bobrek

Question 1

causes of Unintentional weight loss in elderly and next step maangment

Answer 1

ckd, copd, hf
nutritional supplement

Question 2

All diabetic patients with a urinary ACR of 3 mg/mmol or more should be started on —–

Answer 2

ACE inhibitor or angiotensin-II receptor antagonist

Question 3

Diabetic nephropathy: management

Answer 3

dietary protein restriction
tight glycaemic control
BP control: aim for < 130/80 mmHg
ACE inhibitor or angiotensin-II receptor antagonist
should be start if urinary ACR of 3 mg/mmol or more
dual therapy with ACE inhibitors and angiotensin-II receptor antagonist should not be started
control dyslipidaemia e.g. Statins

Question 4

screening of diabetic neuropathy

Answer 4

all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
should be an early morning specimen
ACR > 2.5 = microalbuminuria

Question 5

drugs causing hyperthyroidims

Answer 5

amiodarone, lithium, chemo drugs

Question 6

Wilms’ nephroblastoma features

Answer 6

Features
abdominal mass (most common presenting feature)
flank pain
painless haematuria
other features: anorexia, fever
unilateral in 95% of cases
metastases are found in 20% of patients (most commonly lung)

Question 7

painless visible hematuria-elderly-dx

Answer 7

transitional cell carcinoma of bladder

Question 8

The maximum recommended rate of potassium infusion via a peripheral line is

Answer 8

10 mmol/hour, whereas rates above 20 mmol/hour require cardiac monitoring

Question 9

maintenance fluid requirements
—– ml/kg/day of water and
approximately
—-mmol/kg/day of potassium, sodium and chloride and
approximately ——g/day of glucose to limit starvation ketosis

Answer 9

25-30 ml/kg/day of water and
approximately 1 mmol/kg/day of potassium, sodium and chloride and
approximately 50-100 g/day of glucose to limit starvation ketosis

Question 10

0.9% saline
if large volumes are used there is an increased risk of ——–

Answer 10

0.9% saline
if large volumes are used there is an increased risk of hyperchloraemic metabolic acidosis

Question 11

aki prerenal

Answer 11

hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis

Question 12

aki intrinsic

Answer 12

glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome

Question 13

postrenal aki

Answer 13

kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter

Question 14

aki symptoms

Answer 14

reduced urine output
pulmonary and peripheral oedema
arrhythmias (secondary to changes in potassium and acid-base balance)
features of uraemia (for example, pericarditis or encephalopathy)

Question 15

aki detection

Answer 15

U&Es=sodium
potassium
urea
creatinine

Urinalysis
all patients with suspected AKI should have urinalysis

Imaging
if patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have a renal ultrasound within 24 hours of assessment.

Question 16

management aki
-Stabilisation of the cardiac membrane
-Short-term shift in potassium from extracellular to intracellular fluid compartment
-Removal of potassium from the body

Answer 16

Stabilisation of the cardiac membrane
* Intravenous calcium gluconate
Short-term shift in potassium from extracellular to intracellular fluid compartment
* Combined insulin/dextrose infusion
* Nebulised salbutamol

Removal of potassium from the body
* Calcium resonium (orally or enema)
* Loop diuretics
* Dialysis

Question 17

Causes of transient or spurious non-visible haematuria

Answer 17

urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse

Question 18

Causes of persistent non-visible haematuria

Answer 18

cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease

Question 19

Spurious causes - red/orange urine, where blood is not present on dipstick
foods
drugs

Answer 19

foods: beetroot, rhubarb
drugs: rifampicin, doxorubicin

Question 20

hyperkalemia management

Answer 20

-iv gluconate
-insulin/dextrose infusion
-nebulised salbutamol
-calcium resonium
-loop diuretics
-dialysis
-stop ace-i

Question 21

Primary hyperaldosteronism causes —–, by retaining more —- and excreting more ——. As a consequence, more —— will be expelled, causing —–.

Answer 21

Primary hyperaldosteronism causes metabolic alkalosis, by retaining more sodium and excreting more potassium. As a consequence, more hydrogen ions will be expelled, causing alkalosis.

Question 22

The anion gap is calculated by:
A normal anion gap is

Answer 22

(sodium + potassium) - (bicarbonate + chloride)

A normal anion gap is 8-14 mmol/L

Question 23

Causes of a normal anion gap or hyperchloraemic metabolic acidosis

Answer 23

gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease

Question 24

Causes of a raised anion gap metabolic acidosis

Answer 24

lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
5-oxoproline: chronic paracetamol use

Question 25

Patients with chronic kidney disease should be started on ==== if they have an ACR > 30 mg/mmol

Answer 25

Patients with chronic kidney disease should be started on an ACE inhibitor if they have an ACR > 30 mg/mmol

Question 26

ckd-diabetic nephropathy –clinical sign

Answer 26

proteinuria
ACR-albumin/creatinine ratio for quantification of proteinuria

Question 27

The most likely renal outcome for the 13-year-old girl with Henoch-Schonlein purpura (HSP) and mild renal impairment is ====. HSP, also known as IgA vasculitis, is a small-vessel vasculitis that predominantly affects children. While it can cause kidney involvement in the form of IgA nephropathy, most cases of HSP with renal involvement have a good prognosis and recover fully without any long-term complications.
features:
treatment:

Answer 27

The most likely renal outcome for the 13-year-old girl with Henoch-Schonlein purpura (HSP) and mild renal impairment is full renal recovery.

=Features
palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure

=Treatment
analgesia for arthralgia
treatment of nephropathy is generally supportive. There is inconsistent evidence for the use of steroids and immunosuppressants

=bp monitor and urinalysis to detect renal involvement

Question 28

Normocytic anaemia==, thrombocytopaenia and AKI following diarrhoeal illness - consider ==

investigations:
managements:

Answer 28

Normocytic anaemia-microangiopathic hemolytic anemia, thrombocytopaenia and AKI following diarrhoeal illness - consider HUS
e.coli-0157:h7

Investigations
full blood count
anaemia: microangiopathic hemolytic anaemia characterised by a haemoglobin level less than 8 g/dL with a negative Coomb’s test
thrombocytopenia
fragmented blood film: schistocytes and helmet cells
U&E: acute kidney injury
stool culture
looking for evidence of STEC infection
PCR for Shiga toxins

Management
treatment is supportive e.g. Fluids, blood transfusion and dialysis if required
there is no role for antibiotics, despite the preceding diarrhoeal illness in many patients
the indications for plasma exchange in HUS are complicated
as a general rule plasma exchange is reserved for severe cases of HUS not associated with diarrhoea
eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS

Question 29

Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome and chronic kidney disease. It generally presents in young adults.

Causes:

Answer 29

idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport’s syndrome
sickle-cell

Question 30

Membranous glomerulonephritis histology:

Answer 30

Membranous glomerulonephritis histology:
basement membrane thickening on light microscopy
subepithelial spikes on sliver stain
positive immunohistochemistry for PLA2

Question 31

Membranous glomerulonephritis causes

Answer 31

idiopathic: due to anti-phospholipase A2 antibodies-dvtye neden oluyo
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid

Question 32

==== is the first indicator of diabetic nephropathy. Management includes blood pressure and proteinuria control with an ==== or ==

Answer 32

Microalbuminuria is the first indicator of diabetic nephropathy. Management includes blood pressure and proteinuria control with an ACE-inhibitor or ARB

Question 33

lactic acidosis type A: ====
lactic acidosis type B: ===

Answer 33

lactic acidosis type A: sepsis, shock, hypoxia, burns
lactic acidosis type B: metformin

Question 34

Causes of normal anion gap metabolic acidosis

Answer 34

Diarrhea
Fistulae (eg, pancreatic, ileocutaneous, etc.)
Carbonic anhydrase inhibitors
Renal tubular acidosis
Ureteral diversion (eg, ileal loop)
Iatrogenic

Question 35

Non-anion gap metabolic acidosis and hyperkalemia that occur out of proportion to the renal dysfunction indicate a ——–.

Answer 35

Non-anion gap metabolic acidosis and hyperkalemia that occur out of proportion to the renal dysfunction indicate a renal tubular disorder.

Question 36

rta 4

Answer 36

Impaired function of the cortical collecting tubule due to aldosterone deficiency or resistance will cause retention of H+ and K+ and is termed hyperkalemic RTA Hyperkalemic RTA is commonly seen in elderly patients who have poorly controlled diabetes with damage to the juxtaglomerular apparatus, which causes a state of hyporeninemic hypoaldosteronism.

Question 37

loop diuretics cause

Answer 37

hypokalemia, metabolic alkalosis

Question 38

laxative abuse causes

Answer 38

hypokalemic metabolic alkalosis

Question 39

primary hyperaldesteronism causes

Answer 39

hypokalemia metabolic alkalosis

Question 40

renal artery stenosis causes

Answer 40

secondary hyperaldesteronism, hypokalemia, metabolic alkalosis, hypertension

Question 41

vomiting causes

Answer 41

hypochloremic metabolic alkalosis-due to loss of gastric hcl, hypokalemia can happen due to increased aldosterone secretion due to volume depletion

Question 42

sarcoidosis manifestations
pulm-
cutaneous-
opht-
neuro=
cvs=
gastro=
systemic=

Answer 42

Pulmonary

Hilar lymphadenopathy*
Interstitial infiltrates

Cutaneous

Papules, nodules & plaques
Erythema nodosum*

Ophthalmologic

Anterior & posterior uveitis
Keratoconjunctivitis sicca

Neurologic

Facial nerve palsy
Central diabetes insipidus
Hypogonadotropic hypogonadism

Cardiovascular

AV block
Dilated or restrictive cardiomyopathy

Gastrointestinal

Hepatosplenomegaly
Asymptomatic LFT abnormalities

Other

Hypercalcemia
Peripheral lymphadenopathy
Parotid gland swelling
Polyarthritis*
Constitutional symptoms (fever,* malaise)
*Manifestations of Löfgren syndrome.

AV = atrioventricular; LFT = liver function test.

Question 43

causes of hypercalcemia

Answer 43

-hyperpth
-solid malignancies
-osteolytic malignancies
-granulomatous disease, lymphoma

Question 44

calcium metabolism
-pth
-vit d
-calcitonin

Answer 44

-pth=↑ Bone resorption
↑ Renal reabsorption of calcium & ↓ reabsorption of phosphate
↑ Conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D

-vit d=↑ Intestinal absorption of calcium & phosphate
↑ Renal reabsorption of calcium & phosphate
↓ Parathyroid hormone secretion
↑ Mineralization of bone

-calcitonin=↓ Bone resorption
↓ Renal calcium reabsorption

Question 45

sarcoidosis pathophys

Answer 45

-extrarenal calcitriol conversion in macrophages of lungs and lymph nodes
-pth independent
-increased calcitriol=intestinal calcium absorption increases=hypercalcemia
-pth decreases due to negative feedback by hypercalcemia and increased calcitrio
-Renal calcium reabsorption decreases due to low PTH; because serum calcium is high, renal calcium excretion increases=hypercalciuria

Question 46

Refeeding syndrome occurs in the setting of ==, typically due to ===(eg, alcohol use disorder, anorexia). Patients with alcohol use disorders are at particularly elevated risk due to alcohol-induced ===(reduces intestinal == absorption) and == (==-based antacids bind intestinal ===).

Answer 46

Refeeding syndrome occurs in the setting of hypophosphatemia, typically due to chronic malnutrition (eg, alcohol use disorder, anorexia). Patients with alcohol use disorders are at particularly elevated risk due to alcohol-induced chronic diarrhea (reduces intestinal phosphate absorption) and gastritis (calcium-based antacids bind intestinal phosphorus).

Question 47

Glomerulonephritis is typically accompanied by evidence of

Answer 47

glomerular damage on urinalysis (eg, dysmorphic red blood cells, red blood cell casts).

Question 48

Chronic pyelonephritis may cause

Answer 48

Chronic interstitial nephritis with WBCs and WBC casts. However, this typically occurs as a sequela of recurrent acute pyelonephritis with prior symptoms of dysuria, fever, and recurrent flank pain (absent in this patient).

Question 49

aki=
oliguria/anuria
signs of uremia=anorexia/nausea/asterixis/pericarditis/platelet dysfunction, fatigue, confusion
how to manage?

Answer 49

-confirm aki diagnosis and stage
-labs-cbc/bmp/calcium, phosphate, magnesium, and ABG or VBG
-Urine studies: urinalysis, urine microscopy, urine chemistry (sodium, urea, osmolality, creatinine)
- Consider urgent ultrasound and/or foley catheter placement (if urinary tract obstruction is suspected).
- Consider early nephrology consult.
-Optimize volume status.
-Identify and treat any metabolic complications (e.g., acidosis, hyperkalemia).
-Identify and treat the underlying cause.
-Hold nephrotoxic medications and renally-dose other medications.
-Strict input/output monitoring
-Provide additional supportive care (e.g., nutritional support, VTE prophylaxis)

Question 50

prerenal aki causes

Answer 50

• decreased renal blood flow (RBF) and GFR.
• decreased RBF may be 2ndary to hypovolaemia per se, decreased effective RBF (decreased cardiac
  output, vasodilatation in sepsis), or intrarenal vasomotor changes (e.g.
  NSAIDs and ACE-I).
• Potentially reversed by restoration of RBF.
• Kidneys remain structurally normal.

Question 51

commonest cause of intrinsic aki

Answer 51

atn

Question 52

Dialysis disequilibrium syndrome
risk factors
management
complications

Answer 52

the development of acute cerebral edema secondary to the rapid extraction of osmotically active substances (e.g., urea, NaCl) from the blood
-Risk factors [18]
First dialysis sessions
Extremely elevated BUN
Metabolic acidosis
Preexisting neurological abnormalities
Hyperglycemia or hypernatremia
-Management: Monitor patients for symptoms of cerebral edema and initiate management of raised ICP if present.
-Other complications [2][7]
Acquired cystic kidney disease [19]
Cramps
Electrolyte abnormalities, e.g., hypophosphatemia
Dialysis-related amyloidosis, which can cause carpal tunnel syndrome [20][21]
Allergic reaction to the equipment or dialysate [3]

Question 53

the leading cause of death in patients on dialysis and kidney transplant recipients

Answer 53

cardiovascular disease

Question 54

A unique phenotype of kidney injury in patients with cirrhosis and ascites in the absence of hypovolemia or other kidney pathology

Answer 54

hepatorenal syndrome