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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
Lab in Pre renal AKI GFR Urea Na and urine osmolality
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.
26
Causes of Pre renal AKI
-Hypovolemic (hemorrhage, D&V diuretics) - Hypervolemic states where there’s a low effective circulating volume. sHF (cardiorenal syndrome). -systemic vasodilation, (sepsis)
27
Lab in Inter renal AKI GFR Urea Na and urine osmolality
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.
28
Causes of inter-renal AKI -damage to the tubules, the glomerulus, or the kidney interstitium (4)
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
29
Drug causes of Renal AKI ATN (7)
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
30
Causes of acute interstitial nephritis (5)
type I or type IV hypersensitivity 1. NSAIDs(analgesic nephropathy) 2.penicillin, 3. Rifampin, 4. PPI'sand 5. Diuretics
31
Acute interstitial nephritis triad
* fever, rash, eosinophilia (rare) arthralgia * mild renal impairment * hypertension
32
Labs/urine: Acute interstitial nephritis
WBC, WCB clasts
33
Labs/urine in ATN
Muddy brown clasts Epithelial cells
34
Outcomes of CKD Electrolytes Lipids and RBC
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
Hyperacute rejection (minutes to hours) - Which anti-'s involved -type of hypersensitivity rnx - Results
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
Acute graft failure (< 6 months) Cause SX/Lab
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
Causes of chronic graft failure (> 6 months)
both antibody & cell-mediated = fibrosis to the transplanted kidney (chronic allograft nephropathy) recurrence of original renal disease (MCGN > IgA > FSGS)
38
Relative importance of HLA antigens in transplant
HLA antigens are as follows DR > B > A
39
Renal transplants CMV infection
20% 6-12wk after transplant
40
Renal transplants CMV infection prophylaxis & rx mild infections
valganciclovir
41
Sx of severe CMV infection & Rx
myocarditis, encephalitis, retinitis ganciclovir
42
Prophylaxis of PJP in renal transplant
co-trimoxazole for 6 mo
43
Drug that alter the blood flow to the Kidney
NSAID Prostaglandins reduce bl to kidney ACEi & ARB- Ciclosporin & Tacrolimus
44
Drugs that have tubular toxicity (ATN)
Aminoglycosides Cisplatin Amphotericin
45
What does lithium desensitizes the kidney's ability to
respond to ADH in the collecting ducts DI (h20 = low, dex= low )
46
ADPKD type 1 gene
chromosome 16 = 85% of cases
47
ADPKD type 2 gene
Chromosome 4, later renal failure
48
Screen in family and Rx of ADPKD
screening investigation for relatives is abdominal ultrasound tolvaptan (vasopressin receptor 2 antagonist)
49
What is a normal anion gap
(sodium + potassium) - (bicarbonate + chloride) A normal anion gap is 8-14 mmol/L
50
management of proteinuria in CKD
ACEi & SGLT-2 inhibitors
51
**Anti-phospholipase A2 antibodies** are associated with
Idiopathic membranous glomerulonephritis
52
renal biopsy demonstrates a thickened basement membrane with subepithelial electron dense deposits on electron microscopy.
membranous glomerulonephritis
53
Membranous glomerulonephritis Causes (5)
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
Extra-renal manifestations of ADPKD
Liver cysts berry aneurysms (8%) Mitral valve prolapse
55
Reduces renal perfusion in HF causes
High levels of aldosterone
56
what causes Causes 'swimmer's itch' Sx risk factor Rx
**Schistosoma haematobium** From snails, flukes - frequency, haematuria. Risk factor for squamous cell bladder cancer Praziquantel
57
What causes Renal cell cancer
* more common in middle-aged men * smoking + obesity * Mutations chrom 3 * von Hippel-Lindau syndrome * tuberous sclerosis
58
Where does Renal cell cancer start
proximal convoluted tubule’s epithelial cells
59
most common type of RCC ?
is a clear cell carcinoma
60
How does RCC led to a left varicocele? & Why cant it happen on the right
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
RCC associated paraneoplastic syndromes
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
Rx RCC
- 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
Calcium phosphate - Ass - Imaging -Urinary acid - Rx
Assoc w/ RTA 1&3, Urinary acid: Normal- alkaline Radio-opaque stones (composition similar to bone) RX : low Na diet & Thiazides
64
Calcium Oxalate stone - Ass - Imaging -Urinary acid - Rx
**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
Urate stones - Ass - Imaging -Urinary acid - Rx
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
Struvite stone/ Magnesium ammonium phosphate - Ass - Imaging -Urinary acid - Rx
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
Cystin Stones - Ass - Imaging -Urinary acid - Rx
in patients with inherited cystinuria Moderately radiopaque Urinary acid : Normal
68
Rx of renal stones
Stones < 5 mm will usually pass spontaneously. Lithotripsy and nephrolithotomy may be for severe cases.
69
When are stones an emergency Rx (3)
Ureteric obstruction + infection =surgical emergency -nephrostomy tube placement, -insertion of ureteric catheters - ureteric stent placement)
70
Wilms tumor/nephroblastoma Mutation
- 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
Causes of painless Hematuria
Transitional Carcinoma of the Bladder Squamous Carcinoma of the bladder
72
Causes of squamous cell carcinoma of the bladder (4)
Scsc
73
Causes of transitional cell carcinoma of the bladder (4)
74
Causes of transitional cell carcinoma of the bladder (4)
75
Rx Minimal change disease
**oral corticosteroids**: majority of cases (80%) respond **cyclophosphamide** is the next step for steroid-resistant cases
76
Renal transplant which HLA matching is most important
DR
77
Diffuse proliferative glomerulonephritis, causes (2)
post-streptococcal SLE
78
Indication for renal replacement

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