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
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
3
Q
Quadratus eumborum
A
Fixes rib during inspiration, stabilizes diaphragm
4
Q
Psoas major
A
Flex hip
Medial posterior ab wall
5
Q
Gonadal v tributary to
A
L- L renal
R-ivc
6
Q
Bladder a
A
Superior and inferior vesicle a
Both from internal iliac a
F- also uterine a
7
Q
Kidney lymph tributary to
A
Para-aortic and para-caval nodes
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
9
Q
Mesangial cells
A
Debris phagocytosis, cytokine secretion,
Blood flow regulation
ECM production
10
Q
Nephrosis nephritis
A
,osis-protein
Itis - blood
11
Q
Macula densa-where
A
DCT
12
Q
Bowman capsule cells
A
Podocyte= visceral epithelial cells
Parietal epithelial cells
13
Q
Renal tubular necrosis causes
A
Drugs
-Radiology contrast
-Aminoglycosides (-mycin/micin)
Hypoxia/ischemic
14
Q
Loop diuretics
A
E.g. Furosemide
Block NaCl reabsorption at thick ascending limb
Sodium diuresis
K wasting
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
16
Q
Thiazide diuretics
A
@Dct
Na and k wasting
17
Q
Ad h target
A
Principal cells @ collecting duct
18
Q
Aldosterone tar yet
A
Principal cells @collecting duct - Na and k
Alpha intercalated cells @collecting duct- acid-base
19
Q
Alpha intercalate cells
A
@Collecting duct
Acid-base
Hco3 reabsorb H+ out
Re: acidosis, aldosterone
20
Q
PT H responsive element
A
Reabsorb Ca @dct
21
Q
Urinary epithelium
A
Transitional
Stratified, impertheable to salt and water
Expands
22
Q
Kidney embryo origin
A
Intermediate mesoderm
23
Q
Provephros
A
Week 4
Primitiveglomeruli
24
Q
Mesonephros
A
Week 4-8/first tri
Interimfiltration
Into mesonephire duct
MD will later become male genitals
25
Metanephros
Week 5 -32+
Ureticduct- me somephric duct outgrowth → collecting tubes, urinary system sans bladder
Metanephric blastema- rest of nephron
26
Kidney ascend
'really rest of embryo moving down
Sacral → lumbar
Week 6-9
27
Cloaca
→ bladder
28
Trigone
Mesonephric duct → trigone → sensation of bladder distention
29
Urachal fistula
Failure of allantois degeneration
Fistula between bladder and umbilicus
30
Pelvic kidney
Umbilical arteries prevent ascent
Complications:
-Reflux, hydronephrosis
- dt ureter obstruction, urinary reflex, improper rotation
31
Horseshoe kidney
Fusion
Inferior mesenteric a-blocksascent
Complication:
- obstruction
- stones
-Infection
32
Amniotic fluid source late gestation
Fetal urine and lung secretions
33
Oligohydramnios
Insufficientamniotic frid '
Lethal if severe
Usually dt kidney agenesis or-malformation or obstruction
34
Potter sequence
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
Alport Syndrome
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
D x Alport
Skin biopsy for collagen
37
Adpkd gene
Pkd1 chr. 16
~80%
Polycystin -1
cAMP → epithelial profiler
Ons-t ~50 y/o
Incomplete penetrance
38
Adpkd clinical
Asymptomatic
Flank pain
Cyst/pyelo E coli
Uric acid stones
RAAS → hy pertenten
Liver cysts
Berry aneurysms
Mitral value prolapse
39
-arpkd gene
Pkhd-1 most common
40
Struvite_stones
~15%
Associated with recurrent upper UTIs with urease producing bacteria
- proteus
- staph
Urine ph>7
Coffin lid
Aka ammonium magnesium phosphate
41
Stones risk factors
Dehydration
Recurrent UTI
Gout
Hyper-pth
Fatty malabsorption - bariatric surgery, IBD
Family Hx
42
Calcium stones
Most common
If high serum Ca high suspicion for hyper-pth
Envelope or dumbbell appearance
43
Urate stones
Tx with-gout agents
Mostly don't have other gout sx
Gout, leukemia, chemo,
Rhomboi d or rosette
44
Stones in type 1 RTA
Usually Ca dt low urine citrate dt kidney not secreting H
45
Stones Tx
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
Allopurinol
Inhibits xanthine oxidase
Prevents hypoxanthine→ xanthine
47
Ace inhibitors
- Sartan
Inhibit angiotensin 2 formation
Efferent arteriole dilation
Benefit of decreasing glomerular pressure > decreased GFR
48
Jg stimuli
- low bp
- low NaCl
- more sympathetic input
49
ANP and BNP
Natriaresis - Na and water
Released by heart
Re: high bp
50
Endotheli n
Made by kidney endothelium
Vasoconstrictor a fferent and efferent
Low RB F and GFR
51
K sparingdiaretics site of action
Proximal collecting duct
52
Acetazolamide
Pct
Carbonic anhydrase inhibitor
Na and hco3 excretion
Weak diuretic
Uses:
- open-angle glaucoma _ intraocular
- serum s ' ickness
53
Loop diuretics
-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
Thiazide diuretics
Na cl symporter @. Dct
Compensatory Na Ca exchanger action → hyper-ca
K wasting
H wasting → alkalosis
Uses:
- First line htn
. Calcium kidney stones
55
Spironolactone
- Aldosteronereceptor blocker @collecting duct
K sparing
H retention → acidosis
Use:
- chf
- liver failure/acites
- Maintain k
- Hyper-aldosterone
- feminizing: PCOS, trans-f
56
Na channel blocker
.inhibit enac - @collecting duct
K sparing
H retention →acidosis
Amiloride
Triamterene
57
Non renal uses CA in hibitors
Respiratory alkalosis _ COPD -, sleep apnea, altitude sickness
Pressure- glaucoma, ICP
Epilepsy- nerve de polarization inhibitor
58
CA inhibitors c/i
acidosis
sulfa allergy
cirrhosis (--> hepatic encephalopathy)
59
SIADH
excess ADH = water retention
hyponatremia
but usually euvolemic (total body water) d/t compensatory water loss by ANP/BNP
cerebral edema - potentially lethal
60
SIADH tx
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
loop diuretics c/I and AEs
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
osmotic diuretics c/i
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
thiazide diuretics e.g.
HCTZ
chlorthalidone
metolazone
indapamide
64
High bicarb
"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
bicarb reabsorbtion Mx
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
Chronic . Hyperkalemia bicarb
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
Isoniazid acid base
High anion gap Metabolic acidosis
68
Met formin acid base
High anion gap metabolic acidosis
69
Methanol acid base
High anion gap metabolic acidosis
Dt Formic acid
70
Uremia acid base
Metabolic acidosis
Low gfr → low acid secretion
71
Ingestions acidosis
Ethylene glycol
Propylene glycol
Methanol
72
Drugs acidosis
Isoniazid
Met formin
Salicylates - aspirin (starts with respiratory alkalosis fromhyperventilation then salicylic acid acidosis sets in)
73
Normal anion gap metabolic acidosis
Bicarb loss dt:
- diarrhea
- proximal RTA (type 2) -
Both are hypokalemic
H buildup dt:
- distal and hyperkalemic RTA (1 and 4)
74
Type 2 RTA
Proximal tubule
Hypo - K
Mild acidosis
Impaired bicarb reabsorbtion
Dt:
- acetezolamide
- other drugs/toxins
- excess ig -multiple myeloma
- fanconi syx - pan pct failure
75
Type 1 RTA
Distal
Failed H excretion @ collecting duct
Can be severe
Dt:
- interstitial CKD
-Amphoterrible
- lithium
- lupus
- sjorgen
- amyloidosis
76
Type 4 rta
Hyperkalemi c
Most common
Failed ammonia/um excretion@ pct
Mild acidosis
Dt:
- low aldosterone
-E.g. Low renin in diabetics
77
Fomepizole
Alcohol dehydrogenase inhibitor
Methane and glycol tox
78
When to give bicarb
Normal anion gap metabolic acidosis
79
Enzyme defects metabolic alkalosis
11-b-hydroxyls e and 17-a- hydroxyls e, which result in *high_mineralecorticoids and aldosterone-like effects _
80
Transporter defects alkalosis
Bartter
Liddle
Gitleman
Salt, water, H loss in all
