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Hard stuff to remember > Renal > Flashcards

Renal Flashcards

1
Q

grade 1 chronic kidney disease description

A
  • eGFR over 90

- urine findings, genetic traits or structural abnormalities which point to kidney disease

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2
Q

grade 2 chronic kidney disease description

A
  • eGFR 60-89
  • mildly reduced kidney function
  • urine findings, genetic traits or structural abnormalities which point to kidney disease
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3
Q

grade 3a and 3b chronic kidney disease description

A
  • G3a = eGFR 45-59
  • G3b = eGFR 30-44
  • moderately reduced kidney function
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4
Q

grade 4 chronic kidney disease description

A
  • eGFR 15-29

- severely reduced kidney function

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5
Q

grade 5 chronic kidney disease description

A
  • eGFR less than 15

- established renal failure

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6
Q

what is a high risk albumin creatinine ratio

A

over 30 mg/mmol

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7
Q

what are the symptoms of uraemia?

A
  • yellow colour of skin
  • uraemic frost
  • twitching (restless legs)
  • confusion
  • encephalopathic flap
  • pericardial rub/effusion
  • kussmaul breathing
  • itch
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8
Q

common diet restrictions in those with CKD

A
  • low salt
  • restricted fluid
  • low K+
  • low phosphorus i.e. no dairy (lots of phosphate in blood leached calcium from bones)

-protein (sometimes, depends on dialysis status)

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9
Q

useful drugs in CKD

A
  • calcium resonium (stops absorption of K+ in GI tract)
  • adcal, aluminium, lanthanum (phosphate binders)
  • alfacalcidol (active vit D to increase calcium absorption)
  • iron supplements
  • sodium bicarbonate (for acidosis)
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10
Q

electrolyte abnormalities in CKD

A
  • hyperkalaemia
  • hypocalcaemia
  • hyperphosphataemia
  • metabolic acidosis (bicarb deficiency)
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11
Q

AKI definition

A

abrupt decline in kidney function:

  • increase in creatinine by 26.4umol/l or more than 50%
  • reduction in urine output

ABOVE CAN ONLY BE APPLIED AFTER ADEQUATE FLUID RESUSCITATION

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12
Q

what are the ECG changes seen in hyperkalaemia

A
  1. tall ‘tented’ T waves
  2. P wave flattens, prolonged PR, depressed ST
  3. broad QRS complexes
  4. sine wave pattern
  5. ventricular fibrillation
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13
Q

what are the indications for dialysis in AKI

A
  • K+ over 7 (or 6.5 post medical intervention)
  • PH under 7.15 (severe acidosis)
  • fluid overload
  • urea over 40 (may cause pericardial effusion)
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14
Q

Man post MI with an AKI. why?

A
  • AKI caused by intra-arterial contrast used in coronary angiogram post MI
  • can reduce risk by giving fluid before and after
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15
Q

main features of nephrotic syndrome

A
  • proteinuria over 3g/day
  • hypoalbuminaemia
  • oedema
  • hypercholesterolaemia
  • increased susceptibility to infection (due to loss of antibodies in urine)
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16
Q

Type of damage in nephrotic syndrome

A
  • podocyte damage

- non-proliferative process

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17
Q

main features on nephritic syndrome

A
  • oliguria (little/no urine output)
  • oedema/fluid retention
  • hypertension
  • haematuria and proteinuria with granular casts
  • AKI
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18
Q

type of damage in nephritic syndrome

A
  • damage to endothelial and mesangial cells

- proliferative

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19
Q

patient intermittent claudication is perscribed ACEI/ARB. Develops an AKI Why?

A
  • he had renal artery stenosis

- kidney now super hypoperfused

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20
Q

side effects of renal artery stenosis

A
  • malignant hypertension due to kidney being hypoperfused and over-activating RAAS
  • flash pulmonary oedema in those with congestive heart failure
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21
Q

features of minimal change disease

A
  • antibodies against podocytes
  • nephrotic syndrome
  • kids
  • biopsy of glomerulus will look pretty normal
  • responds well to steroids
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22
Q

features of focal segmental glomerulosclerosis (FSGS)

A
  • areas of damage
  • risk factors: heroin, HIV, obesity, reflux nephropathy
  • kids and adults can get it
  • responds well to steroids
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23
Q

features of membranous nephropathy

A
  • immune complex deposition in basement membrane
  • often caused by infection e.g. HepB malaria, syphilis
  • also CTD (esp. SLE) , malignancy, drugs
  • respond to steroids, alkylating agents and B cell monoclonal antibodies
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24
Q

features of IgA nephropathy

A
  • misfolded IgA forms complexes that can’t be cleared
  • causes mesangial cell porliferation with IgA deposits
  • worse after resp/GI infections (secretory areas)
  • associate with HSP and coeliac disease
  • nephritic
  • no cure only management or symptoms
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25
Q

features of rapidly progressive glomerulonephritis (RPGN)

A
  • crescent formation
  • associated with vasculitis (ANCA pos and neg), goodpastures, SLE
  • treated with strong immunosuppression and dialysis
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26
Q

Pathophysiology of diabetic glomerulonephritis

A
  1. efferent arteriole becomes stiff/narrow/glycated
  2. pressure inside glomerulus increases
  3. transient increase in GFR before mesangial cells get damaged and secrete extra structural matrix
  4. masangial expansion thickens basement membrane so gaps between podocyte processes gets larger
  5. GFR decreases
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27
Q

classic histology finding associated with diabetic nephropathy

A

kimmelsteil-wilson nodules

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28
Q

Autosomal dominant polycystic kidney disease pathophysiology

A
  • mutation in PKD1 (85%)
  • epithelial cysts arise from small population if renal tubules
  • epithelium of cysts have mutated water channels so cysts get large and larger
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29
Q

what is the defect in Alport syndrome

A
  • defective type IV collagen

- leads to glomerulonephritis, sensorineural deafness and ocular defects

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30
Q

what is Anderson Fabry’s disease?

A
  • inborn error of glycophosphingolipid metabolism (possibly due to misfolded enzymes)
  • wide range of symptoms
  • renal failure
  • angiokeratomas
  • cardiomyopathy/ valvular disease
  • pain in extremities
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31
Q

pathophysiology of medullary cystic kidney

A
  • abnormal renal tubules/collecting ducts
  • cysts form at corticomedullary junction (gives kidney sponge appearance)
  • increased likelihood of developing renal calculi
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32
Q

what is an angiomyolipoma and who is likely to get one?

A
  • benign kidney tumour containing mix of blood vessels, smooth muscle and fat
  • those with tuberous sclerosis
  • main risk is that of haemorrhage
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33
Q

features of an oncocytoma

A
  • benign
  • mahogany brown with central stellate scar
  • cells contain large amounts of mitochondria
  • cells look very similar to that of chomophobe renal cell carcinoma!!
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34
Q

features of clear cell carcinoma

A
  • malignant
  • most common renal cancer
  • bright yellow!
  • cystic with heterogenous surface
  • tendency to invade renal vein, IVC
  • risk factors: VHL, issues with enzymes involved in krebs cycle, obesity
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35
Q

why might someone get a varicocele?

A
  • tumour (in particular clear cell ca) obstructs renal vein and thus gonadal veins
  • more common in left due to asymmetric anatomy
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36
Q

what are some of the other more rare types on renal cell cancer?

A
  • papillary renal cell carcinoma
  • collecting duct renal cell carcinoma
  • mudullary renal cell carcinoma
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37
Q

what is stauffer’s syndrome?

A
  • fever
  • anorexia
  • deranged LFTs
  • link to paraneoplastic syndrome
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38
Q

common paraneoplastic syndromes of renal cell carcinoma

A
  • erythropoietin -> polycythaemia
  • renin/renal artery compression -> hypertension
  • insulin -> hypoglycaemia
  • ACTH -> cushings
  • GnRH -> gynaecomastia, amenorrhea, baldness, reduced libido
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39
Q

usual causes of LUTI

A
  • E.Coli
  • klebsiella
  • enterococcus fecaelis
  • staphylococcus saphrophyticus (young women)
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40
Q

more unusual causes of LUTI (associated with catheter use and structural problems)

A
  • proteus (large stones and bad smell)

- pseudomonas

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41
Q

what antibiotics do you give a pregnant women with asymptomatic bacteriuria

A
  • 1st and 2nd semester -> nitrofurantoin
  • 3rd trimester -> trimethoprim
  • any semester (second line) -> cefalexin
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42
Q

important points when counselling a patient about PSA

A
  • normal PSA does not exclude prostate cancer
  • 65% if raised PSA tests are not due to prostate cancer
  • raised PSA can also be due to things like: BPH, prostatitis, UTI, rectal exam before bloods are taken
  • PSA is still useful though as it can identify prostate cancer up to 6 years earlier
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43
Q

medical treatments for BPH

A
  • alpha blockers e.g. tamsulosin

- S-alpha reductase inhibitors e.g. finasteride

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44
Q

how are prostate cancers graded?

A
  • gleason’s scoring system
  • 6 = low grade
  • 10 = high grade
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45
Q

common metastasis of prostate cancer

A
  • pelvic lymph nodes

- bone -> sclerotic lesions (most other cancers have lytic lesions)

46
Q

most common type of bladder cancer

A

transitional cell carcinoma

47
Q

who is more likely to get SCC of the bladder?

A
  • those with indwelling catheters

- particularly bad is paraplegic as can’t feel there is a problem so Ca presents at late stage

48
Q

what is cryptochidism?

A

having an undescended testicle

49
Q

features of a seminoma

A
  • men in 40s
  • uniform and potato coloured
  • risk factor = having an undescended testes
  • use alkaline phosphatase to monitor
50
Q

features of non-seminomatous testicular cancer + examples of types

A
  • men in 30s (so younger)
  • more aggressive and tendency to metastasise
  • teratoma (3 germ layers)
  • yolk sac
  • embryonal (metastasises v fast)
  • trophoblast
  • choriocarcinoma
51
Q

what may yolk sac tumours produce?

A

alpha feto protein

note hepatocellular carcinoma also produces this

52
Q

what may trophoblast or choriocarcinoma produce?

A

beta HCG

53
Q

which type of testicular cancer is responsive to radiotherapy?

A

seminomas

54
Q

which type of testicular cancer is responsive to chemotherapy?

A

non-seminomatous

55
Q

what is a hydrocele?

A

-accumulation of fluid between tunica vaginalis and mesothelial lining of scrotum

56
Q

what is a spermatocele?

A

cystic change within the vas deferens area (top bit) of the epididymus

57
Q

what is balanitis xerotic obliterans (BXO)?

A
  • lichen sclerosis of the penis
  • can affect foreskin causing phimosis
  • continuous inflammation means its a risk factor for penile SCC
58
Q

where is the most risky place to have penile cancer?

A
  • corpus cavernosum

- rich blood supple to Ca more likely to metastasise

59
Q

what is myeloma?

A
  • unregulated/abnormal proliferation of B cells
  • leads to overproduction of immunoglobulins
  • abnormal plasma cells can accumulate in bone marrow and cause lytic lesions
  • immunoglobulins produced tend to get trapped in glomeruli/renal tubules
60
Q

main features of myeloma

A
  • lytic bone lesions
  • renal dysfunction (pos AKI)/light chain cast nephropathy
  • fatigue
  • weight loss
  • infections
61
Q

tests for myeloma

A
  • urine bence jones protein
  • serum free light chains
  • serum protein electrophoresis
62
Q

how can you manage hypercalcaemia?

A

biphosphonates

-also helpful for osteoporosis

63
Q

what are the 4 main types of amyloidosis?

A
  1. primary light chain (AL) e.g. myeloma?
  2. secondary inflammatory (AA) e.g. RA, IBD, psoriasis
  3. dialysis related (AB2M) (some proteins can’t cross dialysis filter) e.g. 5 years+ of dialysis
  4. hereditary/old age related (ATTR)
64
Q

tests for amyloidosis

A
  • renal biopsy -> congo red staining would show bifringent apple green amyloid under polarised light)
  • abdominal fat pad or rectal biopsy (amyloid commonly collects here)
  • serum amyloid P scan -> shoes areas of amyloid deposits (have to go to london for this)
65
Q

what is cyclophosphamide, when is it used?

A
  • chemotherapy agent and immunosuppressant
  • life threatening autoimmune conditions/states which are not responding to DMARDs (especially lupus nephritis)
  • immediate post transplant immunosuppression
  • sometimes AL amyloidosis
66
Q

medical management of stress incontinence

A

-duloxetine (also SSRI)

67
Q

medical management of urge incontinence

A
  • oxybutynin (alpha blocker)

- mirabegron (B3 adrenoreceptor agonist)

68
Q

what might help success when trialling without a catheter post acute retention

A

-tamsulosin (alpha blocker)

69
Q

what type of stones are radio opaque, how might you investigate for them

A
  • uric acid stones

- non-contrast enhanced CT stone search

70
Q

helpful medication in patients with frequent renal calculi

A
  • thiazide diuretics

- reduce urinary calcium excretion

71
Q

what predisposes men to testicular torsion?

A

bell clapper deformity

-why its important to fix both testes if one torts

72
Q

pathophysiology of non-ischaemic priapism

A
  • traumatic disruption of penile vasculature

- causes unregulated blood entry/filling of corpora

73
Q

pathophysiology of ischaemic priapism

A

-low blood flow/vascular stasis leads to compartment syndrome

74
Q

how to differentiate between ischamic and non-ichemic priapism

A
  • aspirate blood from corpus cavernosum

- look to see if bood is dark (low O2) or normal arterial blood colour

75
Q

what causes emphysematous pyelonephritis

A
  • gas forming uropathogens e.g. E.Coli

- commonly occurs in female diabetics

76
Q

when should you investigate trauma to flanks?

A
  • frank haematuria
  • microscopic haematuria in children
  • any penetrating injury presenting with haematuria
77
Q

what is best investigation for renal trauma

A

CT with contrast!

-show defects in collecting system

78
Q

what is associated with fracture to pubic rami in men?

clinical sign?

A
  • posterior urethral injury

- butterfly perineal haematoma (bruising around scrotum which extends to anus)

79
Q

what are the contraindications of renal biopsy?

A
  • small kidneys
  • uncontrolled hypertension
  • untreated UTI
  • only having one kidney
  • thombocytopaenia

most of above are because of risk of haemorrhage

80
Q

treatment for renal mass less then 3cm

A
  • unless v malignant type then regular follow-up

- tumours less than 3cm rarely metastasise

81
Q

what is cells type of ureters, bladder and proximal urethra

A

transitional epithelium

82
Q

ECF has high conc. of what?

A

Na+

83
Q

ICF has high conc. of what?

A

K+

84
Q

name of less common nephron with long loops of henle

A

juxtamedullary nephrons

85
Q

name of common nephron with short loop of henle

A

cortical

86
Q

what senses Na+ conc. within kidney?

A

macula densa

87
Q

what produces renin within the kidney?

A

granular layer

88
Q

if BP increases what happens to renal arterioles

A

they constrict

89
Q

if more NaCl flows through tubules (eGFR rises) what happens to arterioles

A

constriction of afferent arterioles

90
Q

what does ureteric obstruction do to eGFR?

A
  • decreases it

- due to increased bowman’s capsule fluid pressure

91
Q

what do dehydration do to eGFR?

A
  • decreased it

- decreased capillary hydrostatic pressure

92
Q

what does loss of protein e.g. due to burns do to GFR?

A
  • increases GFR

- decreased capillary oncotic pressure (blood has less pull on fluid)

93
Q

what occurs in proximal convoluted tubule?

A
  • 67% of all Na+ and water are reabsorbed
  • 100% of amino acids and glucose are absorbed
  • NOTE: fluid remains iso-osmotic when is leaves the tubule due to similar amounts of ions and water being excreted/absorbed
94
Q

what occurs in descending limb of loop of henle?

A
  • reabsorption of water

- NO reabsorption of NaCl

95
Q

what occurs in the ascending limb of the loop of henle?

A
  • Na+ and Cl- absorption
  • done by Na+K+Cl- co-transported (the one loop diuretics work on)
  • NO movement of water
96
Q

what are transplant patients given prophylaxis for?

A

-pneumocystis jivorecii pneumonia

97
Q

what could really fuck up a transplant?

A
  • cytomegalovirus

- if donor had had CMV but recipient had not

98
Q

action of aldosterone

A
  • increases Na+ reabsorption

- increase H+/K+ secretion

99
Q

what occurs in the distal tubule?

A
  • NaCl reabsorption
  • H+ secretion
  • Ca2+ reabsorption
  • K+ reabsorption/secretion (aldosterone dependant)
  • NO movement of water and urea
100
Q

what occurs in the collecting ducts

A
  • varying reabsorption of urea and water depending on ADH secretion
  • LOW permeability to ions
101
Q

what is water diuresis?

A

increased urine flow BUT no increased solute excretion

102
Q

what is osmotic diuresis?

A

-increase urine flow WITH increase solute excretion (usually due to failure of Na+ reabsorption)

103
Q

side effect of acidosis

A

-CNS depression

104
Q

side effect of alkalosis

A

-over-excitability of NS and CNS

105
Q

what can be used as buffers in body?

A
  • bicarbonate
  • phosphate
  • ammonia (ammonia travels in blood as glutamine)
106
Q

what inhibits the secretion of ADH?

A

alcohol

107
Q

what enhances the secretion of ADH?

A

nicotine

108
Q

function of prostaglandins on kidney

A
  • secreted when kidney under stress
  • stimulate vasodilation of afferent arteriole (and constriction of efferent through renin)
  • this can help to maintain/increase GFR
109
Q

why is it such a bad idea to give ACEI and NSAIDs to at risk patients

A
  • NSAIDs would block prostaglandins and stop afferent artery vasoconstriction
  • ACEI would block angiotensin II action and stop efferent artery constriction
  • so kidney has no way of maintaining a decent blood pressure for filtration
110
Q

what stage of drug metabolism responsible for most adverse reactions?

A
  • phase 1
  • oxidation, reduction and hydrolysis of compounds
  • done through cytochrome P450 enzyme
111
Q

adverse effect of sulphonamide medication e.g. antibiotics, sulphonylureas

A

-Stevens-Johnson syndrome

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