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Internal Medicine > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Thiazide action

A

On distal convoluted tubule

Block NaCl symporter

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2
Q

Furosemide

A

On loop of Henle

Block NaK2Cl channel

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3
Q

Spironolactone

A

On collecting duct

Competitive antagonist of aldosterone

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4
Q

Amiloride

A

On collecting duct

Directly blocking Na channel

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5
Q

Glomerular filtraction rate

A

120mL/min

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6
Q

Renal autoregulation mechanisms

A

Myogenic mechanism: local release of vasoactive factors in response to perfusion (afferent arteriole)
Tubuloglomerular feedback: Na conc changes in macula densa lead to changes in afferent arteriolar tone

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7
Q

Renin

A

Released by JGA, converts angiotensinogen to angiotensin I.

Stimulated by:
Decrease stretch in afferent arteriole
JG cell B sympathetic nerve stimulation
Low Na at macula densa

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8
Q

ACE

A

Produced in the lungs, converts angiotensin I to angiotensin II

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9
Q

Angiotensin II effects

A 
Vasoconstriction
Increase vascular smooth muscle growth
Increase Na reabsorption
Increase aldosterone
Increase bicarbonate products
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10
Q

Aldosterone

A

Minerocorticoid produced by the adrenal.

Acts on CT, stimulates Na retention and K excretion

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11
Q

Hypervolaemic hyponatraemia

A

Low urinary Na: CHF, cirrhosis, ascites, pregnancy

High urinary Na: ARF, CRF

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12
Q

Euvolemic hyponatraemia

A

High urine osmolality: SIADH, adrenal insufficiency, hypothyroidism

Low urine osmolality: psychogenic polydipsia

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13
Q

Hypovolaemic hyponatraemia

A

High urinary Na: diuretics, salt-wasting nephropathy

Low urinary Na: diarrhea, excessive sweating, third space

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14
Q

Iso-osmolar or Hyperosmolar hyponatraemia

A

Pseudohyponatraemia (severe hyperlipidaemia, paraproteinemia)
Hyperglycaemia
Mannitol

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15
Q

SIADH criteria

A

Urine inappropriately concentrated for serum osmolality
High urinary sodiem (>20mmol/L)
High FEna

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16
Q

SIADH disorders

A

Tumour: small cell Ca, bronchogenic Ca, pancreatic adenoca, Hodgkin’s disease, thyoma

Pulmonary: pneumonia, lung abscess, TB, acute respiratory failure, positive pressure ventilation

CNS: mass lesion, encephalitis, subarachnoid haemorrhage, stroke, head trauma, acute psychosis, acute intermittent porphyria

Drugs: antidepressants, antineoplastics, carbamazepine, barbituates, oxytocin

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17
Q

Diabetes insipidus

A

Deficit of ADH release or renal response to ADH. Acts on collecting tubules to reabsorb water.
Diagnosis: dehydration test, desmopressin test

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18
Q

Hypokalaemia ECG

A

U waves
Flattened or inverted T waves
depressed ST segment
Prolongation of QT segment

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19
Q

Hypokalemia (cellular redistribution)

A

Metabolic alkalosis (K/H exchange)
Insulin (Na/K/ATPase)
Catecholamines, beta agonists (Na/K/ATPase)
Tocolytic agents
New cellular growth (treatment of pernicious anaemia)

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20
Q

Hypokalemia (GI causes)

A

GI losses: diarrhea, laxatives, villous adenoma

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21
Q

Hypokalemia (hypertensive renal losses)

A

1* hyperaldosteronism: Conn’s syndrome,
2* hyperaldosteronism: Renovascular disease, renin tumour,
Non-aldosterone: Cushings’s

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22
Q

Hypokalemia (normotensive, based on pH)

A

Acidemic: DKA, RTA
Variable: hypomagnesium, vomiting
Alkalemic: diuretics, Bartter’s, Gitelman’s

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23
Q

Hyperkalemia ECG

A 
Peaked and narrow T waves
Decreased amplitude of P waves
Prolonged PR interval
Widening QRS and T wave merging
AV block
Ventricular fibrillation
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24
Q

Hyperkalemia causes

A

Increased intake: diet, KCl tablets, IV KCl
Cellular release: intravascular hemolysis, rhabdomyolysis, insulin deficiency, hyperosmolar, metabolic acidosis (except keto and lactic), tumour lysis syndrome, drugs (beta blockers, digitalis overdose, succinylcholine)
Decreased excretion: renal failure, hypovolaemia, NSAIDs in renal insufficiency, hypoaldosteronism.

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25
Q

Hyperkalemia - normal GFR with decreased K excretion

A

Decreased aldosterone stimulus (low renin, low aldosterone):
hyporeninemic, hypoaldosteronism, DM2, NSAIDs, chronic interstitial nephritis

Decreased aldosterone production (normal renin, low aldosterone):
adrenal insufficiency, ACEi, ARBs, heparin, congenital adrenal hyperplasia with 21-hydroxylase deficiency

Aldosterone resistance (decreased tubular response):
K sparing drugs (spironolactone, amiloride), renal tubular disease, trimethoprim, cyclosporin, tacrolimus
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26
Q

Hyperkalemia treatment

A

Heart protection: Calcium gluconate
Intracellular K shift: insulin, NaHCOs, salbutamol
Enhance K removal: furosemide, dialysis

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27
Q

Anion gap

A

AG = Na - (HCO + Cl)

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28
Q

Osmolar gap

A 
OG = measured osmolality - calculated osmolality
CO = 2xNa + urea + glucose
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29
Q

Anion gap metabolic acidosis (KARMEL)

A 
Ketoacidosis
Aspirin
Renal failure
Methanol
Ethylene glycol
Lactic acid
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30
Q

Non-anion gap metabolic acidosis

A

Diarrhea

Renal tubular acidosis

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31
Q

Renal infarction

A

Acute renal artery occlusion - trauma, surgery, embolism, vasculitis

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32
Q

Renal artery stenosis

A 
Atherosclerotic plaques (90%) - proximal 1/3 renal artery
Fibromuscular dysplasia (10%) - distal 2/3 renal artery, in young females
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33
Q

Renal vein thrombosis

A

Hypercoagulable states (nephrotic syndrome), ECF depletion, malignancy, extrinsic compression

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34
Q

Small vessel renal disease

A

Hypertensive nephrosclerosis
Atheroembolic renal disease
Thrombotic microangiopathy (HUS, TTP, DIC, preeclampsia)
Calcineurin inhibitor nephropathy (cyclosporine and tacrolimus)

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35
Q

Nephrotic Syndrome

A

Proteinuria, hypoalbumina, oedema, hyperlipidaemia (raised LDL, fatty casts in urine), hypercoagulability (antithrombin III, protein C + S urinary loss).
Frothy urine

FSGS
Membranous glomerulopathy
Minimal change

36
Q

Nephritic Syndrome (PHAROH)

A 
Proteinuria
Hematuria
Azotemia
RBC casts
Oligouria
Hypertension
37
Q

Proteinuria - physiologic

A 
Orthostatic
Transient (exercise, fever)
38
Q

Proteinuria - tubulointerstitial

A

Impaired resorption: Fanconi’s syndrome

39
Q

Proteinuria - glomerular

A

Primary: minimal change, membranous, FSGS, mebrano-proliferative, PSGN, IgA nephropathy

Secondary: systemic (SLE, diabetes, vasculitis), infectious (HIV, Hep B/C, IE), herefitary (Alport’s, Fabry’s sickle cell, PCKD)
drugs (NSAIDs, gold, heavy metals), cancer (lymphoma, solid tumour), others (cryoglobulinemia)

40
Q

Proteinuria - overflow

A

Overproduction of LMW proteins: multiple myeloma, amyloidosis, Waldenstrom’s macroglobinemia

41
Q

RPGN I - anti-GBM mediated

A

Linear immunofluresence with IgG and C3 deposition along capillary loops:
Lung haemorrhage = Goodpasture’s disease
No lung haemorrhage = Anti-GBM disease

42
Q

RPGN II - immune complex mediated

A

Granular pattern with subendothelial or subepithelial deposits of IgG and C3:
C3 normal = IgA nephropathy, HSP
Decreased C3 = membranoproliferative GN, SLE, IE, PSGN, cryoglobinemia

43
Q

RPGN III - non-immune mediated

A

Pauci-immune, no immune staining, ANCA +ve:
c-ANCA = Wegener’s granulomatosis
p-ANCA = Churg-Strauss, microscopic polyangitis

44
Q

Red urine

A

-ve dipstick, -ve RBC: beets, rifampicin
+ve dipstick, -ve RBC: myoglobin/rhabdomyolysis
+ve dipstick, +ve RBC: hemaglobin

45
Q

Hematuria

A

Hematological: coagulapathy, sickle cell

Urologic: nephrolithiasis, trauma, tumour, prostatitis, urethritis

Renal:
Primary - membranoproliferative, PSGN, RPGN, interstitial nephritis, papillary necrosis, IgA nephropathy
Secondary - CTD (Wegener’s, Goodpastures, SLE, Churg-Strauss, HSP), infection (pyelonephritis), hereditary (Alport’s PCKD)

46
Q

Acute nephritic syndrome

A

Subset of nephritic syndrome, proceeds over days

Clinical features: PHAROH

47
Q

Rapidly progressive gomerulonephritis (RPGN)/ cresenteric glomerulonephritis

A

Subset of nephritic syndrome, proceeds over weeks to months.

Fibrous cresents typically seen on histology, RBC casts.

48
Q

RPGN IV - double antibody positive

A

Has features of type I + III (anti-GBM + ANCA)

49
Q

Asymptomatic urinary abnormalities

A

Isolated proteinuria - postural

Isolated hematuria - IgA nephropathy, Alport’s (X-linked), thin membrane disease (AD), exercise, febrile illness

50
Q

Minimal change

A

2nd causes: Hodgkin’s lymphoma
Drug causes: NSAIDs
Rx: Steroids

51
Q

Membranous glomerulonephropathy

A

2nd causes: HBV, SLE, solid tumours
Drug causes: gold, penicillamine
Rx: decrease BP, ACEi, steroids

52
Q

Focal segmental glomerulosclerosis

A

2nd causes: reflux nephropathy, HIV, HBV, obesity
Drug causes: heroin
Rx: steroids, ACEi/ARB for proteinuria

53
Q

Membranoproliferative glomerulonephritis

A

2nd causes: HCV, malaria, SLE, leukemia, lymphoma, infected shunt
Rx: aspirin, ACEi

54
Q

Nodular glomerulosclerosis

A

2nd causes: diabetes, amyloidosis

Rx: treat underlying cause

55
Q

Amyloidosis

A

Deposits of amyloid in mesangium (amyloid light chains). Presents as nephrotic proteinuria with progressive renal insufficiency.

56
Q

Systemic Lupus Erythematous

A

Deposition of immune complex in glomerulus. Present with nephrotic syndrome/nephritis, low complement levels, ANA, RF and anti-dsDNA positive.

57
Q

Henoch-Schonlein purpura

A

Commonly in children. Present with purpura on buttocks and legs, abdominal pain, arthralgia, fever. IgA and C3 staining.
Benign and self-limiting, 10% progress to CKD

58
Q

Goodpasture’s disease

A

Antibodies against type IV collagen (lungs and GBM).
Present with RPGN I and hemoptysis.
Treat with plasma exchange, cyclophosphamide, prednisone.

59
Q

Wegener’s granulomatousis

A

80% with renal involvement, c-ANCA positive. Treat cyclophosphamide, prednisone.

60
Q

Cryoglobulinemia

A

Monoclonal IgM and polyclonal IgG. Presents with purpura, fever, Raynaud’s arthralgias, 50% Hep C.
Treat hep C, plasmapheresis

61
Q

Infectious related renal disease

A 
HIV
Infective endocarditis
Hep B
Hep C
Syphilis
Malaria
62
Q

Acute tubulointerstitial nephritis

A

Acute inflammatory infiltrates into renal interstitium, rapid (days to weeks) decline in renal function.
Present: AKI, hypersensitivity reaction, pyelonephritis

Etiology:
Hypersensitivity - antibiotics, NSAIDs, allopurinol, furosemide, thiazides, PPIs, phenytoin
Infection - bacterial pyelonephritis, strept, brucellosis, legionella, CMV, EBV, toxoplasmosis
Immune - SLE, acute allograft rejection, Sjogren’s, sarcoidosis

63
Q

Chronic tubulointerstitial nephritis

A

Fibrosis of interstitium with atrophy of tubules, mononuclear cell inflammation. Slow progressive renal failure, moderate proteinuria and signs of abnormal tubule function

Etiology: UT obstruction, chronic pyelonephritis, nephrotoxins, vascular disease (ischemic, atheroembolic), malignancies (MM, lymphoma), granulomatous, immune (SLE, Sjogren’s, cryoglobulinemia, Goodpasture’s, amyloidosis, vasculitis), hereditary (PCKD, sickle cell)

64
Q

Acute tubular necrosis

A

Abrupt and sustained decline of GFR within days after ischaemic/nephrotoxic insult.
Present: abrupt rise in urea and Cr after initial insult.
Complications: hyperkalaemia, metabolica acidosis, decreased Ca, increased PO, hypoalbuminemia.

65
Q

ATN - toxins

A 
Exogenous
Antibiotics: aminoglycosides, cephalosporins, amphotericin B
Antiviral
Antineoplastic: cisplatin, methotrexate
Contrast media
Heavy metals

Endogenous
Endotoxins
Myoglobin
Hemoglobin

66
Q

ATN - ischaemia

A 
Decreased circulating volume:
Hemorrhage
Skin losses
GI losses
Renal losses
Decrease effective circulating volume:
Heart failure
Liver failure
Sepsis
Anaphylaxis

Vessel occlusion

67
Q

Analgesic nephropathies

A

Vasomotor acute kidney injury - NSAIDs decrease prostaglandin, renal ischemia

Acute interstitial nephritis - fenopren, ibuprofen, naproxen causes nephrotic proteinuria

Chronic interstitial nephritis - excessive paracetamol + NSAID consumption, causes papillary necrosis (hematuria, flank pain, decrease GFR)

Acute tubular necrosis - paracetamol overuse, spontaneous recovery in 4 weeks

Other effects - Na retention, hyperkalemia, HTN, excess water retention

68
Q

Diabetic renal complications

A

Albuminuria (ACR). Renal function declines once macroalbuminuria is established, progressing to ESRD in 50% by 7-10 years.

Progressive glomerulosclerosis:
Kimmelstiel-Wilson nodular lesions, increase in mesangial matrix with diffuse glomerular sclerosis. 
Stage 1 - increased GFR, compensatory
Stage 2 - microalbuminuria, ACR 2-10
Stage 3 - macroalbuminuria, ACR >20
Stage 4 - ESRD

Accelerated atherosclerosis:
Common finding

Autonomic neuropathy:
Bladder functional obstruction and urinary retention

Papillary necrosis:
Type 1 DM susceptible to ischaemic necrosis of meullary papillae

69
Q

Scleroderma renal involvement

A

Mild proteinuria, high Cr, HTN

Rx: BP control with ACEi

70
Q

Multiple myeloma nephropathy

A 
Kidney damage mechanisms: 
Hypercalcemia
Light chain cast nephropathy (LCCN - large casts light chains + Tamm-Horsfall protein)
Hyperuricemia
Infection
Secondary amyloidosis
Monoclonal Ig deposition disease (MIDD - nodular glomerulosclerosis)
Diffuse tubular obstruction

Features: Bence-Jones proteins

71
Q

Multiple myeloma (CARLI)

A 
Calcium
Anemia
Renal failure
Lytic bone lesions
Infections
72
Q

Malignancy - renal involvement

A

Solid tumours: mild proteinuria, membranous GN
Lymphoma: minimal change (Hodgkin’s), membranous (non-Hodgkin’s)
Renal cell carcinoma
Tumour lysis syndrome: hyperuricaemia, diffuse tubular obstruction
Chemotherapy (cisplatin): ATN or chronic TIN
Pelvic tumours: obstruction
Secondary amyloidosis
Radiotherapy

73
Q

Hypertensive nephrosclerosis

A

Chronic nephrosclerosis: slow vascular sclerosis with chronic hypertensive disease.

Malignant nephrosclerosis: fibrinoid necrosis of arterioles, acute BP elevation, HTN encephalopathy

74
Q

Adult polycystic kidney disease

A

AD involvement of PKD1, PKD2, PKD3.
Extrarenal manifestations: hepatic cysts, cerebral aneurysm, diverticulosis, mitral valve prolapse.
Common complications: UTI, HTN, CRF, nephrolithiasis, flank and chronic back pain

75
Q

Medullary sponge kidney

A

AD multiple cystic dilitations in CT or medulla.

Complications: renal stones, hematuria, recurrent UTIs, nephrocalcinosis

76
Q

Autosomal recessive polycystic kidney disease

A

Prenatal diagnosis by enlarged kidneys, perinatal death from respiratory failure.

77
Q

Acute kidney injury

A

Abrupt decline in kidney function leading to increase urea.

78
Q

AKI - prerenal causes

A

Disordered regulation:
NSAIDs, ACEi, Calcineurin inhibitors, hypercalcemia

Hypovolaemia:
Hemorrhage, GI loss, skin loss, renal loss, low CO, cirrhosis, sepsis, 3rd space

79
Q

AKI - renal causes

A 
Vascular:
Vasculitis, malignant HTN, thrombotic microangiopathy, cholesterol emboli, large vessel disease
Glomerular nephritis
Acute interstitial nephritis
Acute tubular necrosis
80
Q

AKI - postrenal causes

A

Neurogenic

Anatomic

81
Q

Chronic kidney disease

A

Progressive irreversible loss of kidney function

Stage 2 GFR

82
Q

Renal failure

A

Volume overload
Electrolyte abnormalities: high K, PO, uric acid; low Na, Ca, HCO
Uremic syndrome: nausea, vomiting, anorexia, lethargy, muscle cramps, restless legs, prutitus, confusion, pericardial rub

83
Q

Dialysis indications

A 
Acidosis
Electrolyte imbalance - K
Intoxication
Overload
Uremic encephalopathy, pericarditis
84
Q

Renal failure complications

A

CNS: decreased LOC, seizure
CVS: cardiomyopathy, CHF arrhythmia, pericarditis, atherosclerosis
GI: ulcers
Hematologic: anemia, platelet dysfunction, infection
Endocrine: decrease testosterone, estrogen, progesterone; increase FSH, LH
Metabolic: renal osteodystrophy, hypertriglyceridemia, insulin changes
Dermatologic: pruritus, ecchymosis, hematoma

85
Q

Dialysis options

A

Peritoneal dialysis: slow, via peritoneum, multiple exchanges per day, will wear out.

Hemodialysis: fast, via artificial membrane, few exchanges per week.

86
Q

Renal transplant complications

A

Interstitial fibrosis/tubular atrophy (graft loss)
Immunosupressant therapy (infections, malignancy)
Acute rejection
De novo glomerulonephritis (membranous)
New onset DM (prednisone)
Cyclosporin or tacrolimus nephropathy
Chronic allograft nephropathy (previous acute rejections, antibody injury)
CMV infection (1-6months)

Internal Medicine (12 decks)

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