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MRCP Master > Renal: General > Flashcards

Renal: General Flashcards

1
Q

GPA ass renal finding

A

Pauci-immune crescentic glomerulonephritis

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2
Q

Muddy brown granular casts indicate

A

Acute tubular necrosis

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3
Q
  1. rash,
  2. fever and
  3. eosinophilia
    urine sediment, if present, = WBC (and/or red cell) casts/pyuria.
A

interstitial nephritis

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4
Q

Bartter’s syndrome
- What is defective & where
-inheritance
- Results
-What drug acts like this

A

Bartter’s syndrome
AR
- defective Cl- absorption at the Na+ K+ 2Cl- cotransporter (NKCC2)
- ascending loop of Henle
HYPO K -normotension-
metabolic alkalosis

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5
Q

Where do Loop work
MOA
Examples
SE

A

Ascending Loop of Henle
Na/K cotransporter blked

  • ide-Bumetanide , Ethacrynic acid,
    Furosemide ,Torsemide
    -HypoNa & HypoK
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6
Q

Gitelman syndrome
- What is defective & where
-inheritance
- Results
-What drug acts like this

A

Defect NaCL cotransporter in the DCT
-AR
HypoK + Norm tension
metabolic ALKalosis.
hypocalciuria/ hyperCa2+

Thiazides - HyperGluc

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7
Q

Causes of Hypok with htn

A

Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Liddle’s syndrome
11-beta hydroxylase deficiency*

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8
Q

Hypokalaemia without hypertension

A
  1. diuretics
  2. GI loss (e.g. Diarrhoea, vomiting)
    renal tubular acidosis (type 1 and 2**)
  3. Bartter’s syndrome
  4. Gitelman syndrome
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9
Q

What does HyperGLUC stand for

A

Hyper: Glucose, Lipids, Uremia, Ca2
SE of thiazides

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10
Q

SE thiazides
And site of action

A

Hyper: Glucose, Lipids, Uremia, Ca2
HypoK + metabolic ALKalosis
-DCT
NaCl cotransporter

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11
Q

Liddle syndrome
- What is defective & where
-inheritance
- Results
-What drug acts like this

A
  • Collecting ducts
    -AD
  • Hypo K with HTN & Metabolic alkalosis
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12
Q

Fanconi Syn
where does it effect
Hereditary causes
Acquired
Drug

A

-PCT defect
Causes
- Hereditary: Wilsons, tyrosinemia, Glycogen storage disorders
- Acquired: Ischemia, MM
- Drug :Cisplatin, expired tetracyclines, Ifsofamine

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13
Q

Where do N/K transporter work

A

Ascending loop of Henle
(Defect batters)

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14
Q

Where do Nacl cotransporters work

A

DCT
(Gitelmen syn)

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15
Q

What is reabsorbed in PCT
( nep–>cir)

A

Lipids
Small proteins
HCO3-
H2O
Glucose -100%
Na- 65%
K- 60%
CL- 60%
Urea -50%

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16
Q

What is reabsorbed in DLOH

A

H20

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17
Q

What is reabsorbed in thick ascending loop of Henle
Defect and drugs

A

reabsorbs K, Cl & Na
via Na/K/Cl, cotransporter or NKCC2,
Bartter’s
Loops

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18
Q

What is reabsorbed in DCT
Defect
Drug

A

reabsorbs Na, Cl-, Via a Na -Cl cotransporter,
as well as Ca2+ & mg.
- Gitelman
- Thiazide

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19
Q

Causes Respiratory acidosis (4)
Hypoventilation

A
  • decompensation resp d e.g. life-threatening asthma / pulmonary oedema
  • neuromuscular disease
  • obesity hypoventilation syndrome
  • sedative drugs: benzodiazepines, opiate overdose
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20
Q

Causes Respiratory Alkalosis (4)
Hyperventilation

A

due to hyperventilation
- normal pregnancy
- hysteria
- hypoxemia (e.g., high altitude)
- salicylates (early)
- PE
- pneumonia
CNS disorders: stroke, SAH, encephalitis

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21
Q

normal anion gap metabolic acidosis
(Normal Hardass)

A

Hyperalimentation
Addison’s disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
mnemonic: HARDASS

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22
Q

Elevated anion gap metabolic acidosis
(elevated mudpiles )

A

Methanol (formic acid)
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets or isoniazid
Lactic acidosis (such as by metformin toxicity)
Ethylene glycol
Salicylates (late)

mnemonic: MUDPILES

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23
Q

PH

A

HCO3/CO2

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24
Q

Explain metabolic Acidosis with resp compensation

A

Is this what you expect to happen to this PH:

Low PH = acidosis

HCO3 (metabolic) is proportional to PH thus if decreased = met acid

CO2 (respiratory) is inversely proportional you would expect a rise; if it isn’t then compensation.

PH always matches the primary defect

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25
Q

Lab in Pre renal AKI
GFR
Urea
Na and urine osmolality

A

Pre renal
Decrease bl. Flow = decrease GFR

less urea and creatinine are filtered out, and more stays in the blood, so levels of BUN and creatinine will be high.
aldosterone (low bp)= reabsorb sodium= Na reabsorption is also tied to urea reabsorption, = urea gets reabsorbed and so even more urea gets into the blood = > 20:1 creat
Na is retained, = urine Na is < 20 mEq/L
urine is more concentrated (less water excreted) urine’s > 500 milliosmoles per kilogram.

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26
Q

Causes of Pre renal AKI

A

-Hypovolemic (hemorrhage, D&V diuretics)
- Hypervolemic states where there’s a low effective circulating volume. sHF (cardiorenal syndrome).
-systemic vasodilation, (sepsis)

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27
Q

Lab in Inter renal AKI
GFR
Urea
Na and urine osmolality

A

Hindered reabsorption
Urea isn’t reabsorbed = less urea stays in the blood relative to creatinine, and the BUN: creatinine ratio < 20:1
NA NOT reabsorb =urine Na+ >40 mEq/L

H20 not reabsorbed = urine osmolality falls below 350 mOsm/kg.

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28
Q

Causes of inter-renal AKI
-damage to the tubules, the glomerulus, or the kidney interstitium (4)

A
  1. Mainly ATN (prolonged ischemia & Nephrotoxins )
  2. acute interstitial nephritis
  3. infections -Mycoplasma
  4. autoimmune conditions,
    Sjogren syndrome, sarcoidosis or SLE
  5. acute glomerulonephritis
  6. HUS
  7. diffuse cortical necrosis -Combination of vasospasm & DIC
  8. renal papillary necrosis- ass. SS
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29
Q

Drug causes of Renal AKI ATN (7)

A

1.contrast dyes,
2. aminoglycosides
3. cisplatin,
4. heavy metals like lead,
5. myoglobin (rhabdomyolysis),
6. ethylene glycol
7. radiocontrast dye, and hemoglobinuria
Think: Heave metal signer drinking ethylene glycol

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30
Q

Causes of acute interstitial nephritis (5)

A

type I or type IV hypersensitivity
1. NSAIDs(analgesic nephropathy)
2.penicillin,
3. Rifampin,
4. PPI’sand
5. Diuretics

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31
Q

Acute interstitial nephritis triad

A
  • fever, rash, eosinophilia (rare)
    arthralgia
  • mild renal impairment
  • hypertension
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32
Q

Labs/urine: Acute interstitial nephritis

A

WBC, WCB clasts

33
Q

Labs/urine in ATN

A

Muddy brown clasts
Epithelial cells

34
Q

Outcomes of CKD
Electrolytes
Lipids and RBC

A
  1. Lose H+, K+,
    –High serum phosphate (as not excreted) = low Ca lead to high PTH
    retain Na and H20 (= oedema, HTN, HF peri& lung oedema),
    Uremia (asterixis, encephalopathy )
    * Increase in Lipids
    * Reduced production of EPO = Bone marrow not stim to produce RBC = normocytic normochromic anemia additionally they have an iron deficiency note rx EPO = increased bl. Pressure
35
Q

Hyperacute rejection (minutes to hours)
- Which anti-‘s involved
-type of hypersensitivity rnx
- Results

A

Hyperacute rejection (minutes to hours)
- pre-existing antibodies against ABO or HLA antigens
-Type II hypersensitivity

=widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ
Rx: graft must be removed

36
Q

Acute graft failure (< 6 months)
Cause
SX/Lab

A
  1. mismatched HLA. Cell-mediated (cytotoxic T cells)
    usually asymptomatic ;rising creatinine, pyuria & proteinuria
  2. cytomegalovirus infection

may be reversible with steroids and immunosuppressants

37
Q

Causes of chronic graft failure (> 6 months)

A

both antibody & cell-mediated = fibrosis to the transplanted kidney (chronic allograft nephropathy)
recurrence of original renal disease (MCGN > IgA > FSGS)

38
Q

Relative importance of HLA antigens in transplant

A

HLA antigens are as follows DR > B > A

39
Q

Renal transplants CMV infection

A

20%
6-12wk after transplant

40
Q

Renal transplants CMV infection prophylaxis & rx mild infections

A

valganciclovir

41
Q

Sx of severe CMV infection & Rx

A

myocarditis, encephalitis, retinitis
ganciclovir

42
Q

Prophylaxis of PJP in renal transplant

A

co-trimoxazole for 6 mo

43
Q

Drug that alter the blood flow to the Kidney

A

NSAID Prostaglandins reduce bl to kidney
ACEi & ARB-
Ciclosporin & Tacrolimus

44
Q

Drugs that have tubular toxicity (ATN)

A

Aminoglycosides
Cisplatin
Amphotericin

45
Q

What does lithium desensitizes the kidney’s ability to

A

respond to ADH in the collecting ducts
DI (h20 = low, dex= low )

46
Q

ADPKD type 1 gene

A

chromosome 16 = 85% of cases

47
Q

ADPKD type 2 gene

A

Chromosome 4, later renal failure

48
Q

Screen in family and Rx of ADPKD

A

screening investigation for relatives is abdominal ultrasound
tolvaptan (vasopressin receptor 2 antagonist)

49
Q

What is a normal anion gap

A

(sodium + potassium) - (bicarbonate + chloride)

A normal anion gap is 8-14 mmol/L

50
Q

management of proteinuria in CKD

A

ACEi & SGLT-2 inhibitors

51
Q

Anti-phospholipase A2 antibodies are associated with

A

Idiopathic membranous glomerulonephritis

52
Q

renal biopsy demonstrates a thickened basement membrane with subepithelial electron dense deposits on electron microscopy.

A

membranous glomerulonephritis

53
Q

Membranous glomerulonephritis Causes (5)

A
  1. idiopathic: due to anti-phospholipase A2 antibodies
  2. infections: hepatitis B, malaria, syphilis
  3. malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
  4. Drugs: gold, penicillamine, NSAIDs
  5. Autoimmune diseases: SLE (class V disease), thyroiditis, RA
54
Q

Extra-renal manifestations of ADPKD

A

Liver cysts
berry aneurysms (8%)
Mitral valve prolapse

55
Q

Reduces renal perfusion in HF causes

A

High levels of aldosterone

56
Q

what causes Causes ‘swimmer’s itch’
Sx
risk factor
Rx

A

Schistosoma haematobium
From snails, flukes
- frequency, haematuria. Risk factor for squamous cell bladder cancer
Praziquantel

57
Q

What causes Renal cell cancer

A
  • more common in middle-aged men
  • smoking + obesity
  • Mutations chrom 3
  • von Hippel-Lindau syndrome
  • tuberous sclerosis
58
Q

Where does Renal cell cancer start

A

proximal convoluted tubule’s epithelial cells

59
Q

most common type of RCC ?

A

is a clear cell carcinoma

60
Q

How does RCC led to a left varicocele?
& Why cant it happen on the right

A

RCC invades the left renal vein, then the venous drainage of the left testis is blocked, leading to a varicocele.

his can never happen on the right side, because the venous drainage from the right testis goes directly into the inferior vena cava.

61
Q

RCC associated paraneoplastic syndromes

A
  1. Erythropoietin=polycythaemia,
  2. PThr =hypercalcaemia,
  3. Renin= HTN,
  4. ACTH= cushing syndrome

Stauffer syndrome.-paraneoplastic hepatic dysfunction syndrome. Typically presents as cholestasis/hepatosplenomegaly. It is thought to be secondary to increased levels of IL-6

62
Q

Rx RCC

A
  • surgery or ablation of the tumor can be done.
    If there’s metastasis, then immunotherapy with aldesleukin or targeted therapy can be done in selected cases.
63
Q

Calcium phosphate
- Ass
- Imaging
-Urinary acid
- Rx

A

Assoc w/ RTA 1&3,
Urinary acid: Normal- alkaline
Radio-opaque stones (composition similar to bone)
RX : low Na diet & Thiazides

64
Q

Calcium Oxalate stone
- Ass
- Imaging
-Urinary acid
- Rx

A

Most common cause of stones

Risk factors: Hypercalciuria, Hyperoxaluria, Hypocitraturia (citrate forms complexes with ca2+ making it more soluble)
- radio-opaque

  • associated w/ short bowel syndrome, antifreeze, vitamin C abuse

Urinary acid : Variable
Rx: Thiazide diuretics Potassium citrate, low Na diet
* cholestyramine reduces urinary oxalate secretion
* pyridoxine reduces urinary oxalate secretion

65
Q

Urate stones
- Ass
- Imaging
-Urinary acid
- Rx

A

Caused: d’s w/ extensive tissue breakdown/turnover e.g. malignancy, gout, Dehydration, leukaemia, children with inborn errors of metabolism
Urinary acid: Acid

Radiolucent (No seen)

Rx: Alkalinization (bicarb) of urine, allopurinol

66
Q

Struvite stone/ Magnesium ammonium phosphate

  • Ass
  • Imaging
    -Urinary acid
  • Rx
A

Presents as infection formed by urea-splitting bacteria,
-Proteus,
-Staph saprophyticus,
- klebsiella

Often staghorn calculi =chronic obstruction and failure to clear UTI adequately

Urinary acid : Alkaline

Radiopaque

67
Q

Cystin Stones
- Ass
- Imaging
-Urinary acid
- Rx

A

in patients with inherited cystinuria

Moderately radiopaque
Urinary acid : Normal

68
Q

Rx of renal stones

A

Stones < 5 mm will usually pass spontaneously.
Lithotripsy and nephrolithotomy may be for severe cases.

69
Q

When are stones an emergency
Rx (3)

A

Ureteric obstruction + infection =surgical emergency
-nephrostomy tube placement,
-insertion of ureteric catheters
- ureteric stent placement)

70
Q

Wilms tumor/nephroblastoma
Mutation

A
  • early childhood and appears between the ages of 2 to 4.
  • The tumor contains embryonic glomerular structures
  • mutations of tumor suppressor genes WT1 and WT2 on chrom 11
71
Q

Causes of painless Hematuria

A

Transitional Carcinoma of the Bladder
Squamous Carcinoma of the bladder

72
Q

Causes of squamous cell carcinoma of the bladder (4)

A

Scsc

73
Q

Causes of transitional cell carcinoma of the bladder (4)

A
74
Q

Causes of transitional cell carcinoma of the bladder (4)

A
75
Q

Rx Minimal change disease

A

oral corticosteroids: majority of cases (80%) respond
cyclophosphamide is the next step for steroid-resistant cases

76
Q

Renal transplant which HLA matching is most important

A

DR

77
Q

Diffuse proliferative glomerulonephritis, causes (2)

A

post-streptococcal
SLE

78
Q

Indication for renal replacement

A

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