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Y3/4- 5 Nephrology > passmed > Flashcards

passmed Flashcards

1
Q

renal replacement therapy used when

A

Renal replacement therapy (e.g. haemodialysis) is used when a patient is not responding to medical treatment of complications, for example hyperkalaemia, pulmonary oedema, acidosis or uraemia (e.g. pericarditis, encephalopathy).

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2
Q

what drugs cause rhabdo

A

statin

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3
Q

myoglobinuria

A

dark or reddish-brown colour

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4
Q

how to potassium lowering medications work

A

Calcium and sodium cations are exchanged for hydrogen ions in the stomach. These hydrogen ions are then exchanged for potassium ions in the large intestine and the potassium ions are excreted from the bowel as part of the resin complex.

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5
Q

ADPKD features

A

hypertension
recurrent UTIs
flank pain
haematuria
palpable kidneys
renal impairment
renal stones

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6
Q

moa of how SGLT-2 inhibors help in CKD

A

patients who have proteinuric CKD need SGLT2 inhibitors
they primarily act by blocking reabsorption of glucose in the proximal tubule → lowers the renal glucose threshold → glycosuria

by blocking the cotransporter, they also reduce sodium reabsorption → natriuresis reduces intravascular volume and blood pressure, but it also increases the delivery of sodium to the macula densa → normalizes tubuloglomerular feedback and thereby reduces intraglomerular pressure

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7
Q

You are reviewing a 65-year-old in the renal clinic. He has been on haemodialysis for chronic kidney disease for the past 6 years. What is he most likely to die from

A

Ischaemic heart disease

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8
Q

Which one of the following is the most important step in reducing the risk of contrast-induced nephropathy?

A

Intravenous 0.9% sodium chloride pre- and post-procedure

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9
Q

calcium binders such as calcium acetate cause what problems

A

hypercalcaemia and vascular calcification
anxiety
abdo and back pain
muscle weakness

Calcium acetate is a calcium-based binder used to treat hyperphosphataemia.

used in CKD

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10
Q

Severe hyperkalaemia in the context of an AKI requires immediate discussion with critical care/nephrology to conside

A

haemofiltration/haemodialysis

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11
Q

causes of large kidneys in CKD

A

amyloidosis is one
diabetes - most common

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12
Q

causes of small kidneys in ckd

A

A blocked urinary tract leads to pressure on the kidneys and damages the nephrons.
Untreated kidney stones.
Other long-lasting kidney infections like pyelonephritis and reflux nephropathy.
Narrowing of the artery supplying the kidney with blood.

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13
Q

3 things SGLT2 inhibroes excrete in urine

A

secrete sodium ketones and glucose in urine

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14
Q

can you use SGLT2 inhibors in type 1

A

no risk for dka

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15
Q

most common cause of end stage renal failure ( CKD 4,5)

A

diabetes
HTN
IgA nephropathy

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16
Q

insulin helps transport what other molecule into the cell

A

potassium

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17
Q

when do you use fixed rate and varibale rate inuslin in DKA

A

start fied then variable when dka resoltution criteria met

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18
Q

difference between craniotomy and burr hole

A

craniotomy – a section of the skull is temporarily removed so the surgeon can access and remove the haematoma. burr holes – a small hole is drilled into the skull and a tube is inserted through the hole to help drain the haematoma.

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19
Q

HSP you need to check there what

A

blood pressure and urine dipstick

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20
Q

most common cause of inhertied kidney disease

A

Autosomal dominant polycystic kidney disease (ADPKD

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21
Q

mx of ADPKD

A

tolvaptan - vasopressin receptor 2 antagonist to slow progression of cyst development adn renal insufficency

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22
Q

what are the extra renal manifestations of ADPKD

A

liver cysts
cerebral berry anerysms
cysts in other organs sich as pancreas and spleen

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23
Q

what glomerulonephritis is associated with malignancy

A

membranous glomerulonephritis

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24
Q

triad of acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia

all foloowing a diarhoeal illness

A

Haemolytic uraemic syndrome

get scattered petechiae

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25
Q

mx of HUS

A

supportibve and fludis

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26
Q

This question has a 55-year-old man presenting with progressive weakness and dyspnoea, hepatomegaly, proteinuria and worsening renal functio

A

amyloidosis

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27
Q

HSP do they most likely make a full renal recovery

A

yes

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28
Q

unexplained visible haematuria without UTI

next best steps

A

2ww

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29
Q

if someone has haemuatria what is the first thing you should do

A

rule out UTI

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30
Q

right sided testicular swelling - bag of owrms

A

RCC

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31
Q

A 45-year-old female with nephrotic syndrome develops renal vein thrombosis. What changes in patients with nephrotic syndrome predispose to the development of venous thromboembolism?

A

Loss of antithrombin III in the urine

leading to hypercoagulable state this and increased risk of thrombus formation

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32
Q

famialil hypercholesteromaia values

A

TC over 7.5
LDL over 4.9

kids
6.7 TC an 4 LDL

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33
Q

how long beofre conecption shtop staitns

A

3 months

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34
Q

crohns causes what type of renal stones

A

calcium oxalate

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35
Q

uti infection what kind of renal stones

A

striuvite

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36
Q

thiazide diuretics do they raise or lower potassium?

A

lower it

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37
Q

mononeutitis multiplex

A

seen in vasuclitis and in one particualr nerve

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38
Q

to be diagnosed with renal artery stenosis have much of artery has to be occluded

A

60%

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39
Q

Antistreptolysin-O

A

recent strep infection

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40
Q

renal vasucalr disease get bruit - in renal artery stenosis what is major cuase in young people

A

fibromuscular dysplasia

41
Q

ureaemia sx

A

Patients with uremia typically complain of nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, pruritus, or changes in mental status. The clinical presentation of uremia can be explained by the metabolic disturbances associated with the condition.

42
Q

tolvapatan moa

A

t counteracts the actions of vasopressin by blocking the V2 receptor, thereby decreasing the expression of the aquaporin channels (Figure 1B). This causes (i) an increase in free water clearance, (ii) a decrease in urine osmolality and (iii) an increase in serum sodium concentration.

43
Q

recurrent UTI makes you think of

A

posterior urethral valves

44
Q

hyaline cast scaued by

A

loop diuretics and exercise

nephritic red cell casts

45
Q

sterile pyuria caused by

A

TB sti and ANW

46
Q

ketamine cystitis

A

thcikened bladder wall

47
Q

how logn till you can drive after successful angio

A

1 week

48
Q

how long can you drive aftr unsucceeful angio

A

6w

49
Q

reinfarction of MI

A

CK_mB

50
Q

sexual activity how long after angio

A

2w

51
Q

fibromuscular dysplasia

A

under 50 RAS hx and restiricitve and high bP

e abnormal development or growth of cells in the walls of arteries that can cause the vessels to narrow or bulge.

52
Q

lupus nephritis how many syndromes

A

6

4 - nephriict - high dose steriod
type 1 - GBM

53
Q

following tx with ACEi in HTN in RAS what scan do you need

A

CT MRI renal angiography

54
Q

unexlianed AKI what do you need

A

USS

55
Q

calcitriol does what

A

increase uptake of Ca from GI

56
Q

why do creatinine levels rise on ACEi

A

reduced glomerular filtatration pressure to sless creatine is excreted

57
Q

gram postiive or negative produce nitries

A

gram negative

58
Q

drug cause of nephrogenic DI

A

lithium

59
Q

what drug can cuase SIADH

A

fluoxetine

60
Q

maxamine time bag of potassium can be infused through peripheral line

A

4 hours

The maximum recommended rate of potassium infusion via a peripheral line is 10 mmol/hour, whereas rates above 20 mmol/hour require cardiac monitoring

61
Q

4 things to remember to examine with AV fistula

A

Skin integrity
Aneurysms
Palpable thrill (a fine vibration felt over the anastomosis)
A “machinery murmur” on auscultation over the fistula

62
Q

complications with a fistula

A

Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High-output heart failure

63
Q

what is STEAL syndrome

A

STEAL syndrome occurs when there is inadequate blood flow to the limb distal to the fistula. The AV fistula “steals” blood from the rest of the limb. Blood is diverted away from the part of the limb it was supposed to supply, leading to ischaemia. Instead, it flows through the fistula and into the venous system.

64
Q

ckd mostly asx what are some sx if they present

A

Fatigue
Pallor (due to anaemia)
Foamy urine (proteinuria)
Nausea
Loss of appetite
Pruritus (itching)
Oedema
Hypertension
Peripheral neuropathy

65
Q

Medications that help slow the disease progression in ckd are:

A

ACE inhibitors (or angiotensin II receptor blockers)
SGLT-2 inhibitors (specifically dapagliflozin)

66
Q

Reducing the risk of complications in ckd involves:

A

Exercise, maintain a healthy weight and avoid smoking
Atorvastatin 20mg for primary prevention of cardiovascular disease (in all patients with CKD)

Oral sodium bicarbonate to treat metabolic acidosis
Iron and erythropoietin to treat anaemia
Vitamin D, low phosphate diet and phosphate binders to treat renal bone disease

67
Q

ACE inhibitors are offered to all patients in ckd with:

3 things
DM
htn

A

Diabetes plus a urine ACR above 3 mg/mmol
Hypertension plus a urine ACR above 30 mg/mmol
All patients with a urine ACR above 70 mg/mmol

68
Q

6 top causes of nephortic syndrome in adults

A

The top causes of nephrotic syndrome in adults are:

Membranous nephropathy
Focal segmental glomerulosclerosis

Other causes of nephrotic syndrome include:

Membranoproliferative glomerulonephritis
Henoch-Schönlein purpura (HSP)
Diabetes
Infection (e.g., HIV)

not including minimal change

69
Q

sx of nephrotic

what are you predisposed too

A

Proteinuria (more than 3g per 24 hours)
Low serum albumin (less than 25g per litre)
Peripheral oedema
Hypercholesterolaemia

Nephrotic syndrome presents with oedema. Patients might notice frothy urine due to the high protein content. Nephrotic syndrome predisposes patients to thrombosis, hypertension and high cholesterol.

70
Q

what is HUS

A

HUS leads to the classic triad of:

Microangiopathic haemolytic anaemia
Acute kidney injury
Thrombocytopenia (low platelets)

The formation of blood clots consumes platelets, leading to thrombocytopenia. The blood flow through the kidney is affected by thrombi and damaged red blood cells, leading to acute kidney injury.

Microangiopathic haemolytic anaemia (MAHA) involves the destruction of red blood cells (haemolysis) due to pathology in the small vessels (microangiopathy). Tiny blood clots (thrombi) partially obstruct the small blood vessels and churn the red blood cells as they pass through, causing them to rupture.

this all follows an episode of gastroenteritis - abx or anti motility medicine leads to this

71
Q

presentation of HUS

A

E. coli O157 and Shigella cause gastroenteritis. Diarrhoea is the first symptom, which turns bloody within 3 days. Around a week after the onset of diarrhoea, the features of HUS develop:

Fever
Abdominal pain
Lethargy
Pallor
Reduced urine output (oliguria)
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion

confusion ureamia
brusng low platelets
abdo pain
pallor anaemia
renal failure - HTN

72
Q

what is the management of HUS

A

Stool culture is used to establish the causative organism.

HUS is a medical emergency and requires hospital admission and supportive management with treatment of:

Hypovolaemia (e.g., IV fluids)
Hypertension
Severe anaemia (e.g., blood transfusions)
Severe renal failure (e.g., haemodialysis)

73
Q

all diabetic patients require annual screening for what test

A

Albumin:creatinine ratio (ACR) in an early morning specimen

74
Q

in addition to low platelets in HUS what else is low

A

Serum haptoglobins (which bind haemoglobin) and the platelet count are decreased in haemolytic uraemic syndrome.

75
Q

how does an insulin dextrose infusion work

A

work by shifting potassium from extracellular to intracellular fluid compartments

76
Q

what electrolyte balance indicates whether kidney disease is acute or chronic

A

Hypocalcaemia is an indication that kidney disease is chronic and not acute

77
Q

acute graft failure what signs

A

rising creatinine, pyuria and proteinuria

78
Q

A 65-year-old woman is admitted to the Emergency department with sepsis and is also found to have an acute kidney injury. Which of the following would be the most likely finding on her arterial blood gas?

A

Patients who have sepsis often have a raised serum lactate due to the hypoperfusion of their peripheries. This gives them a metabolic acidosis with a raised anion gap.
If the anion gap is raised, this suggests that there is increased production, or reduced excretion, of fixed/ organic acids e.g.
Lactic acid (sepsis, tissue ischaemia)
Urate (renal failure)
Ketones (diabetic ketoacidosis)
Drugs/ toxins (salicylates, methanol, ethylene glycol)

79
Q

Nephrotic syndrome is associated with a hypercoagulable state due to loss of what via kidneys

A

antithrombin 3

80
Q

left variocele - (due to occlusion of left testicular vein)

A

RCC

endocrine effects: may secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH

80
Q

v A 21-year-old female complains of dysuria for the past week, despite just completing a three day course of trimethoprim. Urine dipstick is positive for blood + and leucocytes +. A MSSU shows no organism.

A

Features of Chlamydia
asymptomatic in around 70% of women and 50% of men
women: cervicitis (discharge, bleeding), dysuria
men: urethral discharge, dysuria

80
Q

A 13-year-old girl presents to her GP with her father as she is concerned about recently gaining weight. She feels that her hands and feet have got ‘fatter’ in the last few weeks and she has had to buy larger shoes as her old ones no longer fit. She also says that her face looks rounder and puffier than it used to. A routine review of symptoms reveals no other problems except when passing urine, she has noticed her urine looks very frothy.

ph 6.1
protinuria
albumin low

A

Oral prednisolone + urgent outpatient referral to paediatrics

This girl has presented with a classical nephrotic syndrome. The majority of cases in childhood are due to minimal change disease which is nearly always responsive to oral steroid therapy. For this reason, a renal biopsy is not indicated unless there is no response to steroid therapy. Treatment with cyclophosphamide would be second line in people not responding fully to oral steroids.

81
Q

Causes of bilaterally enlarged kidneys - mnemonic change of SHAPE:

A

Scleroderma
HIV nephropathy
Amyloidosis
Polycystic kidneys
Endocrinology i.e. diabetes

81
Q

Sevelamer

A

non-calcium based phosphate binder that treats hyperphosphataemia in patients with CKD mineral bone disease

82
Q

nephrotic syndrome do you get DVT

A

yes

hypercoagulable state due to loss of antithrombin 3 and plasmingoen via kidneys

83
Q

what is the daily glucose requirement of a person

A

When prescribing fluids, the glucose requirement is 50-100 g/day irrespective of the patient’s weight

84
Q

Renal impairment, flank masses, hypertension →

A

ADPKD

85
Q

A 69-year-old woman with a history of well-controlled temporal arteritis presents to the emergency department following a collapse at home, and is complaining of severe persisting abdominal pain. Her husband reports that she has been following her daily steroid regime, and that she has recently been recovering from ‘a nasty bout of flu’. Initial observations and examination identify a low-grade fever and generalised abdominal tenderness, with a GCS of 13/15.

Which of the following acid-base imbalances would be most expected in this patient, given the likely underlying pathology?

A

Hyperkalaemic metabolic acidosis

Addison’s disease/adrenal insufficiency can cause hyperkalaemic metabolic acidosis

86
Q

what drug can cause polyuria

A

lithium

87
Q

look for uraemia in ckd as

A

need dialysis

88
Q

what problem in the lungs is often an indication for haemodialysis in a patient with aKi

A

pulmonary oedema

89
Q

pt with polydipsia an dpolyuria

Plasma osmolality 315 mOsm/kg (275-300 mOsm/kg)
Urine osmolality 190 mOsm/kg (100-1000 mOsm/kg)
Na+ 152 mmol/l

what is problem

A

DI

Diabetes insipidus (DI) is characterized by impaired water resorption by the kidney as a result of lack of ADH secretion by the posterior pituitary (cranial DI) or reduced sensitivity of the kidneys to the action of ADH (nephrogenic DI). Biochemistry reveals a high/borderline high plasma osmolarity (patient always feels thirsty and tries to replace the lost fluid to lower plasma osmolarity) with an inappropriately low urine osmolarity (the patient complains of production of large amounts of very dilute urine as a result of reduced water resorption in the kidney).

In normal physiology an increase in urine osmolarity (ADH working normally to maintain homoeostasis) will occur in response to water deprivation. This acts to maintain a normal plasma osmolarity. However, in cranial DI patient there is a rise in plasma osmolarity with production of low osmolarity urine until exogenous ADH (vasopressin) is given. In nephrogenic DI patients, the same plasma and urine osmolarity changes occur but there is no response to the exogenous vasopressin.

90
Q

can hyperacute trasnpalnt rejection be treated

A

no you need to remove the graft

91
Q

Paracetamol overdose: risk factors

A

The following groups of patients are at an increased risk of developing hepatotoxicity following a paracetamol overdose:
patients taking liver enzyme-inducing drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s Wort)
malnourished patients (e.g. anorexia nervosa) or patients who have not eaten for a few days

Interestingly, acute alcohol intake, as opposed to chronic alcohol excess, is not associated with an increased risk of developing hepatotoxicity and may actually be protective

92
Q

Ciclosporin side-effects:

A

everything is increased - fluid, BP, K+, hair, gums, glucose

93
Q

metformin in mi yes or no

A

Metformin should be stopped following a myocardial infarction due to the risk of lactic acidosis. It may be introduced at a later date. Diabetic control may be achieved through the use of a insulin/dextrose infusion (e.g. the DIGAMI regime)

94
Q

Extra-renal features of ADPKD include:

A

Extra-renal features of ADPKD include:
Hepatic cysts which manifest as hepatomegaly
Diverticulosis
Intracranial aneurysms
Ovarian cysts

95
Q

what is antithrombin III and its function

A

Antithrombin III is a naturally occurring anticoagulant. It is a serine protease inhibitor that inactivates thrombin and factors IXa, Xa, XIa, and XIIa, and thereby limits the coagulation cascade.

Y3/4- 5 Nephrology (10 decks)

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