Renal Flashcards
(223 cards)
In rhabdo the myoglobin is directly nephrotoxic and causes an AKI in what way? Electrolytes in rhabdo? Same as?
Acute tubular necrosis
HyperK, HyperPO4
HypoCa (due to hyperPO4 which causes calcium deposition)
[Same as tumour lysis]
Why DIC in rhabdo
thromboplastin release during muscle damage
3 things that stimulate renin release
HypoNa (in distal convolute tubule by macula densa cells)
HypoVolaemia (detected by afferent arteriole)
Sympathetic stimulation of B1 receptors
RAAS system
Renin converts angiotensin (produced in liver) to angiotensin I.
ACE (produced in lung vasculature) converts Angiotensin I -> Angiotensin II
Effects of angiotensin II on
Vasculature?
Kidney?
Pit?
Nervous system?
Hypothalamus?
Vasculature - binds to g coupled protein -> vasoconstriction,
Kidney - Increases Na reabsorption in proximal convoluted tubule
-Stimulates aldosterone release from the adrenal cortex
-Contstrics efferent arteriole
Pit - Stimulates release of ADH
Nervous system - Release of noradrenaline
Hypothalamus - increases thirst
Where in adrenal cortex is aldosterone released? what does it do?
Zona glomerulosa
Acts on Distal convoluted tubule [Last part of RAAS acts distal]
- Increases Na reabsorption and potassium excretion
-> Increases osmolarity
Glomerular nephritis includes nephrotic (protein loss predominant) and nephritic syndrome (blood predominant). Most common in Kids? Adults? Black adults?
Kids - minimal change disease
Adults - IgA nephropathy (Bergers) disease
Black - FSGN (nephrotic)
Urine protein excretion and albumin levels in nephrotic. Key complications?
Urine >3.5g protein excretion / day
Albumin <25
Thrombosis
hyperlipidaemia
Infection
Kid with minimal change on steroids? Rx of hypertension first line? Steroid sparing agent first line? Bar steroids what other Rx is needed?
ACEi
Cyclophosphamide
Anticoag - Eg enox / warfarin
Bone disease in diabetic patients (especially if on dialysis) ?
Adynamic bone disease
PTH, Ca, PO4 in osteoporosis
NORMAL
Who gets osteitis fibrosis cystica
HyperPTH
Who gets osteitis fibrosis cystica
HyperPTH
What stimulates PTH.
Effects?
Low Ca
Increase Ca from bone.
Less Ca exerted in urine
Stimulates vit D -> Increased Ca absorption from intestines
Vit D in CKD ? Why?
Low - part of hydroxylation process occurs in kidney
Also high PO4 levels suppress
CKD and PTH
Get secondary HyperPTH (low ca)
Or eventually tertiary [high pth high Ca]
1st line phosphate binder (may be used in CKD)
Calcium acetate
CKD statins?
All CKD 3 or over should be on atorvostatin
HTN on thiazide. What are key biochem side effects causing nephropathy? Rx?
Hypercalcaemia, hyperUric acid -> deposition
Change to alternative - eg amlodipine
Why urine dipstick positive for nitrites in UTI?
Bacteria -Eg E coli
Break down nitrates into nitrites in urine
What is pollakiuria?
Increased urinary frequency
Eg in antipsychotic meds
Most common histological type of RCCs
Clear cell adenocarcinoma
Renal tumours, retinal haemangiomas, pancreatic islet cells tunours
Von-hippel lindau
Epithelium from urological Cancer
transitional