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MBBS VI Medicine > Nephrology notes > Flashcards

Nephrology notes Flashcards

1
Q

What are the indications for emergency haemodialysis?
What are dialyzable drugs/toxins?

A
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2
Q

How can serotenergic syndrome affect the kidneys?
What should the management be?

A
  • Due to increased muscle rigidity it can result in rhabdomyolysis (releases K (arrhythmia), myoglobin, creatine kinase, phosphate) which may further lead into compartment syndrome (compromising blood supply to limbs)
  • Myoglobin has toxic effect on renal tubules (esp proximal renal tubules). Interacts with Tamm-Horsfall protein in the distal tubules and result in cast formation in the presence of acidic urine. This leads to urinary obstruction.

Mangement
* If myoglobinuria –> should IV fluid resuscitation
* Sodium bicarbonate to make the urine alkali and prevent formation of renal casts (reduce chance of urinary obstruction) further worsening renal function

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3
Q

What are the prognostic factors of PKD?

A

PKD1 has early presentation and more severe with median starting dialysis around 50 years old (PKD2 median dialysis starting age around 70 years old)

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4
Q

What is the most common presenting SS of PKD and why?
What CBC and urinanalysisresults will be present?

A
  • Loin pain (enlarged kidney) will stretch the surrounding muscles
  • Refractory hypertension
  • Family history (autosomal dominant if presentation in adulthood, autosomal recessive in children)

CBC results
* Occult polycythemia: cysts become stretched and compress on blood suppplies supplying kidney inducing hypoxia causing a reflex increased EPO production.
* There will be less anemia than non PCK patients with same dgree of renal dilatation

Urinanalysis: no significant proteinuria in most cases (if present think underlying DM)

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5
Q

Uremic encephalopathy

  • Pathophysiology

Bedside teaching - Max

A

Accumulation of amino acid metabolites alter neuronal metabolism, alter balance of excitatory and inhibitory effects, eventually causing neuronal cellular damage and cell death

Notable metabolites that are neurotoxic include Guanidine compounds (guanidinosuccinic acid and guanidine, methyguanidine), Kynurenine, 3-hydroxykynurenine

Neurotoxic effect is compounded by metabolic disturbances such as acidosis, electrolyte disturbances (i.e. HypoNa, HyperK, HypoCa, HyperMg), dehydration or over-hydration, leading to neuronal inflammation and increased brain microvascular leakage

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6
Q

Uremic encephalopathy

Clinical presentation

A

Clinical presentation:
- May be the first indication of metabolic disturbances
- Wide range of S/S: Loss of memory, impaired concentration, depression, delusions, lethargy, irritability, fatigue, insomnia, psychosis, stupor, catatonia, and coma
- Myoclonic jerks, asterixis, chorea; Dysarthria, seizure, tetany

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7
Q

Uremic encephalopathy

Ix and diagnosis

A
  • BUN for urea level: over 40mg/dL (normal <8)
  • CBC (NcNc anemia)
  • Electrolyte profile (HypoNa, HyperK, HypoCa, HyperPO4)
  • Arterial blood gas (Metabolic acidosis with high Anion gap)
  • RFT
  • urinalysis for proteinuria (+/- Autoimmune markers, SFLC assays…)

EEG:
- Acute uremia: EEG is characterized by irregular low voltage with slowing of the posterior dominant alpha rhythm and occasional theta bursts.
- Characteristic findings are prolonged bursts of bilateral, synchronous slow and sharp waves or spike and waves.

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8
Q

Uremic encephalopathy

Treatment

A

General: Low-sodium, low phosphate, low potassium diet, Low-protein diet, 30kcal/kg/day, bed rest, adequate hydration

Correction of electrolyte disturbances: HyperK, HypoCa with calcium gluconate or calcium carbonate, metabolic acidosis with sodium bicarbonate

Renal replacement therapy

Seizure: Anticonvulsants at lower-than-normal doses due to low albumin levels, Levels of anticonvulsant drugs must be closely monitored to prevent toxicity

Surgery: renal transplantation, neurosurgical care for subdural hematoma or ICH

Manage cardiovascular complications: ultra-filtration related arterial hypotension causing ischemic stroke; thromboembolic ischemic CVA, concomitant hypertensive encephalopathy…etc

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9
Q

Uremic pericarditis

Pathophysiology

A

Pathophysiology
Inflammation of visceral and parietal pericardium by accumulated metabolic toxins

Notable metabolites: urea, creatinine, methylguanidine, guanidinoacetate, parathyroid hormone, beta2-microglobulin, uric acid

Types: Uremic pericarditis, dialysis-associated pericarditis

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10
Q

Uremic pericarditis

Clinical presentation

A

Uremic pericarditis: slow onset anterior chest pain/ present with isolated pericardial friction rub
Potentially fatal progression into cardiac tamponade: tachycardic, hypotensive, and has distended neck veins

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11
Q

Uremic pericarditis

Ix and diagnosis

A

Blood test:
- BUN >40mg/dL
- CBC, inflammatory markers, renal and liver function tests: raised erythrocyte sedimentation rate and C-reactive protein
- creatine kinase troponins: may be elevated (not diagnostic)

Imaging:
- Electrocardiogram: diffuse ST and T-wave elevations (typically diffuse and not localized to coronary artery territory c.f. STEMI)
- Chest X-ray: increased cardiac silhouette,
- Echocardiogram: restrictive pattern due to the stiffness of the fibrous pericardium as a result of adhesions, systolic right atrial collapse, with equalization of pressure in all cardiac chambers and swinging septal position

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12
Q

Uremic pericarditis

Treatment

A

General: Low-sodium, low phosphate, low potassium, low-protein diet, 30kcal/kg/day, bed rest, adequate hydration

Correction of electrolyte disturbances HyperK, HypoCa with calcium gluconate or calcium carbonate, metabolic acidosis with sodium bicarbonate

Intensive dialysis (HD) for 5-7 days with heparin-free hemodialysis (reduce the risk of intrapericardial haemorrhage)

No fluid removal to avoid hypotension and cardiovascular collapse

Refractory to intensive dialysis: systemic or intrapericardial NSAIDs and corticosteroids (e.g. Triamcinolone hexacetonide (synthetic corticosteroid))

Refractory to all medical treatment for 7 days or hemodynamically unstable: pericardiocentesis or pericardiectomy

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13
Q

Dermatological manifestations of uremia

A
  • Xerosis (abnormally dry skin or mucosa)
  • Pruritis: starts at stage 4 CKD, 6 months after starting dialysis. Cutaneous manifestations of pruritus include excoriations, prurigo nodularis, and lichen simplex chronicus

Pigmentary alterations:
- brown–to–slate-gray discoloration: hemosiderin deposition in association with iron overload from excessive transfusions
- yellowish hue: retained urochromes and carotene deposited in the epidermis and subcutaneous tissues
- Hyperpigmentation: increase in melanin production due to increase in poorly dialyzable beta-melanocyte stimulating hormone

Half and half nails

Alopecia

Uremic frost (rare): due to concentration of urea in sweat and evapouration of sweat deposit crystals in skin

Bullous disease of dialysis: secondary to iron overload

Arterial steal syndrome: proximal shunting of blood causing hand ischemia

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14
Q

Uremic anemia

Causes

A

Deteriorating renal function – deficient erythropoietin

Medications and dietary restriction

Anemia of chronic illness

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15
Q

Uremic anemia

Treatment target
Indication of treatment
Options

A

Goal of treatment:
- mitigate symptoms
- reduce blood transfusion
- treat absolute or functional iron deficiency
- target Hb should be individualized: within 10 to 11.5 g/dL. Excessive Hb can lead to hyperviscosity syndrome and directly increase mortality

Indications:
- Hb <11 g/dL
- Symptomatic anemia
- CKD stage 4/5 with no other cause identified (eg blood loss, folic acid or vitamin B12 deficiency)

Treatment options:
- Iron repletion: oral iron, iv iron dextran, iv iron sucrose, iv iron carboxymaltose
- Oral iron for PD, IV iron for HD
- ESA (Erythropoiesis Stimulating Agents): SC or IV
- Hypoxia inducible factor proline hydroxylase inhibitor (HIF proline hydroxylase inhibitor)
- Blood transfusion (indicated by acute blood loss, hemolysis, severe sepsis)

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16
Q

CKD - BMD

Clinical presentation

A
  • Fractures, bone and joint pain
  • Skeletal deformities, growth retardation in children
  • Deposition of calcium-phosphate complexes in vascular tissue (medial calcification-> hypertension, stroke, MI)
  • Deposit in valvular tissue (valvular dysfunction, MI)
  • Deposit in soft tissue (metastatic calcification, most commonly in periarticular regions)
  • Calciphylaxis (ulcers, infection with sepsis)
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17
Q

CKD - BMD

Types of renal osteodystrophy

A

High bone turnover
- Secondary hyperPTH
- changes in material composition and nanomechanical properties (mineral-to-matrix ratio, carbonate-to-phosphate ratio, hardness, and shape-independent material stiffness)

Low bone turnover/adynamic bone disease
- More commonly in PD and HD patients
- Oversuppression of PTH with normal mineralization due to early usage of vit D analogs and Ca-containing PO4 binders
- changes in microstructural parameters (low cancellous bone volume, and trabecular thickness, absent osteoid accumulation)

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18
Q

CKD - BMD

Ix and diagnosis

A

RFT: GFR <60mL/min

Electrolytes and metabolites:
- serum calcium, phosphate, PTH, 25(OH)D (calcidiol) levels
- Bone-specific alkaline phosphatase for bone turnover

BMD testing: by dual energy X-ray absorptiometry to assess fracture risk

Gold standard for evaluation and diagnosis of renal osteodystrophy is bone biopsy. (NOT routinely done)

Lateral AXR for vascular calcification, echocardiogram for valvular calcification

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19
Q

CKD - BMD

Treatment

A

Based on serial assessments of phosphate, calcium, and PTH levels

Dietary restriction (<900mg/d): avoid excessive milk, cheese, eggs, protein-rich food (esp processed)

Phosphate binders: sevelamer, lanthanum (non-Ca), CaCO3, Ca acetate (Ca-based)

Treatment of ↓Ca, ↓vitamin D, ↑PTH: should be done AFTER correction of ↑PO4:
- Calcitriol/synthetic analogue: active form of vitamin D, usually first choice (might correct Ca but exacerbate PO4 level due to concomitant increase absorption of both in gut)
- Calcimimetics (cinacalcet, etelcalcetide): ↑sensitivity of parathyroid calcium-sensing receptor to calcium → ↓PTH secretion
- Parathyroidectomy

Treatment of bone disease:
- Bisphosphonate, denosumab and other Tx of osteoporosis
- guided by BMD, fragility fractures ± bone biopsy

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20
Q

What are the 2 associated viruses with renal transplantation?

A
  • BK virus
  • CMV
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21
Q

Algorithm for arterial pH<7.35

A
22
Q

What urinary pH in distal RTA?
Which RTA is prone to renal stones?

A

urine pH >5.5 in the presence of acidemia i.e. inappropriate urine acidification (as defective H+ ATPase in distal tubule)

Distal RTA prone to renal stones. Acidosis induced increased bone breakdown –> decreased tubular calcium/po4 reabsorption –> hypercalciuria, hyperphosphaturia. Increased urine pH –> decreased solubility of calcium and phosphate –> increased risk of crystallization.
Bone diseases are also common due to acidosis –> increased bone breakdown

23
Q
A
24
Q

What drugs used in T2DM for ESRD?

A
  • Sulphonylureas: prefer short acting ones with renal doseing (glipizide)
  • Meglitinides: prefer repaglinide (metabolized by liver, <10% renally excreted)
  • DPP4 inhibitors: prefer linagliptin (trajenta)
  • TZD: avoided due to fluid retention effects
  • alpha glucosidase inhibitors: avoided due to a/w decreased postprandial sugar peaks –> increased hypoglycemia
  • SGLT2 inhibitors: C/I when eGFR <30 due to dehydrating effects
  • Metformin C/I if eGFR <30 due to lactic acidosis
25
Q

What is non immunosuppressivce therapy in CKD?

A
  • Aggressive BP control: BP target of 120/80 for HBPM, 130/80 for office BP
  • Anti proteinuric therapy: indicated in patients with proteinuria CKD only. ACEI is most effective among anti HTN drugs in decreased proteinuria
  • Lipid lowering therapy: statins indicated in all CKD patients as CKD is a major risk factor for CVD and often a/w increased triglycerides, Ch, lipids
  • Anticoagulation considered in high risk nephrotic syndrome patients
26
Q

How to monitor renal allograft function?

A
  • Urine output: should slowly increase from preop baseline
  • Serial Cr, GFR: generally lower than native kidney
  • Proteinuria: presence may indicate acute rejection and predicts decreased long term graft function
  • Transplant kidney biopsy: genereally performed if any evidence of allograft dysfunction
27
Q

Immunosuppressive therapy for renal transplant

A
  • Induction (perioperative): heavy initial immunosuppression to prevent acute rejection.
    Usually biologics (antithymocyte globulin, anti IL2) + high dose glucocorticoids

Maintenance (lifelong): usually triple therapy at intensive dose at first and gradually step down
* Calcineurin inhibitor (CNI): tacrolimus (preferred due to decreased acute rejection rate). If CNI nephrotoxicity develops, then consider sirolimus (mTOR inhibitor)
* Antimetabolite: MMF preferred (C/I in women of childbearing age –> then prefer azathioprine)
* Glucocorticoids

28
Q

How to make dx of acute renal allograft rejection?
Mechanism of rejection?
Tx?

A

Ix: suggested by new increased creatinine >20% from baseline
Dx: renal allograft biopsy
Acute T cell mediated rejection (TCMR): lymphocytic infiltration of tubules, interstitium
Acute Ab mediated rejection (ABMR): arteriolar fibrinoid necrosis, fibrin thrombi in glomerular capilaries + demonstration of donor specific antibodies

Tx:
ABMR: IVIG + steroids + plasmaphresis (if <1st year post op)
TCMR: IV pulse steroids and rATG thymoglobulin + increased maintenance immunosuppression

29
Q

Long term complications of renal transplant

A
  • Infections
    CMV. PCR for CMV DNA. Tx: stop antimetabolite, give IV ganciclovir or oral valganciclovir
    PKP. BAL fluid for microscopy with silver stain. Mx: high dose septrin
    BK virus nephropathy: urine/serum for BKV DNA. Tx by decreasing immunosuppressive therapy
  • Post transplant lymphoproliferative diseases due to prolonged immunosuppression
  • Cardiovascular disease
  • Drug related SE
  • Chronic allograft nephropathy which is leading cause of late graft failure. Immunologic (cell and Ab mediated), non immunologic (HTN, glomerular scarring)
  • Recurrence of primary disease: esp in IgAN, membranous nephropaty, FSGS
30
Q

How to dx hepatorenal syndrome?

A

dx by exclusion
Urinanalysis: urine sodium

31
Q

ESRD patient with pericardial effusion, what is most likely cause?
What are other causes?

A
  • Uremic pericarditis
  • Viral (cox, herpes, echovirus, mumps), bacterial (pneumococcus, streptoccus, staphylococcus, TB (can be non mycobacterial), fungal = rare (candidiasis)
  • Autoimmune: SLE, scleroderma. Arteritis: polyarteritis nodosa, post MI syndrome
  • Drug induced: isoniazid, cyclosporine, phenytoin
32
Q

What sort of malignancy prone in renal transplant with immunosuppression?

A
  • Lymphoma
  • Lymphoproliferative diseases
  • Solid organ tumors also possible
33
Q

MoA of cyclosporin A and rapamycin?

A

CyA inhibits NFAT protein
Rapamycin inhibits the mammalian target of rapamycin

34
Q

Physical signs of cardiac tamponade

A

Pulsus paradoxus
Kussmauls sign
Distant heart sounds

35
Q

Patient presents with vomiting and diarrhea, what to worry about?
What will hypoK present as?

A

Dehydration and electrolyte disturbances: hypoK, hypoNa, metabolic alkalosis

Arrhythmias: prominent U wave, ST depression, wide QRS and flattened P wave
Paralytic ileus, vomiting, altered mental status

36
Q

If patient on 1st line TB drugs suddenly has increased Cr, what is the reason?

A
  • Rifampicin induced acute TIN
  • Due to type 2/3 hypersensitivity reaction iinduced by rifampciin
  • Anti rifampicin antibodies form immune complexes that are deposited in renal vessels, glomerular endothelium and interstitial area

Presentation of acute TIN
Hypersensitivity: fever, eosinophilia, skin rash
AKI: oliguria, anorexia, nausea/vomiting, malaise

37
Q

Why does serum creatinine rise after transplant?
What ix for each of them?

A

Acute graft rejection (highly suspect when serum creatinine level rises >25% of its normal value. Usually occurs on day 8-11 after transplantation.
Other causes
* Vascular complication: renal vein thrombosis
* Infection: UTI, viral infections
* Drug toxicity: calcineurin inhibitor, nephrotoxicity

38
Q

Bedside tests for ddx for increased serum Cr after renal transplant?

A
  • Monitor I/O, hourly urine output (for oliguria/anuria) as 1st signs of acute graft rejection
  • Body temp (for fever as sign of infection)
  • Urine dipstix for UTI (nitrite, leukocyte esterase, high pH)
  • Tender kidney in acute allograft rejection
  • Renal bruit for RAS
  • Bedside USG and doppler (for acute graft rejection and renal vein thrombosis)
39
Q

Lab ix for increased serum creatinine in renal transplant?

A
  • CBC DC: look for WCC to r/o infection (lymphocyte predominance with presence of atypical lymphocytes in CMV infection)
  • LRFT: highly suspect acute graft rejection if serum Cr>25% its normal value)
  • Cyclosporin A/ tacrolimus trough level to see whether there is insufficient immunosuppression
  • qPCR for BK polyomyavirus, CMV pp65Ag
40
Q

What prophylaxis/tx given for renal transplant

A

Antimicrobial and antiviral prophylaxis for first 6 months to 1 year after transplantation
CMV prophylaxis: valganciclovir
Septrin for PJP

Vaccinations for immunocompromised host 3-6 months post transpantation
Safe to give inactivated vaccines
Cannot give live or live attenuated vaccines

41
Q

SE of each immunosuppressant

A
42
Q

Role of HLA testing in renal transplant

A

If the transplant is between genetically different individuals, the allogeneic graft (allograft) is recognized as foreign predominantly because of differences between donor/recipient major histocompatibility complex (MHC) molecules, which are also known as the human leukocyte antigens (HLAs).

HLA testing focuses on predicting antibody mediated alloimmune response.
HLA mismatch = HLA antigen found on the cells of the donor allograft but not in the recipient. Greater the disparity between the donor and recipient the more foreign the allograft and higher chance of developing alloimmune response.
In renal transplant only HLA-A, HLA-B, and HLA-DR loci are examined (other HLA-C. HLA-DP, HLA-DQ) does not have to be matched

43
Q

Causes of isolated microscopic haematuria?

A
  • IgA nephropathy
  • Alport syndorme
  • Thin basement membrane nephropathy

GN
* IgA nephropathy: history of URTI or GIT infection
* MPGN: HBV/HCV infection, malignancy, AI disease (SLE)
* PSGN: history of skin infection, pharyngitis

44
Q

some ddx for bilateral pitting LL edema?
If there is frothy urine what can be the underlying cause?

A

Heart: CHF
Liver: cirrhosis
Kidney: nephrotic syndrome (loss of albumin)

Frothy urine –> proteinuria –> nephrotic syndrome
Illicit below history to find underlying cause

Primary nephrotic syndrome: FSGN, membranous nephropathy –> must screen for malignancy (anti PLA2R), minimal change disease. Others: IgA nephropathy, MPGN, crescenteric
Secondary nephrotic syndrome
* HBV, HCV, syphilis/HIV, TB/mycoplasma, CMV/rubella/toxoplasmosis
* Systemic diseases: DM, SLE, IE, HSP, vasculitis
* Structural glomerular disease: Alport disease
* Malignancy: leukemia, lymphoma, ovarian, lung, breast cancer
* Drug induced: NSAIDs, Abx (ampicillin/ rifampicin/ cephalosporins), sulfasalazine

45
Q

Ix for nephrotic syndrome/

A
  • CBC with differentials
  • Clotting profile
  • Lipid profile
  • LFT, RFT (eGFR, Cr, BUN)
  • Urinalysis: dysmorphic RBC, RBC casts
  • 24 hr urine protein excretion: >3.5g/day
  • Urine protein-to-Cr ratio
  • MSU for C/ST
  • anti-PLA2R
  • AI markers: ANA, ds-DNA
  • Serum C3/ C4 levels
  • Serum Ig pattern
  • SPEP and immunofixation
  • Serological tests: HBV, HCV, HIV, syphilis, EBV, CMV
  • Renal USG
  • Renal biopsy
46
Q

What is lupus nephritis?
Class 4 or 5 more severe?
Where are crescents found?
If histology was both sclerosing and diffuse proliferative what is dx?

A
  • Deposition of circulating immune complexes –> activates complement cascade (hence if C3/4 low –> active disease) damgae, leukocyte infiltration, activation of procoagulant factors and release of cytokines
  • Class 4: diffuse nephritis >50% GN affected with crescent formation (LM), subendothelial and mesangial immune deposits (EM) full house stainging of IgGAM, C3, C1q (IF)
  • Class 5: membranous nephriits –> thickened GBM (LM), subepithelial and mesangial immune deposits (can do oral prednisolone)
  • Class 4 is most severe form of lupus nephritis –> requires high dose IV pulse methylprednisolone
  • Crescents are found in Bowmans capsule (between bowmans capsule and the glomerulus): injury to glomerular capillary wall results in movement of plasma products including fibrinogen into bowmans space
  • Rapidly progressive glomerulonephritis
47
Q

What are causes of hypoCa in rhabdomyolysis?

A

Release of phosphate which binds to the calcium (so free calcium is low)

48
Q

Induction immunosuppression for renal transplant?

A
  • Biologics (antithymocyte globulin, anti-IL2)
  • High dose glucocorticoids
49
Q

What is used to assess efficacy of peritoneal dialysis?

A
  • Peritoneal equilibration test
  • Serum and dialysate samples are analyzed for urea, creatinine and glucose
  • Urea and creatinine is calculated as the dialysate to plasma or D to P ratio. This means that the concentration of urea or creatinine in the dialysate at each point is divided by the concentration of urea or creatinine in the plasma or serum.
  • For glucose dividing the dialysate glucose concentration at each time point by the glucose concentration in the O-hour dialysate sample results in the equilibrium ratios.
50
Q

Early vs late complications of peritoneal dialysis

A

Encapsulated peritoneal sclerosis (abd caccoon) is late PD complication

51
Q

How can ESRF cause tetany/cramps?

A

Hypocalcemia induced by increased phosphate (which binds to free calcium) and decreased renal production of 1,25OH2 vit D due to renal malfunction.

In comparison to hyper/hypoK which causes muscle weakness

MBBS VI Medicine (98 decks)

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