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
mx of HUS
supportibve and fludis
26
This question has a 55-year-old man presenting with progressive weakness and dyspnoea, hepatomegaly, proteinuria and worsening renal functio
amyloidosis
27
HSP do they most likely make a full renal recovery
yes
28
unexplained visible haematuria without UTI next best steps
2ww
29
if someone has haemuatria what is the first thing you should do
rule out UTI
30
right sided testicular swelling - bag of owrms
RCC
31
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?
Loss of antithrombin III in the urine leading to hypercoagulable state this and increased risk of thrombus formation
32
famialil hypercholesteromaia values
TC over 7.5 LDL over 4.9 kids 6.7 TC an 4 LDL
33
how long beofre conecption shtop staitns
3 months
34
crohns causes what type of renal stones
calcium oxalate
35
uti infection what kind of renal stones
striuvite
36
thiazide diuretics do they raise or lower potassium?
lower it
37
mononeutitis multiplex
seen in vasuclitis and in one particualr nerve
38
to be diagnosed with renal artery stenosis have much of artery has to be occluded
60%
39
Antistreptolysin-O
recent strep infection
40
renal vasucalr disease get bruit - in renal artery stenosis what is major cuase in young people
fibromuscular dysplasia
41
ureaemia sx
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
tolvapatan moa
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
recurrent UTI makes you think of
posterior urethral valves
44
hyaline cast scaued by
loop diuretics and exercise nephritic red cell casts
45
sterile pyuria caused by
TB sti and ANW
46
ketamine cystitis
thcikened bladder wall
47
how logn till you can drive after successful angio
1 week
48
how long can you drive aftr unsucceeful angio
6w
49
reinfarction of MI
CK_mB
50
sexual activity how long after angio
2w
51
fibromuscular dysplasia
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
lupus nephritis how many syndromes
6 4 - nephriict - high dose steriod type 1 - GBM
53
following tx with ACEi in HTN in RAS what scan do you need
CT MRI renal angiography
54
unexlianed AKI what do you need
USS
55
calcitriol does what
increase uptake of Ca from GI
56
why do creatinine levels rise on ACEi
reduced glomerular filtatration pressure to sless creatine is excreted
57
gram postiive or negative produce nitries
gram negative
58
drug cause of nephrogenic DI
lithium
59
what drug can cuase SIADH
fluoxetine
60
maxamine time bag of potassium can be infused through peripheral line
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
4 things to remember to examine with AV fistula
Skin integrity Aneurysms Palpable thrill (a fine vibration felt over the anastomosis) A “machinery murmur” on auscultation over the fistula
62
complications with a fistula
Aneurysm Infection Thrombosis Stenosis STEAL syndrome High-output heart failure
63
what is STEAL syndrome
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
ckd mostly asx what are some sx if they present
Fatigue Pallor (due to anaemia) Foamy urine (proteinuria) Nausea Loss of appetite Pruritus (itching) Oedema Hypertension Peripheral neuropathy
65
Medications that help slow the disease progression in ckd are:
ACE inhibitors (or angiotensin II receptor blockers) SGLT-2 inhibitors (specifically dapagliflozin)
66
Reducing the risk of complications in ckd involves:
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
ACE inhibitors are offered to all patients in ckd with: 3 things DM htn
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
6 top causes of nephortic syndrome in adults
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
sx of nephrotic what are you predisposed too
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
what is HUS
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
presentation of HUS
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
what is the management of HUS
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
all diabetic patients require annual screening for what test
Albumin:creatinine ratio (ACR) in an early morning specimen
74
in addition to low platelets in HUS what else is low
Serum haptoglobins (which bind haemoglobin) and the platelet count are decreased in haemolytic uraemic syndrome.
75
how does an insulin dextrose infusion work
work by shifting potassium from extracellular to intracellular fluid compartments
76
what electrolyte balance indicates whether kidney disease is acute or chronic
Hypocalcaemia is an indication that kidney disease is chronic and not acute
77
acute graft failure what signs
rising creatinine, pyuria and proteinuria
78
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?
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
Nephrotic syndrome is associated with a hypercoagulable state due to loss of what via kidneys
antithrombin 3
80
left variocele - (due to occlusion of left testicular vein)
RCC endocrine effects: may secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH
80
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.
Features of Chlamydia asymptomatic in around 70% of women and 50% of men women: cervicitis (discharge, bleeding), dysuria men: urethral discharge, dysuria
80
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
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
Causes of bilaterally enlarged kidneys - mnemonic change of SHAPE:
Scleroderma HIV nephropathy Amyloidosis Polycystic kidneys Endocrinology i.e. diabetes
81
Sevelamer
non-calcium based phosphate binder that treats hyperphosphataemia in patients with CKD mineral bone disease
82
nephrotic syndrome do you get DVT
yes hypercoagulable state due to loss of antithrombin 3 and plasmingoen via kidneys
83
what is the daily glucose requirement of a person
When prescribing fluids, the glucose requirement is 50-100 g/day irrespective of the patient's weight
84
Renal impairment, flank masses, hypertension →
ADPKD
85
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?
Hyperkalaemic metabolic acidosis Addison's disease/adrenal insufficiency can cause hyperkalaemic metabolic acidosis
86
what drug can cause polyuria
lithium
87
look for uraemia in ckd as
need dialysis
88
what problem in the lungs is often an indication for haemodialysis in a patient with aKi
pulmonary oedema
89
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
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
can hyperacute trasnpalnt rejection be treated
no you need to remove the graft
91
Paracetamol overdose: risk factors
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
Ciclosporin side-effects:
everything is increased - fluid, BP, K+, hair, gums, glucose
93
metformin in mi yes or no
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
Extra-renal features of ADPKD include:
Extra-renal features of ADPKD include: Hepatic cysts which manifest as hepatomegaly Diverticulosis Intracranial aneurysms Ovarian cysts
95
what is antithrombin III and its function
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.