increase in plasma volume:
- CHF
- pulmonary edema

renal impairment: lack of filtration –> accumulation –> volume overload

severe dehydration
hemorrhage incl acute intracranial bleed

63
Q

thiazide diuretics e.g.

A

HCTZ
chlorthalidone
metolazone
indapamide

64
Q

High bicarb

A

”Side effect” of conditions that reabsorb Na
- dehydration, hemorrhage
- metabolic
- dt na-hco3-cotransport

Compensation for respiratory acidosis
- failure toventilate/ breath off co 2
- respiratory depression

65
Q

bicarb reabsorbtion Mx

A

Mostly pct
Carbonic anhydrase urine → cell
Na-hco 3 cotransporter cell → blood
Can reabsorb less or more bicarb - but limited in how muchbicarb it can get rid of because all passive

66
Q

Chronic . Hyperkalemia bicarb

A

Inhibit ammoniagenesis → can’ I get rid of acid

One primary cause- low aldosterone - also → acidosis because Na and hco3 move in same direction ‘

H K exchange also means- if k is high will get rid of k and keep H to try to compensate _ this is more important for explaining opposite, why low k is associated with alkalosis

67
Q

Isoniazid acid base

A

High anion gap Metabolic acidosis

68
Q

Met formin acid base

A

High anion gap metabolic acidosis

69
Q

Methanol acid base

A

High anion gap metabolic acidosis
Dt Formic acid

70
Q

Uremia acid base

A

Metabolic acidosis
Low gfr → low acid secretion

71
Q

Ingestions acidosis

A

Ethylene glycol
Propylene glycol
Methanol

72
Q

Drugs acidosis

A

Isoniazid
Met formin
Salicylates - aspirin (starts with respiratory alkalosis fromhyperventilation then salicylic acid acidosis sets in)

73
Q

Normal anion gap metabolic acidosis

A

Bicarb loss dt:
- diarrhea
- proximal RTA (type 2) -
Both are hypokalemic

H buildup dt:
- distal and hyperkalemic RTA (1 and 4)

74
Q

Type 2 RTA

A

Proximal tubule
Hypo - K
Mild acidosis
Impaired bicarb reabsorbtion

Dt:
- acetezolamide
- other drugs/toxins
- excess ig -multiple myeloma
- fanconi syx - pan pct failure

75
Q

Type 1 RTA

A

Distal
Failed H excretion @ collecting duct
Can be severe

Dt:
- interstitial CKD
-Amphoterrible
- lithium
- lupus
- sjorgen
- amyloidosis

76
Q

Type 4 rta

A

Hyperkalemi c
Most common
Failed ammonia/um excretion@ pct
Mild acidosis

Dt:
- low aldosterone
-E.g. Low renin in diabetics

77
Q

Fomepizole

A

Alcohol dehydrogenase inhibitor
Methane and glycol tox

78
Q

When to give bicarb

A

Normal anion gap metabolic acidosis

79
Q

Enzyme defects metabolic alkalosis

A

11-b-hydroxyls e and 17-a- hydroxyls e, which result in *high_mineralecorticoids and aldosterone-like effects _

80
Q

Transporter defects alkalosis

A

Bartter
Liddle
Gitleman
Salt, water, H loss in all

STEP1 (15 decks)

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